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182 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What does lipids include?
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glucocorticoids
steroid hormones fat sol vitamins |
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what releases FA from triglycerols?
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lipase
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triglycerides are solid or liquid?
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both
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nutritionally important FA contain up do ___ C-C double bonds?
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6
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most FA double bonds are cis or trans?
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cis
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c16 aka
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palmitic acid and
hexadecanoic acid |
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cis-9 C16:1 =
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palmitoleic acid or
cis-9-hexadecenoic acid |
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CAPRIC ACID AKA
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DECanOIC ACID
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caprylic acid aka
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octanoic acid
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capric acid aka
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hexanoic acid
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lauric acid aka
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dodecanoic acid
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C14 aka
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myristic acid
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oleic acid aka
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C18:1 cis-9
cis-9-octadecenoic acid |
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alpha linolenic acid is
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all cis-15,12,9-octadecatrienoic acid
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gamma linolenic acid is
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all cis-6,9,12-octadecatrienoic acid
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C20 is
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arachidic acid
ecosanoic acid |
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arachidonic acid is
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all cis-5,8,11,14-eicosatetraenoic acid
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eicosanoids include:
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prostaglandins
thromboxanes leukotrienes How are these produced? |
from FA in the body
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how are eicosanoids made?
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oxygen must be added.
What are these reactions called? And what enzymes do this? |
oxygen reactions.
oxygenases |
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FA that are precursors to eicosanoid production
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arachidonic acid
eicosatrienoic acid eicosapentenoic acid (EPA) How do we get these FA? |
from diet, or synthesized
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what is a cholesterol ester?
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FA esterified to a cholesterol
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only place cholesterol and cholesterol esters are found?
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animals
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phosphotidylcholine is a
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phospholipid
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phosphotidylcholine aka
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lechithin
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glycolipids
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lipids with a carb component. serve as cell recognition markers
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enzymes that digest triglycerides and phosphotydalcholines and cholesterols?
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esterases
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where does lipid digestion take place?
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stomach but mostly SI
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lipase is a type of
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esterase
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where is lingual lipase released from?
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glands under the tongue.
Where does this digestion start? |
not until the stomach
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unique property of lingual lipase?
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can digest milk globule. esp important for infants who don't have a working pancreas yet
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this helps to emulsify lipids during digestion?
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peristalsis in the stomach and SI. Benefit of this?
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helps expose surface area of fats for digestion
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effect of undigested lipids in the stomach?
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slows gastric emptying. That's why you are more full when you eat fat
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dietary fat effect on bile?
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causes it to be released into SI
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bile salts effects on lipids?
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emulsifies them further
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bile acids are synthesized from
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cholesterol
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primary bile acids are synthesized in
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the liver
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secondary bile acids are converted by
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intestinal bacteria
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how do bile acids vary?
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in the number of hydroxyl groups they have attached
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bile acids are hydrophobic or philic?
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both (amphipathic)
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functional groups in bile acids
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hydroxyl and carboxyl
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what is sometimes conjugated to the bile acids?
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glycine or taurine. What effect does this have on bile acids?
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more water soluble
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as emulsifiers, bile acids give the lipids what configuration?
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they are in lipid droplets in the aqueous environment
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where is the lipase made that acts on the lipids in the SI?
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pancreas. Therefore it is called
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pancreatic lipase
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pancreatic lipase acts on a triglyceride and leaves what?
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a monoglyceride (FA attached to the middle)
and 2 free FA |
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what does cholesterol esterase do?
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acts on cholesterol ester, leaving a free FA and a cholesterol
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phospholipase A2 acts on
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lecithin. It results in
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a free FA cleaved from C #2.
And lysolecithin |
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covering the enterocytes you have:
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brush border
glycocalyx unstirred water layer |
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why are micelles necessary for lipid absorption into circulation?
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lipids can't cross the unstirred water layer
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where does absorption of lipids occur?
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duodenum and jejunum
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where are bile acids absorbed?
