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371 Cards in this Set
- Front
- Back
- 3rd side (hint)
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fischer projection
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not cyclic
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The O in the haworth projection of monosaccs comes from C #?
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5
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C # 6 is what C# in the haworth projection?
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it is still C#6
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alpha means
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down
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beta means
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up
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sucrose linkages
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1,2
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maltose linkages
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1,4
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lactose linkages
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1,4
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reducing sugar:
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Has a free anomeric C
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NON reducing sugar =
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sucrose
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fatty acids release more energy per unit of
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weight (probably other things too)
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unbranched starch
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amylose
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branched starch
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amylopectin
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two types of starch
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amylose and amylopectin
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cellulose linkages
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beta 1,4
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starch linkages
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alpha 1,4
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major enzyme that hydrolyzes dietary polysaccs
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alpha amylase
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alpha amylase hydrolyzes what kind of linkages?
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alpha 1,4 of glc units
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alpha amylase is found
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a bit in the saliva, but mostly in the stomach and si
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enterocytes
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cells that line the villi of the si
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where are carbs absorbed?
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into the enterocytes
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what kind of cells are enterocytes?
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epithelial
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microvilli aka
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brush border
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where is the brush border found?
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On top of the enterocytes, which are on the villi
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alpha amylase is secreted in the si by
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pancreatic exocrine cells
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enzymes found on the brush border
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isomaltase, maltase, sucrase, lactase,
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two broad types of enyzmes for carb digestion:
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pancreatic and intestinal enzymes are both necessary
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where are disaccharidases found
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on the brush border
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lactase breaks down
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lactose-> glc + gal
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isomaltase breaks down
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alpha dextrins
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maltase breaks down
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maltotriose and maltose
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intestinal enzymes for carb digestion:
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isomaltase, maltase, sucrase, lactase
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surface area of brush border =
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300 m2
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SGLT is
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sodium glc transporter. It transports glc (or gal) with Na into the enterocyte.
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how do enterocytes uptake glc?
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through specific carrier proteins
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does the SGLT require energy?
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no
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absorption process of SGLT relies on
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sodium potassium pump
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SGLT uses up energy?
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nope. But it is energy DEPENDENT.
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SGLT is passive or active transport?
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active
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each mole of glc transported into the enterocytes must be cotransported with:
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a mole of Na
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How the Na/K pump works:
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It takes 1 ATP to pump out 3 Na out of the cell, and at the same time, 2 K are brought in.
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purpose of K in the Na/K pump?
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It helps to replenish the positive charge in the cell that the 3 Na atoms just left. This allows the Na's to continue to move down the concentration gradient.
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SGLT has a high affinity for
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gal.
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Glc competes with ___ to be absorped
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Gal
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GLUT 5 absorption is active or passive?
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passive
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GLUT 5 can absorb:
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Glc, Gal and Fructose
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SGLT can absorb:
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Glc and Gal
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GLUT 5 is what kind of carrier?
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A Concentration dependent carrier
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GLUT 5 transports monosaccs from where to where?
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From the SI into the enterocyte
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Which is slower at transporting molecules into the enterocyte, GLUT 5 or SGLT?
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GLUT 5 (it's passive)
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GLUT 2 transports monosaccs from where to where?
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enterocyte to the blood
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Where is another place GLUT 2 is found?
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liver cells
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why does glc have to go through a carrier protein to be absorbed?
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it's highly polar
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most cells take up glc actively or passively?
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passively
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where is glut1 located?
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bbb, placenta, rbc
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where is glut 2 located?
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pancreatic beta cells
si liver kidneys |
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which glut has bidirectional transport of glc?
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liver
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where does bidirectional transport of glc occur? and which carrier protein?
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liver
glut 2 |
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where is glut3 located?
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brain cells
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where is glut4 located
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adipocytes
muscle |
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conc of what glut is insulin dependent
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glut4
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relationship between insulin and glut4?
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directly proportional
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glut related to type 2 diabetes?
