Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
76 Cards in this Set
- Front
- Back
|
CHO RDA and why
|
130g/day
amount of glucose to fuel brain |
|
|
functions of CHO
|
primary energy source
storage form of energy in liver and muscle - glycogen make up glycoproteins and glycolipids |
|
|
some cells unable to use other fuels
why? |
Because the mitochondria can only use fat for fuel and not all cells have one. Others have to use glucose as fuel.
|
|
|
monosaccharides
Hexoses Pentoses |
hexoses
-glucose -fructose -galactose pentoses -ribose -arabinose |
|
|
disaccharides
|
sucrose
maltose lactose isomaltose |
|
|
polysaccharides (digestible)
|
plant starch
-amylose -amylopectin animal starch - glycogen |
|
|
polysaccharides (undigestible)
|
fiber
-cellulose -hemicellulose -pectin -gums -insulin |
|
|
oligosaccharides
|
raffinose
stachyose |
|
|
Sucrose
|
glucose + fructose
alpha-1,2 |
|
|
Maltose
|
glucose + glucose
alpha-1,4 |
|
|
Isomaltose
|
glucose + glucose
alpha-1,6 |
|
|
Lactose
|
glucose + galactose
beta-1,4 |
|
|
What does USDA term as "added sugars?"
chemically differ from naturally occurring sugars? DRI and why? |
any sugar that's added (added during processing) - not naturally occurring
no chemical difference (only dose is different) DRI- less than 25% of total calories why - minimizing risk of nutrient deficiency |
|
|
amylose
|
linear, unbranched chains (15-20%)
alpha-1,4 glycosidic bonds harder to digest --more resistent starch |
|
|
amylopectin
|
branched chains (80-85%)
alpha-1,4 glycosidic bonds with alpha-1,6 branch points digested much more rapidly |
|
|
glycogen
|
100g stored in liver; 400g stored in muscles
highly branched glucose polysaccharide (Quicker breakdown, synthesis, and more dense [able to fit more in]) |
|
|
Cellulose fiber--food source for intestinal bacterial
|
Part of the plant that cannot be digested
human enzymes cannot breakdown beta-1,4 bonds -- comes out in feces |
|
|
metabolic/physiologic advantages to the highly branched structure of glycogen
|
faster breakdown and synthesis
more energy stored in small space greater solubility |
|
|
mouth
|
break alpha-1,4 bonds in starch by hydrolysis
|
|
|
stomach
|
acidic pH deactivates salivary amylase
|
|
|
small intestine
|
S-cell release secretin -- inhibits gastric mobility
-stimulates pancreas to release bicarbonate major site of absorption K-cells and jejunum release GIP to promote the uptake of glucose into cells -induces insulin secretion |
|
|
pancreas
|
release pancreatic alpha-amylose in the duodenum
-breaks alpha-1,4 bonds to make isomaltase, maltotriose, maltase |
|
|
brush border (lactase)
|
(beta-galactosidase)
hydrolyzes beta-1,4 bond to lactose infants have highest activity of this enzyme |
|
|
brush border (maltase)
|
hydrolyzes alpha-1,4 bonds in maltose
|
|
|
brush border (sucrose-isomaltase complex)
|
two enzyme subunits
sucrase alpha-1,2 subunit hydrolyzes sucrose isomaltase (alpha-dextrinase) subunit hydrolyzes alpha-1,6 bond in isomaltose |
|
|
glucose and galactose absorption process from lumens to intestinal mucosal cell
|
active transport (requires ATP-faster)
transport protein SGLT1(sodium-glucose transporter 1) 1 glucose (0r galactose) and 2 Na+ transported inside (co-transport) |
|
|
fructose absorption process from lumen to intestinal mucosal cell
|
carrier-meditated (GLUT 5) facilitated diffusion
Na independent |
|
|
glucose and galactose absorption process from enterocyte to blood circulation
|
60% transported into blood via GLUT 2
25% diffuses across basolateral membrane into blood |
|
|
fructose absorption process from enterocyte to blood circulation
|
transported into blood via GLUT 2
proceeds down concentration gradient (maintained by liver) |
|
|
examples of medical conditions or genetic disorders that affect CHO digestion and absorption
|
lactose intolerance- inability to digest lactase (genetic disorder)
sucrase-isomaltase complex deficiency- genetic defect Sucrose difficulty breaking α-(1,2), amylopectin [difficulty breaking the branch points α-(1,6) |
|
|
after absorptions glucose from liver gets...
|
gets phosphorylated (hexokinase); glycolysis or glycogen synthesis --stored as glycogen when you don't need the energy (glu-6-P)
|
|
|
after absorptions galactose from liver gets...
