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41 Cards in this Set
- Front
- Back
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Saturated vs unsaturated FA
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-saturated contain no double bonds
--end in anoic -unsaturated contain double bonds spaced at three carbon --end in enoic |
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Nomenclature of FA
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-saturated=anoic
-unsaturated=enoic -a carbon = adjacent to carboxyl carbon -b carbon= carbon 3 -w carbon= end methyl carbon unsaturated: double bond nearest to terminal methyl group (omega 6 etc) |
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Common names, number of carbons and double bonds of FA from table
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-Oleic (18:1(9)) omega 9
-Linoleic (18:2(9,12)) omega 6 -Linolenic (18:3(9,12,15)) omega 3 -Arachidonic(20:4(5,8,11,14) |
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Lauric and myristic acids
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medium chain FA found in palm and coconut ooil
12:0 and 14:0 saturated fats that raise serum cholesterol levels -why coconut oil is so horrible for you |
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Palmitic acid
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-16:0
-most abundant saturated fatty acid -raises serum cholesterol levels |
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Stearic acid
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18:0 saturated fatty acid
-neutral or cholesterol loweing effect |
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Oleic acid
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18:1
-most abundant dietary monounsaturated FA -abundant in olive oil -key component of mediterranean diet -lower serum cholesterol w.out also lowering HDL levels |
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Linoleic acid
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-18:2
-essential polyunsaturated fatty acid -omega 6 -found in veg oil -lowers serum cholesterol |
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Linolenic acid
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-18:3
-essential polyunsaturated FA of omega3 series -found in veg oil, lowers serum cholesterol |
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Arachidonic acid
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-20:4
-polyunsaturated fatty acid made from linoleic acid -precursor for synthesis of w6 eicosanoids |
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Eicosapentanoic and docosahexanoic acids
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-20:5 and 22:6
-polyunsaturated FA made from linolenic acid, precursor for synthesis of w3 eicosanoids -fish oil and canola oil -w3 eicosanoids have beneficial effects on heart disease risk, decosahexanoic acid may be essential for early neural and visual development |
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Trans fatty acids
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-polyunsaturated fatty acids that are partially hydrogenated to make solid at room temp
-convert some of double bonds to saturated state -cis double bonds to trans -raise serum cholesterol as much as saturated fatty acids |
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Triglycerides vs Diglycerides
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-TG
--esters of the alcohol glycerol and fatty acids -DG --intermediates in TG synthesis and signalling molecules |
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Glycerol structure and TG synthesis notes
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-carbon 1 and 3 are NOT identical in glycerol
--enzymes readily distinguish btw them and target spec -Each of the carbons of glycerol may be esterified w a different FA and both synthesis and hydrolysis of TG occurs in highly selective manner |
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Compound phospholipids
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-most abundant compound lipids in membrane
-combo of 2 FA, glycerol, phosphoric acid, and in most cases a nitrogenous base |
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Lecithin
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compound phospholipid
-phosphatidyl choline |
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How is the insolubility of fat overcome so that fat can be digested?
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-disperse fat into small particles w enough exposed surface for rapid attack by digestive enzymes
-due to detergent effect (from fatty acid soaps and bile salts) |
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Structure and action of bile salts
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-bile salts have hphobic and philic sides
-dissolve at oil-water surface -emulsifies fat and yields mixed micelles |
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Action of mixed micelles
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allow attack of fats by water soluble digestive enzymes at surface
facilitate absorbption of lipids through intestinal mucosa transport vehicles for lipids that are less soluble than FA (cholesterol, vit A, D, E, K) |
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Pancreatic lipase
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-important enzyme in fat digestion
-bile salts inhibit activity BUT --colipase binds to micelle surface and pancreatic lipase and prevents inhibition of PL by bile salts |
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Control of fat digestion
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Products of digestion cause release of peptide hormone PZ-CCK
CCK activity -induces emptying of gall bladder -leading to increased concentration of bile salts in intestine PZ activity release of pancreatic digestive enzymes invluding pancreatic lipase |
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Absorption of short and medium chain FA
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-absorbed directly through villi of intestinal mucosa
- empty into portal vein and are transported via lipid carrier proteins directly to the liver -used for energy production |
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Absorption of 2-monog's, long chain FA, cholesterol, lipophospholipids
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-absorbed from lumen by intestinal mucosa cells
- incorporated into lipoproteins and directed to the lymphatic system -w.in intestinal wall TG are resynthesized from mono-g's to DAGS to triglycerides -majority of absorbed lipids appear in form of chylomicrons that pass to lymphatic vessels of abdominal region and later to systemic blood |
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Lipid metabolism in fed state: dietary fat (triglycerides)
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Dietary fat hydrolyzed to free FA and monoacylglycerols in intestine by pancreatic lipase
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Lipid metabolism fed state: What happens to free fatty acids after they have been hydrolyzed from TGs?