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ileum
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what happens to bile acids after they are absorbed?
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go to the liver via the
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portal vein
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recylcization of bile acids aka
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enterohepatic circulation
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%of bile acids recycled?
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95
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what happens after the 2-monoglycerides, FA, cholesterols and lysolecithins are absorbed?
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they are randomly reassembled into cholesterol esters, triglycerides and lecithin.
Then what? |
incorporated into chylomicrons
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what are chylomicrons?
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lipoproteins formed on the ER of the enerocyte
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how do chylomicrons leave the enterocyte?
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exocytosis
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where do chylomicrons go after they leave the enterocyte?
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lacteal. Then waht?
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transported through lymphatic system and eventually enter blood stream
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lipoproteins are composed of:
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proteins and lipids
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what are the proteins called in lipoproteins?
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apolipoproteins
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function of lipoproteins?
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transport lipids among tissues
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What is the structure of a lipoprotein?
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phospholipid layer surrounds everything (with some apoproteins dispersed in it.)
triglycerides and cholesterol esters are contained within the lipoprotein's center |
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are apolipoproteins hydrophilic of phobic?
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hydrophilic
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function of apolipoproteins?
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stabilize the lipoprotein structure
serve as recognition markers |
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types of lipoproteins?
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chylomicrons
VLDL IDL LDL HDL |
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least dense lipoprotein
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chylomicron
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which is more dense, cholesterol or triglycerides?
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cholesterol
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Which would be larger? a lipoprotein full of cholesterol or triglycerides?
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triglycerides
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where are chylomicrons formed?
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enterocyte
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what apolipoprotein is necessary to have to let the chylomicron leave the enterocyte?
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ApoB48
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do chylomicrons enter the bloodstream quickly or slowly?
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slowly. How long after meal does lipid in blood peak?
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30 min - 3 hr
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pathway of chylomicrons:
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Enterocyte
lymphatic duct thoracic duct vena cava circulation |
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significant consumers of dietary fat?
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adipose
muscles. Other consumers of dietary fat? |
heart
kidney liver(last organ to accept dietary fat) |
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how do the products of LPL on triglycerides get into the cells?
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diffuse
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what happens when the products of LPL are in the muscle cell?
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further hydrolyzed into glycerol and free FA. The FA are then oxidized for energy.
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What happens when the products of LPL are in the adipocyte cell?
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The free fatty acids are used to resynthesize triglycerides which is then stored
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effect LPL has on the blood stream?
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it clears the bloodstream of chylomicrons and yields chylomicron remnants
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Composition of chylomicron remnants?
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they have high cholesterol:triglycerol ratios
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what happens to chylomicron remnants?
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go to liver. How do they enter
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endocytosis
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what apolipoproteins do chylomicron remnants have?
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E and B48. How does the liver recognize them?
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by the E apolipoprotein
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where are bile acids synthesize?
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liver
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where is bile stored?
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gall bladder
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where are lipids synthesized from non lipid precursors?
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livere
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if there is an excess of glc in the liver...
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the AcCoA from glc is converted to fats
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aa can be converted to what fat precursors?
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AcCoA
pyruvate |
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what happens to the chylomicron remnant when it goes into the liver
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it's hydrolyzed into: FA, glycerol, monoglycerol, diacylglycerol, inorganic phosphates, and free cholesterol.
The apolipoproteins are hydrolyzed into aa Some of the FA are used for energy. Cholesterol, triglycerides and phospholipids are resynthesized in the liver |
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which lipoproteins contain endogenous lipids?
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HDL and VLDL
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Which lipoproteins contain exogenous lipids?
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chylomicrons
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HDL is made up of
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mostly dense cholesterol esters
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VLDL made up of
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mostly triglycerides
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which is bigger? VLDL or HDL?
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V:LDL
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where are HDL and VLDL released from?
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liver
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where is chylomicron remnant uptake?
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liver (not adipose)
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where is glc uptaken when insulin is high?