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glut 4. The glut4 activity is insufficient, therefore the blood sugar remains high
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where is glut7 located?
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ER of hepatocytes
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glycolysis takes place in the
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cytolsol
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cells that have glycolysis as their only form of energy production
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rbc
lymphocytes testicular cells eye lens cells |
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how many atp are produced in glycolysis
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4
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how many atp are consumed in glycolysis
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2
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net ATP production in glycolysis is
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2
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insulin regulates these enzymes in glycolysis
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glucokinase
phosphofructo 1 kinase pyruvate kinase |
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insulin's effect on glycolysis pathway
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promotes it
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unique quality about all the reactions that insulin regulates in glycolysis
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they are all IRreversible
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1st step of glycolysis:
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glc phosphorylated to form glc-6-P
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what provides the P for the first step of glycolysis?
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ATP
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what steps are the ATP consumed in in glycolysis?
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1 and 3 and
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1st step of glycolysis is catalyzed by
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glucokinase or hexokinase
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glucokinase is found in the
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liver and pancrease
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hexokinase is found in the
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all other cells bu the liver and pancrease
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2nd step of glycolysis?
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glc-6-P to Fru-6-P
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Reaction 2 of glycolysis is catylzed by
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glucose isomerase
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rxn 3 of glycolysis is:
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fru 6 P to Fru 1,6 biP
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rxn 3 of glycolysis is catalyzed by
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PFK
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rate limiting step of glycolysis is
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step 3 (fru6 P) to Fru1,6 bisP
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Fru 1,6 biP turns into:
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DHAP and GA3P
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glc6P turns into
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Fru-6-P
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Fru-6-P turns into
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Fru-1,6-BisP
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Fru-1,6-BiP to the two compounds in catalyzed by
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aldolase
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fru6P to fru1,6biP is catalyzed by
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PFK
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what reactions in glycolysis produce ATP?
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PEP to pyruvate (2 ATP)
1,3 bisphosphoglycerate to 3 phosphoglycerate (2 ATP) |
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benefit of converting pyruvate to lactate?
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NAD is regenerated.
(NADH is oxidized to NAD) |
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Fate of pyruvate if it enters the mitochondria?
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It is oxidized to acetyl coA
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uses of lactate:
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precursor for glc in the liver
fuel for muscles |
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what is a kinase?
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An enzyme that phosphorylates its substrates
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how many moles of ATP are produced per every mole of Glc?
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4 moles of ATP
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where does pyruvate move to when oxygen is present?
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Into the mitochondria to be converted to AcCoA
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TCA stands for
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tricarboxylic acid
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this is used to form AcCoA
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Coenzyme A
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when is NADH utilized for energy?
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When it is oxidized by the ETC
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Hydrogen acceptors in the TCA cycle?
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FAD and NAD
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NAD to NADH is ox or red?
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reduction
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how much energy is in GTP compared to ATP?
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equal amounts
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How does the body obtain energy?
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by oxidizing nutrients
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How are the H atoms and electons removed from nutrients so they can get energy?
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dehydrogenase reactions
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After H atoms and electrons are removed from nutrients how do they produce energy?
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They go through the ETC which results in the release of energy
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The energy released from the ETC is used to do what?
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Generate ATP and produce body heat
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each component of the ETC can donate AND accept electrons?
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yes.
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When a compound donates electrons is it ox or red?
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it is oxidized
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molecule that receives electrons is ox or red?
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reduced
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How is energy liberated in the ETC?
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when electrons flow btw acceptor/donor pairs
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End result of the protons from the ETC?
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transferred to O to form water
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what happens to the protons in the cytochromes?
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They don't go through the cytochromes, but are released from CoQ into the matrix. They eventually combine with O to form water.
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What happens to the electrons in the cytochromes?
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They are released from CoQ into the cytochromes and are transferred amoung the cytochromes. Eventually they are released to combine with O to form water.
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ATP is produced at how many sites in the ETC?
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up to 3
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Why does NADH produce 3 ATP?