|
gets phosphorylated (galactokinase); glucose goes into glycolysis or glycogen synthesis
|
|
|
after absorptions fructose from liver gets...
|
gets phosphorylated (fructose-1-P); goes into glycolysis or triacylglycerol synthesis
|
|
|
type of transport used for glucose uptake by nearly all cells of the body
|
facilitated diffusion through the GLUT family of protein carriers
|
|
|
overall rxn of glycolysis and where it occurs?
|
occurs in cytosol
1 glucose + 2 ATP + 2 NAD+ --> 2 pyruvate + 4 ATP + 2 NADH |
|
|
GLUT transported in insulin sensitive and where its found?
|
Glut 4; found in muscle and adipose tissue
|
|
|
fate of pyruvate if either no oxygen or mitochondria is available?
|
reduction of pyruvate --> lactic acid (oxidation of NADH to NAD+) occurs in cytosol
|
|
|
how overall end products of glycolysis change when the cell is in an anaerobic state and what is the significance of this change?
|
enters the PDH complex and the TCA cycle creating more ATP-- takes place in mitochondria
NADH converts back to NAD+ |
|
|
Glycolysis Step 1
|
Step 1: Hexokinase (glucose glucose-6-P)
Inhibited by glucose-6-P (product inhibition) |
|
|
Glycolysis Step 3
|
Step 3: PFK-1 (fructose-6-P fructose-1,6-bisphosphate)
What influences activity of PFK-1? Availability of substrates Regulatory substances within the cell: Allosteric inhibition by ↑ [ATP] and ↑ [citrate] – Why? You don’t need to make more energy: shows high energy state Allosteric activation by ↑ [AMP] – Why? Tells cell is in low energy state Most potent activator of all…fructose 2,6-bisphosphate, made by the enzyme PFK-2 (active when insulin is high) |
|
|
Glycolysis Step 10
|
Step 10: Pyruvate kinase (PEP pyruvate)
Feed forward activation by fructose-1,6-BP Inhibited by phosphorylation (occurs when glucogon is high) |
|
|
where are glucokinase and hexokinase found and how they are similar and different?
|
hexokinase phosphorylates glucose so it becomes trapped in the cells; high affinity -doesnt phosphorylate more than it can uptake
Glucokinase is in the liver and controls blood glucose levels |
|
|
why is pyruvate dehydrogenase (PDH) complex important and where does it occur? overall, what happens during the PDH complex runs and what vitamin cofactors are required?
|
it converts pyruvate to acetyl CoA for the TCA cycle
occurs in the inner surface of mitochondria vitamins required: thiamin, niacin, riboflavin, pantothenic acid, a-lipoic acid. -decarboxylation of pyruvate, CO2 released -dihydrolipoyl trans acetylase acetyl CoA is made -dihydrolipyl dehydrogenase produces NADH |
|
|
where TCA cycle occurs? why TCA cycle is considered to be an "amphibolic" pathway?
|
mitochondrial matrix --> because it does catabolic and anabolic reactions
|
|
|
in TCA out TCA
how many NADH, FADH2, CO2 and ATP made when 1 acetyl CoA enters a complete turn of the TCA cycle? |
1 Acetyl-CoA + 3 NAD+ + FAD+ + GDP + Pi + 2 H2O
2 CO2 + 3 NADH + FADH2 + GTP +3H+ + CoASH in: acetyl CoA and OAA Out: 2 CO2, 3 NADH, 1 FADH2, GTP(ATP) |
|
|
TCA STEP 1
|
Step 1: Citrate synthase inhibited by:
↑ [ATP] and [NADH] – why?- cuz you don’t need more energy ↑ [Succinyl CoA] – end result of odd chain FA breakdown |
|
|
TCA Step 3
|
Step 3: Isocitrate dehydrogenase (MOST highly regulated step)
Inhibited by ↑ [ATP] and ↑ [NADH] – Why?- you don’t need more Energy Activated by ↑ [ADP] – Why?- You need to make ATP |
|
|
TCA Step 4
|
Step 4: α-ketoglutarate dehydrogenase complex inhibited by:
↑ [ATP] and [NADH] – why?- don’t need more Energy ↑ [Succinyl CoA] (product inhibition)- since this is what’s made in this step |
|
|
How many ATP are made from NADH, FADH2
|
3 NADH = 9 ATP (made in ETC)
1 FADH2 = 2 ATP (made in ETC) 1 GTP = 1 ATP 2 CO2 |
|
|
"FATS BURN IN A CARBOHYDRATE FLAME"
|
in order for fat to burn efficiently without producing toxic ketones, adequate carbs must be available
|
|
|
big picture of CHO metabolism
|
glycolysis --> PDH -->TCA --> ETC
|
|
|
glyconeogenesis
|
making new glucose form non-carb substrates --> provide energy when glycogen and glucose is not available. during fasting when glycogen stores in liver are deleted
|
|
|
where glyconeogenesis occurs?
