Lipids, AA, Protein Metabolism
Cards (73)
- What is dietary fat made of- mainly triacylglycerols- cholesterol- cholestery esters- phospholipids- free fatty acids
- Lipid digestion and absorption steps- digestion = emulsification- micelle formation- absorption- not much in mouth and stomach- mainly in small intestine = emulsification
- Emulsification- occurs when lipids enter duodenum- means mixing of two normally non mixable liquids- increases surface area of lipid = more enzymatic activity- aided by bile and pancreatic acids = hydrolyze lipids into 2-monoacylglycerin, free fatty acid, and cholesterol
- Bile- has bile salts, pigments, and cholesterol- made by liver- stored in gallbladder
- Pancreas- makes pancreatic lipase, colipase, and cholesterol esterase = into small intestine
- Micelle formation- made by free fatty acids, cholesterol, 2-monoacylglycerols, bile salts- cluster of amphiphatic lipids- solubule in aqueous solution- go from duodenum to ileum- ileum = bile salts are reabsorbed for recycleing- any fats that aren't absorbed go into colon = becomes stool
- Lipid absorption- micelles diffuse to brush border- lipids are absobed into mucosa- lipid is re-esterfied = triacylglycerol and cholesteryl = packaged into chylomicrons- water-soluble short-fatty acids are re-absorbed
- Chylomicrons- packages of triacylglcerols, cholesteryl, fat-soluble vitamins, other lipids- leave intestine via lacteals- least dense lipoprotein- high soluble in lymphatic fluid and blood
- Lacteals- vessels of lymphatic systems- allows lipids to re-enter the bloodstream via thoracic duct
- Thoracic duct- long lymphatic vessel- empties into left subcalvian vein- at base of neck
- Postabsorbative state- when we are sleeping- body uses energy stored- does not respond to glucagon levels- responds to fall in insulin = activates hormone-sensitive lipase (HSL)
- HSL- hormone-sensitive lipase- hydrolyzes triacylglyerols = fatty acids and glycerol = transported to liver for glycolysis or gluconeogenesis- activated by fall in insulin, rise in epinephrine, rise in cortisol- effective with adipose tissue, not as much for metabolism of chylomicrons and VLDL
- LPL- lipoprotien lipase- metabolize cylomicrons and VLDL- enxyme that releases fatty acids from triacylglycerols in lipoprotein
- Free fatty acid transportation- associates with albumin = carrier protein- transported through blood
- Triacylglycerols and cholesterol transportation- as lipoprotein- aggregates of apolipoprotiens and lipids- named depending on density = proportional to amount of protein = VLDL, IDL, LDL, HDL, chylomicrons
- VLDL- very low density lipoprotein- transports triacylglycerides and fatty acids from liver to tissue- similar metabolism as chylomicrons- reduced and assembled in liver- have fatty acids from excess glucose or chylomicron remnants
- IDL- intermediate density lipoprotein- VLDL remnants = when VLDL loses tiracylglycerol- some picks up cholestryl from HDL to become LDL- some picked up by liver- some is further processed in bloodstream- transition particle between triacylgylcerol transport and cholesterol transport
- LDL- low density lipoprotein- delivers cholesterol into cells- measured cholesterol is mainly LDL
- HDL- high density lipoprotein- picks up accumulating cholesterol in blood vessels- delivers cholesterol to liver and steroidogenic tissues- transfers apolipoproteins to other lipoproteins- made in liver and intestines- released into blood
- Use of cholesterol- biosynthesis- cell membrane- bile acids and salts synthesis- steroid hormone synthesis
- Apolipoproteins- aka apoproteins- form protein part of lipoproteins- receptor moelcules- involved in signaling
- Types of apolipoproteins- not usually tested- apoA-I = activates LCAT = catalyzes cholesterol esterification- apoB-48 = mediates chylomicron secretion- apoB-100 = permits uptake of LDL by liver- apoC-II = activates lipoprotein lipase- apoE = uptake of chylomicron remnant and VLDL by liver
- Cholesterol- uniquitous component of all cells in human- major role in making:- cell membrane- steroid hormone- bile acids- vitamin D
- Cholesterol sources- most cells take from LDL and HDL- some are de novo
- De novo cholesterol sythensis- in liver- driven by acetyl-CoA and ATP- done by citrate shuttle = carries mitchondrial acetyl-CoA into cytoplasm- NADPH supplies reducing equivalents- rate limiting = synthesis of mevalonic acid
- Synthesis of mevalonic acid- in smooth ER- rate limiting step for cholesterol synthesis- catalyzed by 3-hydroxy-3-methylgutaryl CoA reductase
- Cholesterol synthesis regulation- more cholesterol = inhibits further synthesis- insulin = activates- regulation of HMG-Coa gene expression = activates/inhibits
- Special enzymes that transport cholesterol- LCAT- CETP
- LCAT- lecithin-cholesterol acyltransferase- transport cholesterol- in bloodstream- activated by HDL apoproteins- adds a fatty acid to cholesterol = soluble cholesteryl ester = in HDL = distributed to IDL = become LDL
- CETP- cholesteryl ester transfer protein- transport cholesterol- helps transfer cholesteryl ester between HDL and IDL and LDL
- α-carbon of triacylglycerols- carbon #2- carbon #1 = carboxyl carbon
- How do fatty acids occur in the body- salts- can form micelles- esterfied to other compounds
- Saturated fatty acid- no double bonds
- Unsaturated fatty acid- 1+ double bond = usually cis- humans can only synthesize a few- others come from diet = essential fatty acids = chylomicrons as triacylglycerols from intestine
- Essential fatty acids- α-linolenic acid = precursor of ω-6 family- linoleic acid = precursor of ω-3 family- maintain cell membrane fluidity
- Omega numbering system- used for unsaturated fatty acids- ω = position of last double fond relative to end of chain- identifies major precursor fatty acid
- Lipid and carbohydrate synthesis- fatty acids for fuel = mainly from diet- some is made by body- nontempelate synthesis = does not rely directly on coding
- Fatty acid biosynthesis- in liver- products transported to adipose- adipose can also make small amounts- major enzymes = acetyl-CoA caboxylase and fatty acid synthase = stimulated by insulin- primary end product = palmatic acid = palmitate
- Acetyl-CoA shutteling- acetyl CoA = product of pyruvate dehydrogenase complex = accumulates in m.matrix after large meal = needs to be moved to cytosol or fatty acid- Acetyl CoA couples with oxaloacetate = citrate = accumulates when no energy needed- citrate diffuses to m.membrane- cytosol citrate lipase splits citrate to aCoA and oxaloacetate- ends with aCoA in cytoplasm and citrate goes back to mitochondria to shuttle more aCoA
- Acetyl-CoA caboxylase- aCoA carboxylase acitavtes incorportaion of aCoA into fatty acids = rate limiting- needs ATP and biotin- adds CO2 to aCoA to make malonyl-CoA- activated by insulin and citrate