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lipoprotein lipase

an enzyme that hydrolyzes the ester linkage between a fatty acid and a glycerol in a triglyceride molecule as it circulates in the bloodstream

hormone sensitive lipase

an enzyme that catalyzes the hydrolysis of ester linkages that attach fatty acids to the glycerol molecule; mobilizes fatty acids from adipose tissue


the cyclic metabolic process that results in fatty acid and, ultimately, triglyceride synthesis through the repeated process of adding 2 carbons onto the acetyl CoA starter; requires initial ATP & NADPH (as a hydrogen donor)

lipogenesis steps

acetyl coa condenses w/ malonyl coa (loses co2); malonyl coa is reduced (NADPH) and dehydrated, then further reduced (hydrogenation); repeat process until a 16c saturated fatty acid is produced

lipogenesis: location, enhancers, inhibitors

cytosol of liver (+ some adipose tissue); high simple sugar/low fat diet, insulin, inc acetyl coa carboxylase activity, ATP; glucagon, dietary fat, starvation

cholesterol synthesis has ___ basic stages:

3: formation of HMG-CoA from acetyl CoA, production of squalene from HMG-CoA (rate limiting step requiring HMG CoA reductase), eventual production of hcolesterol from cyclization of squalene

cholesterol synthesis: location

20% liver

digestion of triacylglycerols

1. Mouth: chewing breaks apart food, lingual lipase starts hydrolyzing fatty aicds from glycerol molecules 2. Stomach: lingual lipase continues; stomach releases gastric lipase from gastrin (secreted w/ presence of fat in stomach) but most action occurs via emulsification via contractions 3. small intestine: more conducive pH environment; a) partially hydrolyzed lipids enter as lipid droplets and become further emulsified via mechanical means & bile release from the gallbladder as a result of cck; micelles form w/ phospholipids & cholesteryl esters b) in the duodenum, secretin (SI) stimulates the pancreas to release pancreatic lipase to complete triglyceride digestion into fatty acids and monoacylglycerol from wtihin the micelles

digestion of phospholipids, cholesterol & cholesteryl esters

phospholipids are digested by phospholipase A from pancreas in response to secretin resulting in 1 fatty acid and 1 molecule of lysophospholipid; cholesteryl esters must be broken down into their cholesterol and fatty acid constituents via vile salt dependent cholesteryl ester hydrolase in response to secretin


occurs in the distal duodenum and jejunum; micelles are water soluble enough to get through the layers lining the enterocyte and allow their contents (FFA, 2-monoacylglycerols, cholesterol/esters, lysolecithin) to diffuse out into the enterocytes down a concentration gradient; short & medium FA pass directly into the portal blood to liver bound to albumin; other components reform triacylglycerols, phosphatidylcholine, and cholesteryl esters

transport & storage

lipids are surrounded by lipoproteins and fuse with golgi apparatus to form chylomicrons, leaving the cell membrane and entering lymphatic circulation


the protein portion of any lipoprotein; play an important role in structural and functional relationship among lipoproteins (stabilize the lipoprotein as a whole, act as recognition sites for receptors, stimulate enzymatic reactions)


made in the liver from endogenous triacylglycerol; function in the transport of triacylglycerol from liver to other, non-hepatic tissues; also contain cholesterol & cholesteryl esters; deliver fatty acids to cells via lipoprotein lipase


brief intermediary stage that occurs as triacylglycerol molecules are removed from VLDL; taken up by the liver or remain in circulation; eventually converted to LDLs


type of lipoprotein that IDL's become when enough TAG's are removed; major cholesterol carrier to tissues for membrane construction or conversion into other metabolites; receptors needed to get TAG's into cells and remove LDL from circulation

classes of inadequate LDL functioning

1: no receptors synthesized 2: precursor synthesized but not properly processed 3: synthesized & processed but in a faulty way 4: receptors bind w/ LDL but can't cluster in the coated pits; inadequate # receptors caused by high saturated fat & cholesterol in diets


lipoprotein made in the liver that circulates in the blood to collect excess cholesterol from the cells; reverse cholesterol transport back to liver


adipocytes are major site; constant TAG turnover here

if glucose exceeds glycogen stores, excess is turned into ____ leading to ____

fatty aicds, overproduction of vLDL

chylomicron remnants

the lipoprotein particle that remains after a chylomicron has lost most of its fatty acids; taken up by the liver for reuse or recycling.

uses for glycerol vs. fatty acids

used for energy by the liver through glycolytic pathways; oxidative potential in the krebs cycle

beta-oxidation of fatty acids

a cyclic degradative pathway in the mitochondria of all cells but brain & RBC by which 2-carbon units in the form of acetyl CoA are cleaved one by one from the carboxyl end

beta oxidation: short vs. long chain FA

short pass directly into matrix; long use carnitine as a transport system

beta-oxidation requires ___, but each C-C saturated bond cleavage yields ____


there are ___ ketone bodies:

3: beta-hydroxybutyrate, acetone, acetoacetate

why would ketone formation occur?

accumulation of acetyl coa due to insufficient quantities of oxaloacetate from glucose breakdown to combine with it in krebs

ketone formation process

2 molecules acetyl coa condense to form acetoacetate, which can decarboxylate spontaneously to form acetone (end of the road) or converted to beta-hydroxybutyrate


results from an overproduction of ketone bodies and can disturb acid-base balance and lead to ketoacidosis


severe ketosis leading to lowered blood pH, nausea, coma, death

regulation of fatty acid metabolic processes

linked to carb status: hyperglycemia + insulin promotes glucose transport into adipose cells (lipogenesis); hypoglycemia + low levels of insulin favor lipolysis; hormone sensitive lipase is stimulated by epinephrine, norepinephrine, glucagon, etc. to mobilize fat

ethyl alcohol

neither a carb nor a lipid, but with a structure that resembles a carbohytes and a metabolism that resembles a fatty acid catabolic process; preferentially treated by liver (will break down and ignore sugar, fat, etc.)

ethyl alcohol: source, calorie content

alcoholic beverages, 7kcal/gram

ethyl alcohol: absorption & transport

throughout entire GI tract, transported unaltered in bloodstream

ethyl alcohol: metabolism

oxidatively degraded in tissues (especially liver) via alcohol dehydrogenase (ADH), forming NADH & acetyl CoA, which works until NAD+ is depleted or concentration rises too high

why is ethyl alcohol metabolism lipogenic?

depletion of NAD+ means that the krebs cycle can't run to burn fats for energy

complicationsof alcoholism

acetyaldehyde toxicity, high NADH:NAD+ ratio, substrate competition

acetaldehyde toxicity

Both ADH + MEOS routes produce acetaldehyde, which can attach covalently to proteins to form protein adducts; could impair enzyme activity, impede the formation of microtubules in liver, leads to cirrhosis

high NADH:NAD+ ratio

leads to fatty liver due to upregulation of acetyl coa carboxylase

acetyl coa carboxylase

the enzyme responsible for converting acetyl coa into malonyl coa; key regulatory enzyme for fatty acid synthesis

substrate competition of ethyl alcohol

especially with retinol

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