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B/c it starts at the beginning of the ETC and goes through all 3 ATP production sites.
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why does FADH2 only produce 2 atp?
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B/c it doesn't start at the beginning of the etc, but instead gives its electrons directly to CoQ which means it missed 1 ATP production site.
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how many kcal are in each ATP?
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7.5 kcal = 1 ATP
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when an NADH is oxidized in the ETC, how many kcal of energy is liberated?
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52.6 kcal of energy.
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How much of the energy liberated by the ETC is conserved in ATP?
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40%. The rest is released as body heat.
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chemical reaction for the oxidation of glc:
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C6H12O6 + 6O2 = 6CO2 + 6H2O
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Energy is captured in the bonds of ATP?
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yes
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How many NADH are produced in glycolysis
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2
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whole point of the tca cycle
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to remove hydrogen atoms and ectrons and place them onto FAD and NAD.
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How many H atoms and electrons are involved in dehydrogenase reactions?
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2 H atoms and
2 electrons are transferred to the acceptors in dehydrogenase reactions |
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This is necessary for FADH2 and NADH to be oxidized in the ETC
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Oxygen
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What kind of phosphorylation occurs in glycolysis
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substrate phosphorylation
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including ETC, how many ATP are produced from glycolysis?
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8
(2 ATP) (2 NADH) |
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how many ATP produced from pyruvate dehydrogenase reaction (pyruvate to AcCoA)?
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6 ATP
(2 NADH) |
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how many ATP produced from 1 glc in the tca cycle
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24 ATP
(6 NADH) (2 GTP) (2 FADH) |
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Total ATP produced from 1 glc?
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38 ATP
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Max number of ATP that can be produced from 1 glc?
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38 ATP
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What are the two carriers that can shuttle the H atoms from the NADH produced in glycolysis into the mitochondria?
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malate-aspartate
glycerol 3 phosphate |
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Where does the malate shuttle work
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heart, liver and kidney
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Where does the glycerol 3 phosphate shuttle work?
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brain and muscles
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H acceptor in the malate shuttle?
|
NAD
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H acceptor in the glycerol 3 P shuttle?
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FAD
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Which shuttle system for the NADHs from glycolysis produces the most ATP in the end?
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The malate shuttle. (B/c it uses NAD as its acceptor)
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Which shuttle system for the NADHs from glycolysis produces less ATP in the end?
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The glycerol 3 phosphate system.
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How much ATP is produced if the glycerol 3 phosphate shuttle is used for both NADHs?
|
36
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Malate shuttle cycle goes:
|
malate to Oaa to aspartate to Oaa to Malate.
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What two things actually cross the membrane in the malate shuttle cycle?
|
malate and aspartate
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which is more reduced, malate or Oaa?
|
malate is more reduced
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High levels of NADH inhibit
|
alpha ketogluterate dehydrogenase and isocitrate dehydrogenase.
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what accumulates when NADH inhibits 2 dehydrogenase enzymes in the TCA?
|
citrate accumulates
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Can AcCoA directly cross the mitochondrial membrane?
|
nope. There is no carrier directly for it.
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the energy abudance signal is
|
citrate
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When citrate accumulates it...
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crosses the mitochondrial membrane into the cytosol and is cleaved into AcCoA and OAA
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carbon dioxide plus AcCoA =
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malonyl CoA
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what catalyzes the reaction that forms malonyl CoA?
|
acetyl CoA carboxylase
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what rxn requires biotin as a cofactor?
|
AcCoA + Co2 = malonyl CoA
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What activates AcCoA carboxylase?
|
citrate and insulin
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what are fatty acids formed from?
|
condensed malonyl CoA units
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citrate suppresses ____ how?
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PFK
allosteric modulator |
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The rate limiting step of glycolysis is catalyzed by what enzyme?
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PFK
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Allosteric modulator
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a compound binds to an enzyme somewhere other than the active site and either inhibits or promotes it
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When PFK is inhibited by citrate (when there's an excess of it), what results?