|
mitochondria and cytosol of liver/kidney cells
|
|
|
is gluconeogenesis the exact reversal of glycolysis?
|
no there are detours that need to be taken for roadblocks such as the 3 irreversible steps
|
|
|
substrates for gluconeogenesis
|
tiglycerides (glycerol)
Protein (glucogenic AA) Lactate pyruvate |
|
|
examples of metabolic intermediates that cannot be used for gluconeogenesis
|
acetyl CoA
alcohol fatty acids |
|
|
what effect does hormone glycogon have on gluconeogenesis? 3 ways glycogon promotes gluconeogenesis
|
favors gluconeogenesis
- decreases levels of fructose-2,6-BP (via FBP-2) -inactivates pyruvate kinase (via phosphorylation) which decreases conversion of PEP to pyruvate -increases gene transcription of PEP-carboxykinase |
|
|
overall metabolic conditions which favor glconeogenesis and why
|
High ATP, high acetyl CoA, high glucagon & low insulin
Also high epinephrine & cortisol favor gluconeogenesis |
|
|
How is gluconeogenesis part of both the core cycle and glucose-alanine cycle?
|
combination of transanimation and gluconeogenesis --> both during starvation
|
|
|
what is glycogen, where is it found in the body, and why is it important?
|
storage form of glucose
found in liver and muscle and kidney provides energy to cells when in non-eatting state |
|
|
steps to make glycogen to from glucose
|
1. glucose --> glucose-6-P by hexokinase to glucokinase
2. glucose-6-P --> glucose-1-P by phosphoglucomutase 3. glucose-1-P + UTP --> UDP-glucose + PPi by UDP-glucose pyrophosphorylase 4. glycogen synthase 5. glycosyl alpha-4,6 transferase for branch points intermediate source: UDP glucose |
|
|
steps of glycogenolysis and form of glucose released by action of glycogen phosphorylase
|
1. glycogen phosphorylase - cleaves alpha-1,4 bond until the last 4 glucose units --> glucose-1-phosphate
2. debranching enzyme glucosyl (4:4) transferase - removing glucose units amylo-alpha-1,6-glucosidase - removes the last glucose glucose -1-P |
|
|
what can't muscle glycogen be used to maintain blood glucose levels?
|
because it is still phosphorylated and cannot get out of the cell
|
|
|
key regulatory enzymes for glycogen synthesis and broken down
|
glycogen synthesis
needs ATP and UTP High ATP glycogen breakdown requires PLP; vitamin B6 High AMP Epinephrine/ glucagon |
|
|
effect of insulin have on CHO metabolism in liver, muscle and adipose tissue
|
liver - decrease glycogen breakdown
muscle- increase glycogen synthesis adipose - increase glucose uptake |
|
|
effect of glucagon have on CHO metabolism in liver, muscle and adipose tissue
|
liver - increased production of glucose
muscle - increased glycogen breakdown |
|
|
difference between dietary and functional fiber
|
dietary - nondigestible CHO and lignin that are intact and intrinsic in plants
functional - nondigestible CHO that are isolated, extracted,or manufactured and known to have physiological benefits |
|
|
AI for fiber in men and women ages 19-50
|
28g men
25 g women |
|
|
mechanisms by which fiber can lower blood cholesterol levels and decrease risk of cardiovascular disease
|
substation effect, binding effect, fermentation of fiber, delayed nutrient absorption
|
|
|
mechanisms by which fiber can help prevent colon cancer
|
butyrate, fibers with binding ability, fibers which increase binding to carcinogens
|
|
|
key physiological effects/ benefits of soluble fibers
|
decreases nutrient absorption
longer digestion time delays gastris emptying small increase in fecal bulk |
|
|
key physiological effects/benefits of insoluble fibers
|
decrease transit time
increases fecal bulk doesn't dissolve |
|
|
key physiological effects/ benefits of viscous fibers
|
delayed gastric emptying
slows down digestion and absorption reduced digestive enzyme function delayed absorption in enterocytes |
|
|
key physiological effects/ benefits of ferment fibers
|
digested by gut bacteria then produce gases and short therm fatty acids
|
|
|
key physiological effects/ benefits of non-ferm fibers
|
increases fecal volume
detoxification |
|
|
key physiological effects/ benefits of binding fibers
|
diminished absorption of lipids
lowered serum cholesterol levels altered mineral absorption Increased fecal bile acid excretion |