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adipocyte, liver, maybe others?
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what does adipocyte uptake when insulin is present?
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FA
glc |
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what form of glycerol is used in the adipocyte to make triglycerides?
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glycerol 3 phosphate. (glycerol can't be used b/c the adipose doesn't have glycerol kinase)
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where does the adipose get the glycerol 3 phosphate it needs to make triglycerides?
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from the glc it has uptaken
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what must happen before a FA can be esterified to a glycerol?
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it must be attached to a CoA
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what ways does insulin promote triglyceride storage
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1. inhibits ICL(aka HSL)
2. promotes FA uptake and triglyceride synthesis |
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in the liver, FA can be used to synthesize:
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ketone bodies. to be used for fuel for the brain and muscles.
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upon hydrolysis by LPL, VLDL becomes?
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IDL
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what delivers triglycerides to the fat and muscle cells?
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VLDL or chylomicrons
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IDL is hydrolyzed to
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LDL
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what things have Apo C-II on them?
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chylomicron and VLDL
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job of ApoCII?
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activates LPL
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major carrier of cholesterol in the blood?
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LDL
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what percent of serum cholesterol does LDL contain?
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60%
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what is the cholesterol carried by LDL used for?
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synthesis of steroid hormones
goes into membranes |
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how does LDL enter cells?
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endocytosis
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which is the only apolipoprotein in LDL?
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ApoB100
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what is the receptor called that recognizes LDL?
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LDL receptor
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what percent of serum cholesterol does LDL contain?
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60%
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what is the cholesterol carried by LDL used for?
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synthesis of steroid hormones
goes into membranes |
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how does LDL enter cells?
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endocytosis
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which is the only apolipoprotein in LDL?
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ApoB100
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what is the receptor called that recognizes LDL?
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LDL receptor. what happens nex to this receptor
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it is recycled and goes back to the surface of the membrane (only lives 20 hrs)
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what happens to the apolipoprotein of LDL?
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it is hydrolyzed into aa
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what negatively inhibits uptake of LDL into cells?
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lots of free cholesterol already in the cell. How does it do this?
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It inhibits the production of LDL receptors, therefore they are decreased
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what suppresses the production of LDL receptors?
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increased cholesterol in cells (b/c LDL receptors are what allow LDL to bring cholesterol into the cell)
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what suppresses the production of de novo cholesterol?
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cholesterol in the cells
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what enzyme is the rate limiting step of de novo cholesterol synthesis?
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3-hydroxy-3-methylglutaryl CoA reductase
aka HMG CoA reductase |
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what enzyme catalyzes the formation of cholesterol esters?
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ACAT (acCoA cholesterol acyl transferase)
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how LDL affects Cardiovascular disease?
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LDL receptor mutations occur
cholesterol can't get in de novo synthesis occurs too much cholesterol too much LDL floating around contributes to LDL build up in arteris and hardening of the arteries |
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where deoes HDL dump it's cholesterol?
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liver
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where does the liver put the cholesterol that the HDL dumpe don it?
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in bile acids to be excreted in the feces.
primary means of cholesterol disposal |
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LDL receptor can also bind to
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HDL. but HDL doesn't go into the cell.
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what does LCAT do?
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makes cholesterol esters from the C2 FA on lecithin and cholesterol
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what does ApoA1 do?
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activates LCAT
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where is APo A1located?
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HDL
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in general how does HDL work?
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-binds to LDL receptor b/c it recognizes APoE
-ApoA1 activates LCAT. -LCAT makes cholesterol esters from lecithin and cholesterol located in the plasma membrane of the cells (or from the monolayer of the lipoprotein) -The cholesterol esters migrate into the HDL -HDL transfers them to the liver to be excreted in the bile |
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hyper responders
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people whose serum cholesterol increases significantly with dietary cholesterol intake
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hypo responders
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people who serum cholesterol isn't affected much by the amount of dietary cholesterol they consume
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how much energy per g does cholesterol contribute?