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An increase in Fru 6 Phosphate
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Glc 6 Phosphate can be transformed into
|
D ribose 5 Phosphate
|
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the hexose monophosphate shunt is what?
|
Pathway that turns glc6phosphate into D-ribose-5-phosphate
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Where does the hexose monophosphate shunt take place?
|
adipose
thyroid liver adrenal cortex testicular gland lactating mammary glands |
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Products of the hexose monophosphate shunt?
|
NADPH and pentose phsphates (ribulose-5-phosphate and ribose-5-phosphate)
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What is used to synthesize nucleotides?
|
ribose-5-phosphate
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NADPH is used for
|
synthesis of FA
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How does insulin effect glycogen synthesis
|
positively
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where is glycogen stored?
|
liver and muscles
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How much glycogen is typically in the liver?
|
it varies from meal to meal
|
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What cells are dependent on glc for fuel?
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rbc and brain cells
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Can the brain use any fuel besides glc?
|
yes, can use ketones. but glc is still important for utilization of ketones and proper brain function
|
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minimum carb requirement?
|
80g/d
|
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can FA be used as things to make glc?
|
nope
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What must you have in order to use FA for fuel?
|
you must have a small amount of glc
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what does the body rely on to provide the C's for the OAA
|
glc and aa
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gluconeogenesis occurs in the (where in the body)
|
liver primarily
sometimes the kidney during prolonged starvation |
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insulin effect on glycolysis
|
promotes it
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insulin effect on glycogenesis
|
promotes it
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what hormones promote the breakdown of fuel sources and the synthesis of glucose
|
epi
glucagon glucocorticoids |
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where does glucagon come from?
|
the alpha cells of the pancreas
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primary glucocorticoid
|
cortisol
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where are glucocorticoids produced?
|
adrenal cortex
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what regulates the release of glucocorticoids
|
hypothalamus
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where is epi released from?
|
adrenal medulla
|
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3 groups of glucogenic things:
|
1. glucogenic aa
2. lactate 3. glycerol |
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body part Sources of glc precursors?
|
rbc
muscle adipose |
|
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|
what body part doesn't have a glucoagon receptor?
|
the muscle cells
|
|
|
|
how is the muscle used as a source of glucogenic precursors?
|
1. b/c of no glucagon receptor on muscle cells, GCC can go in and bind to the DNA of the cell.
2. mRNA transcriptions are stimulated that code translations of enzymes that catabolize the muscle 3. AA especially Ala are released into the blood |
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what form is glc in in the muscle?
|
glc 6 phosphate
|
|
|
|
enzyme that the muscles lack? what is the effect?
|
glc 6 phosphatase. The glc from glycogen in muscles is all pretty much used in the muscles, and isn't released into the blood.
|
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what body part provides the most glc to the body?
|
the liver
|
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What two things can the muscles provide as glc precursors?
|
aa and lactate
|
|
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|
effect of Glucagon and epi on adipose cells?
|
stimulate breakdown of triglycerides
|
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|
|
catabolism of triglyceride leaves you with"
|
glycerol
'3 FA |
|
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how are FA transported to the liver?
|
albumin carries tehm
|
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|
build up of AcCoA results in
|
inhibiting pyruvate dehydrogenase
|
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during hypoglycemia when FA are transported to liver, what happens?
|
FA are oxidized to produce ATP
AcCoA is produced |
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when pyruvate dehydrogenase is inhibited by excess AcCoA, what happens to pyruvate?
|
It is instead converted into OAA and then used as a glucogenic precursor
|
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When hypoglycemia is going on, what happens in rbc?
|
their pyruvate is reduced to lactate which is then released into the blood and used as a glucogenic precurosr.
|
|
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The first step for lactate and glucogenic aa in gluconeogenesis?
|
being converted to pyruvate
|
|
|
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pyruvate to lactate reaction is reversible?
|
Yes
|
|
|
|
enzyme that catalyzes pyruvate to lactate is:
|
lactate dehydrogenase
|
|
|
|
How is Ala converted to pyruvate?
|
transamination
|
|
|
|
Is pyruvate a precursor for glc?
|
yes
|
|
|
|
effect of glucagon and epi on adipose cell
|
stimulates breakdown of triglyceride
|
|
|
|
The 3 enzymes in gluconeogenesis that replace the enzymes in the irreversible reactions
|
glucose 6 phosphatase
fru 1,3-bisphosphotase pyruvate carboxylase |
|
|
|
effect of pyruvate carboxylase
|
pyruvate to OAA (first step in gluconeogenesis or reversal of glycolysis)
|
|
|
|
pyruvate carboxylase requires what cofactor?
|
biotin
|
|
|
|
AcCoA effect on pyruvate cavoxylase?
|
positive
|
|
|
|
when insulin is low, effect on glycolysis?
|
suppresses glycolysis
|
|
|
|
In the fasting state does pyruvate come from glc or glucogenic precursors?
|
glucogenic precursors
|
|
|
|
in order for Oaa to go through the mitochondrial membrane it must be transformed into what:
|
Aspartate or malate
|
|
|
|
rate limiting step of gluconeogenesis
|
OAA to PEP (second step)
enzyme: PEP carboxykinase |
|
|
|
what happens to glc after it is made by gluconeogenesis?
|
Transported into the blood through GLUT 2
|
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What happens to the glycerol released from the catabolism of triglyceride by glucagon
|
goes to the liver where it is phosphorylated by glycerol kinase to form glycerol 3 phosphate.
From there it is turned into DHAP and continues on in gluconeogensis. |
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where is most of the glycogen stored?
|
muscles
|
|
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|
ave store of glycogen is
|
350 g (1400 kcal)
|
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|
|
where does the glc come from to fuel the body when glycogen breaks down?
|
liver
|
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|
enzyme that cleaves glc units from glycogen
|
glycogen phosphoylase
|
|
|
|
how is glycogen phosphorylase activated?
|
through a series of enzymatic events or triggers
|
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|
|
The advantage of having a series of enzymes trigger glycogen phosphorylase is:
|
signal amplification, more rapid breakdown of glycogen
|
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|
|
signal amplification in glucose phosphorylase is:
|
100 fold increase in amplification with each successive enzyme. Resulting in an 100 million x greater strength in the final enzyme than if only one enzyme had been used to activate it.
|
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|
phosphorolysis is
|
lysis of a bond with the addition of a phosphate
|
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|
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what cleaves the alpha 1,6 bonds of glycogen
|
debranching enzyme
|
|
|
|
what receptors does the muscle cell have that stimulate glycogen breakdown?
|
epi and gcc
|
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The end product of glycogen lysis in muscles is:
|
glc 6 phosphate.
|
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|
|
the glc 6 phosphate left at the end of glycogen lysis in muscles then does what?
|
goes throuhg glycolysis and tca to make ATP.
OR stops at pyruvate, is converted to lactate and goes to liver to be converted into glc |
|
|
|
why do you get more ATP when you go straight from glycogen to ATP in the muscles?
|
B/c it skips the first step of glycolysis which uses 1 ATP
|
|
|
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insulin drives what pathways?
|
glycogenesis
glycolysis |
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glucagon drives what pathways?
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glycogenolysis
gluconeogenesis |
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what kind of cells are the alpha and beta cells of the pancreas?
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endocrine
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where are the alpha and beta cells of the pancreas located?
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on the islets of langerhans
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what do the exocrine glands of the pancrease secrete?
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digestive enzymes (alpha amylase)
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what do the endocrine glands of the pancreas secrete?
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hormones: glucagon and insulin
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what receptors are the muscles missing?
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glucagon receptors
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Three pathways insulin promotes
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FA synthesis
Glycogen synthesis Glycolysis |
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how does insulin promote glycogenesis?
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supports glycogen synthase
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what does epi stimulate?
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glycogenolysis in the muscles and liver
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What do the gcc's stimulate?
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gluconeogenesis
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how does gcc stimulate gluconeogenesis?