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none
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what happens to cholesterol's steroid ring as it is digested?
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stays in tact
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how is cholesterol excreted?
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in the form of bile acids
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how is cholesterol delivered to the liver?
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by chylomicron remnants, LDL or HDL
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what percent of body cholesterol is endogenous?
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66%
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what parts of the body synthesize cholesterol?
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almost all cells can
The liver and SI synthesize a lot. |
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how does insulin promote storage of TG in adipocyte?
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promotes LPL
inhibits ICL/HSL |
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caproic acid is
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hexanoic acid
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caprylic acid is
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octanoic acid
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capric acid is
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decanoic acid
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c20 is
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eicosanoic acid aka arachidic acid
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which apo protein is necessary for chylomicron to leave the enterocyte?
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B48
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what is ICL stimulated by
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glucagon and epi
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where does beta oxidation occur
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mitochondria
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what is required for a fatty acyl to cros into the mitochondria so it can be oxidized for energy
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CAT 1
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how to oxidize odd number compounds?
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do it normally until 3 C compound left. propionyl CoA goes to succinyl CoA which can be used to synthesize glucose
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how much less energy is from unsaturated FA?
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2 ATP less per double bond (b/c in that step which is skipped an FADH is generated which equals 2 ATP)
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non insulin diabetes?
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type 2
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what is the most prevalent kind of diabetes?
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type 2
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insulin resistance is
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error in cellular response to insulin resulting in: reduced conc. of GLut4 on the plasma membrane
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insulin resistance in the skeletal muscle:
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GLUT4 doesn't translocate to the membrane
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insulin resistance in adipocyte?
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depletion of mRNA to produce GLUT4
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decrease in GLUT4 is correlated with?
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increasing obesity
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what suppresses cholesterol synthesis? and how?
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increased dietary cholesterol. suppresses HMG CoA reductase
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how is the cholesterol delivered to the liver that is to be excreted?
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HDL, LDL, chylomicron remnants
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two forms cholesterol can be excreted into bile as
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free cholesterol or bile acids
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where do we get oaa from?
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you must have glc to get oaa
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what is the state of beta oxidation prior to ketogenesis?
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it is accelarated
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how are ketone bodies utilized for energy?
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acetoacetate and beta hydroxy butyrate travel to tissues where they are converted back into AcCoA and used to make energy
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ketone bodies are produced in the
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liver mitochondira matrix
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where does FA synthesis occur?
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cytosol
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can AcCoA corss the mitochondrial membrane?
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no
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malonyl units part in FA synthesis?
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they are condensed one at a time to form FA
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condensation of malonyl CoA releases what with every condensation?
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CO2
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condensation of malonyl CoA results in (typically)
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palimitic acid
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what is NADPH necessary for?
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synthesis of FA and cholesterol
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where is NADPH produced?
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in conversion of malate to pyruvate. in the cytosol
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what kind of FA are used for elongation and desaturation?
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endogenous and dietary
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what is necessary in the desaturation reactions?
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NADPH
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where do we get EPA and DHA from?
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we make them I think
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what is required to attach a FA to a CoA?
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two high energy bonds
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FA are esterified to
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glycerol 3 phosphate
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malonyl CoA inhibits
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CAT1 (carnitine transferase 1)
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what does CAT1 do?
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catalyzes the reaction that allows carnitine to carry the FAacylCoA into the matrix for beta oxidation
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negative regulator of FA oxidation?
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malonyl CoA
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precursor for FA synthesis that also acts as inhibitor for FA oxidation?
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malonyl CoA
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what suppresses HSL./ICL?
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insulin
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what stimulates ICL/HSL?
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epi and glucagon
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ACAT does what?
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catalyzes the formation of cholesterol esters from cholesterol and free FA in cells. This allows cholesterol to move down its concentration gradient into cells
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increased LDL receptors affects serum cholesterol how?
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decreases it
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increased ACAT effects serum chol. how?
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decreases it
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