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stimulate all of the gluconeogenesis specific enzymes
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Three pathways insulin promotes
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FA synthesis
Glycogen synthesis Glycolysis |
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how does insulin promote glycogenesis?
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supports glycogen synthase
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what does epi stimulate?
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glycogenolysis in the muscles and liver
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What do the gcc's stimulate?
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gluconeogenesis
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how does gcc stimulate gluconeogenesis?
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stimulate all of the gluconeogenesis specific enzymes.
Also, promotes muscle degradation when needed. |
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is it bidirectional movement in the GLUT2 in the SI?
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no. it's unidirectional
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How does the liver maintain a concentration gradient so glc will keep flowing in?
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it converts some glc to glc 6 phosphate
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which has a higher buffering capacity? glucokinase or hexokinase?
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glucokinase
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is the liver capable of buffering the bld glc level?
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yes
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high levels of ____ in the ____ indicate energy abundance
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citrate in the cytosol
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AMP effect on glycolysis
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positive
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AMP effect on gluconeogenesis
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negative
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Fru 1,6 bisphosphate effect on glycolysis
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positive (feed forward mechanism) stimulates pyruvate kinase
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Fru 2,6 bisphosphate effect on glycolysis and gluconeogenesis
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stimulates glycolysis
inhibits gluconeogenesis |
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how does Fru2,6bisphophate inhibit gluconeogenesis
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inhibits fru1,6,bisphophatase
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how does fru2,6bisphophate stimulate glycolysis
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stimulates PFK
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alanine's effect on glycolysis
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inhibits it by inhibiting pyruvate kinase
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is ethanol a nutrient?
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no. but it does have calories
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what causes the ADH way of metabolizing alc to be inhibited?
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excessive alc
not enough NAD available ADH is saturated with ethanol |
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where is the MEOS located
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cytosol
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what is oxidized in MEOS?
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NADPH
ethanol |
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what is used in MEOS instead of NAD?
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NADPH
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what pathway is MEOS similar to?
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ETC
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can MEOS only metabolize alc?
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nope. other stuff too.
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what is reduced in MEOS?
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oxygen (forms water)
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can you develop an ethanol tolerance?
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yes. you can build up a tolerance to ethanol.
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Effect of building up a tolerance to ethanol?
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can increase the body's needs for some other nutrients such as vit A
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what toxic substance do both MEOS and ADH systems produce?
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acetaldehyde
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what is it that causes damages to the body's tissue from alc?
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acetaldehyde. When large amounts are consumed, it can't be metabolized to acetate fast enough before causing damage.
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what is cirrohis?
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liver's ability to store and metabolize nutrients is compromised
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nutrients affected by alcoholism
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vit a, thiamin, folic acid, vit k, nicotinic acid
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what state causes pyruvate to produce lactate?
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high levels of NADH caused by high alcohol intake
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pyruvate to lactate is catalyzed by what enzyme?
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lactate dehydrrogenase
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result of too much NADH during alc consumption?
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lactate is produced, go into lactic acidosis.
Reactions that use NAD are suppressed |
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regular consumption of alc leads to
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fatty liver and fat deposition other places
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why is it that fat deposition occurs with heavy alc consumption?
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b/c of high NADH levels, reactions that utilize NAD are suppressed (dehydrogenase reaction). The first two dehydrogenase reactions in the TCA are suppressed resulting in a rise in citrate. Citrate moves to the cytosol and is cleaved to oaa and acCoA, which is then used to form malonyl CoA.
Also, production of glycerol 3 phosphate occurs. |
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which type is insulin dependent?
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type 1
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What happens when insulin levels are low
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hepatic glc output promoted
glc oxidation is inhibited glycogenysis inhibited lipogenesis inhibited |
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impaired glc utilization effects metabolism of protein and fats?
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yes
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lipids are soluble in ___ solvents
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organic
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lipids include fat soluble vitamins?
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yes
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fatty acids contain how many C atoms
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4 - 24
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C double bonds in FA are in cis or trans form?
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either. mostly in cis form.
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common name for hexanoic acid
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caproic acid
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which one of the irreversible enzymes in glycolysis is not stimulated by insulin?
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hexokinase
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insulin affect on FA synthesis
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insulin promotes it
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low insulin effect on glycogenolysis?
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glycogenolysis is going to be accelarated
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insulin effect on glycogenesis?
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promotes it
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where does the pyruvate dehydrogenase reaction occur?
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mitochondria
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The two essential FA are:
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linoleic acid
linolenic acid |
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why can't our body make the essential FA?
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we can't form C-C double bonds past the 9th C.
(they can still form a double bond at C 9) |
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what is the notation for linoleic acid?
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(C18:2 n-6)
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notation for linolenic acid?
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C18:3 n-3)
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how can the body alter FA?
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elongation: adding 2 C units at the carboxyl end.
Desaturation: |
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how many C do eicosanoids contain?
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20 C
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3 groups of eicosanoids
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prostaglandins
thromboxanes leuktrienes |
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how do we get eicosanoids?
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we produce them in the body. Part of it is by adding oxygen
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which FA are precursors to eicosanoids?
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arachidonic
eicostrienoic acid eicosapentaenoic acid (EPA) |
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how do we obtain the FA that are precursors to eicosanoids?
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from the diet OR
by synthesizing them from essential fa |
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where do prostaglandins and thromboxanes effect?
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only the cells in which they are synthesized
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where do hormones affect?
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can effect tissues other than the ones they are formed in
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are triacylglycerols solid or liquid?
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can be either
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how are FA released from triacylglycerols?
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lipase
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what kinds of organisms are cholesterol and cholesterol esters found in?
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only animals
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what is a precursor for many steroids in the body?
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cholesterol
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what are the glucocorticoids synthesized from?
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cholesterol
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what are phospholipids made up of
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phosphate group and FA
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lechithin is
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phosphotidylcholine
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glyolipid:
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lipids with a carb componet.
serve as recognition markers on cells |
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triacylglycerol in the adipocyte is hydrolyzed by
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intracellular lipase aka hormone sensitive lipase
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intracellular lipase aka
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hormone sensitive lipase
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intracellular lipase is stimulated by
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epi and glucagon
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what happens after glucagon and epi stimulate the fat cell?
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The G protein is acitvated which activates
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adenylate cyclase
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what does adenylate cyclase do?
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converts ATP to cyclic AMP (cAMP)
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where do the FA (which have been released from an adipocyte) go?
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to muscles, liver. Where does the glycerol go?
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liver
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why isn't free glycerol utilized in the adipocyte?
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glycerol kinase is not present in adipocytes. What does glycerol kinase do?
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glycerol --> glycerol 3 phosphate
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where in the cell does beta oxidation take place?
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mitochondria
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how is a FA transported into the mitochondria?
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The FA must be attached to CoA, forming a fatty acyl CoA.
Then what must happen? |
The fatty acyl CoA must be carried by carnitine
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what does CAT 1 stand for?
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carnitine acyltransferase 1.
what does it do? |
forms a covalent bond btw the fatty acyl and carnitine
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what does CAT 2 do?
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Reforms the fatty acyl CoA once it is in the matrix of the mitochondria
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what is the alpha C in a FA?
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C 2
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why is it called beta oxidation?
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b/c the FA is cleaved at the beta C
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how much ATP is USED during the whole process of beta oxidation?
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2 ATP equivalents (ATP --> AMP + PPi)
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oxidation of AcCoA = __ ATP
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12
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how many ATP would be produced from a 14 C saturated FA chain
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129
8 AcCoA X 12 = 96 5 x 7 = 35 - 2 ATP = 129 |
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how many less ATP are generated for unsaturated FA?
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2 less ATP for every double bond.
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unique property of odd numbered FA?
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they are glucogenic. the last 3 C's make propionyl CoA. how?
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propionylCoA is oxidized to succinyl CoA, which can be used to form glc.
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3 ketone bodies
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acetone
acetoacetate beta hydroxy buterate |
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ketogenesis:
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AcCoA used to form ketone bodies
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when is ketogenesis accelarated
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when fat intake is high
when Carb intake is low |
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when is FA oxidation accelarated?
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when fat intake is high
when carb intake is low |
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Where (body parts) does beta oxidation take place?
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in the liver muscles and other orangs
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where does the glycerol go after being released from the adipocyte?
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liver
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what happens when there is no glc available and beta oxidation is taking place?
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AcCoA is elevated in the mitochondria b/c it doesn't have oaa to combine with.
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when AcCoA concentration in mitochondria is high...
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ketone bodies are synthesized
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after ketone bodies are produced, what happens?
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acetoacetate and betahydroxybutyrate go to organs and are converted to AcCoA
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oaa can be made from
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pyruvate
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pyruvate dehydrogenase is inhibited by
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acCoA and ATP and NADH
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where are ketone bodies synthesized?
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liver
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3 ways to get AcCoA
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oxidation of pyruvate
oxidation of FA degradation/transamination of ketogenic aa |
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where does FA synthesis occur?
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cytosol
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how does AcCoA cross the mitochondrial membrane to get to the cytosol
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combines with oaa to form citrate
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can pyruvate cross the mitochondrial matrix?
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yes
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can citrate corss the mitochondrial matrix
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yes
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can oaa cross the mitochondrial membrane?
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nope
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where is AcCoA synthesized?
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in mitochondria
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first step of FA synthesis
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AcCoA combines with oaa to form citrate, and then moves out of the mitochondria and into the cytosol
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NADPH is necessary for
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synthesis of FA and cholesterol
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what is required in the desaturase reactions of FA?
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NADPH (it is oxidized to NADP in the process)
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can a FA be desaturated at C 9?
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yes
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what must happen before a FA can be esterified to a glycerol?
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FA must be attached to a CoA.
what is required to do that? |
2 high energy bonds
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What is the compound that FA are esterified to?
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glycerol 3 phosphate
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hexanoic acid's common name?
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caproic acid
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octanoic acid is aka
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caprylic acid
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decanoic acid
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capric acid
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lauric acid aka
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dodecanoic acid. how many c?
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12
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tetradecanoic acid aka
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myristic acid. how many C?
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14
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hexadecanoic acid aka
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palmitic acid
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formula for oleic acid?
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cis-9 C18:1. systemic name is?
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cis-9-octadecenoic acid
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C20 is aka
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arachidic acid
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arachidonic acid's notation:
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all cis-5,8,11,14-eicosatetraenoic acid
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what happens to hepatic glc output when insulin is low?
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it increases
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what happens to glc oxidation when insulin is low
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it decreases
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what happens to glycogenolysis when insulin is low
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increases
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what happens to lipogenesis when insulin is low?
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decreases
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what does epi control
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glycogenolysis
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what does gcc control?
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gluconeogenesis
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what hormones control glycogenolysis?
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glucagon and epi
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what hormones control gluconeogenesis?
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gcc and glucagon
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benefit of glucokinase low affinity for glucose?
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allows glucokinase to remain significantly active when bld glc is high, allowing large amounts of glc to be trapped in the liver when there is high bld glc. This all works b/c glucokinase doesn't get saturated very easily. Also, keeps it from removing too much glc, when there is low bld glc
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can cells with hexokinase store more or less glc than glucokinase cells?
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glucokinase cells can store more (that's why the liver stores so much glycogen).
why? |
b/c hexokinase is saturated at low concentrations of glc
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what is the action of gluco/hexokinase?
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glc--> glc6 phopshate
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where is most of the glycogen stored in our bodies?
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muscles
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enzyme the muscle is lacking?
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glc 6 phosphate
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what organ(s) provide the glc from glycogen when blood glc is low?
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liver (NOT the muscles. they only provide glc for themselves)
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where in the body are FA oxidized?
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in the liver
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