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-Short chain can enter circulation directly
-all others are resterified with mono-g's in epithelial cells of intestine -these TGs enter circulation as lipoprotein particles called chylomicrons through the lymphatic system -TGs in chylomicrons can be cleared by lipoprotein lipase |
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Lipid metabolism fed state: what are the 3 fates of fatty acids after they have been freed from chylomicrons by lipoprotein lipase?
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1. Can be stored as fat in adipose tissue
--remember TG can also be made from excess glucose/protein in fed state 2. Used for energy --remember most tissues rely on glucose for energy in fed state except for exercising muscle 3. Re-esterified to TG in the liver and exported as lipoproteins called VLDL |
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Difference between VLDL and chylomicrons in fed state lipoprotein metabolism?
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-both have the same fates (used as energy, stored as fat, re-esterified)
-chylomicrons collect TGs in the lymphatic system -VLDL made from re-esterified FFA in liver |
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Insulin regulation of lipid metabolism in the fed state? What enzymes does it act on etc?
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-Stimulates lipoprotein lipase
---stimulates release of FA from chylomicrons -Stimulates FA and TG synthesis in liver and adipose tissue -Inhibits hormone-sensitive lipase in adipose tissue --inhibits hydrolysis of TG into FA (catabolism) |
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Lipid metabolism during fasting and exercise: What tissues are using FA for energy? What tissues are not?
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-RBCs and brain are using blood glucose as energy source
-Resting muscle and most other tissue using FA for energy -Exercising muscle uses both glucose and FA |
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Lipid metabolism during fasting and exercise: Glucagon and epinephrine regulation
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- Stimulate HSL (horomone sensitive lipase)
--fat in adipose tissue hydrolyzed to give glycerol and FA during both fasting and exercise -Inhibit lipoprotein lipase --inhibit cellular uptake of free FFA etc -Inhibits FA and TG synthesis |
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Lipid metabolism during fasting and exercise: ketone bodies
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-During prolonged starvation, FA can be converted to ketone bodies
- can be used as energy source by all tissue w. mitochondria (no RBCs) - brain adapts slowly to the use of ketone bodies |
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Insulin resistance and VLDL irregularity
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-liver normally synth fat and exports as VLDL only in FED STATE
-when become insulin resistant VLDL levels are higher than normal (inhibition of lipoprotein lipase?) -LDL particles produced -lower HDL levels = dislipidemia |
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How does insulin normally control blood glucose and VLDL levels in fed state? (Liver and adipose regulation)
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- Inhibit HSL
--no FA released from adipose tissue -Stimulate glycolysis and inhibit gluconeogeneis in liver --acetyl-CoA used for energy -Stimulates FA and TG synthesis in liver --TGs made in liver and xported as VLDL -Stimulates lipoprotein lipase --FA are removed from VLDL and stored in adipose tissue |
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How does insulin control blood glucose and VLDL levels during the fed state? (Resting muscle regulation)
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Insulin stimulates:
-Glucose uptake via GLUT4 transporter -Glycogen synthesis -Protein synthesis |
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Glycolysis and mass action in resting muscle: implications in diabetes and metabolic syndrome
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-Glycolysis driven by mass action
-long term exposure to increased insulin levels can result in upregulation od enzymes involved in glycolysis -in fed state: 2/3 of G6P converted to glycogen and 1/3 enters glycolysis |
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-Overview of fatty acid metabolism during fasting and starvation: How is it controlled? (liver and adipose)
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-Glucagon activates HSL
--causing fatty acids to be released from adipose tissue -Mass action drives B-oxidation in liver: acetyl-CoA produced -Glucagon inhibits FA and TG synthesis -Acetyl-CoA enters CAC and is used for energy production |
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--Overview of fatty acid metabolism during fasting and starvation (resting muscle)
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-Glucagon has no direct effect on muscle
-Glucose not taken up bc GLUT4 xporter not at membrane (mobilized to membrane when epi present) -Glycogen neither synth or degraded -Protein synthesis not stimulated: net proteolysis (source of aa for gluconeogenesis) |
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-Overview of FA metabolism in Type I Diabetes (liver and adipose)
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-Insulin not produced
--can't inhibit lipolysis and gluconeogenesis --unable to stimulate FA synthesis -Lipid metabolism behaves as if body undergoing prolonged starvation --ketone body synthesis can become excessive -Net result: hyperglycemia and ketoacidosis |
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-Overview of FA metabolism in Type I diabetes: Resting muscle
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-insulin not present, uptake of glucose via GLUT4 transporter does not occur
-enough GLUT1 and GLUT3 driven by mass action (extracellular glucose high) compensate and enough glucose gets into muscle cells -muscle can still use fatty acids as energy source -insulin not stimulating protein synthesis: normal protein results in net degradation of proteins and release of aa's for gluconeogenesis -GLUT4 still activated by exercise, so exercising muscle still capable of using glucose as a primary energy source |
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-Overview of FA metabolism in Type 2 Diabetes (adipose and liver)
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-Liver is insulin resistant, but insulin is overproduced
-Gluconeogenesis stimulated but not to extent of Type I -TNFalpha and other adipokines activate HSL --high levels of FFA released by adipose tissue -most FA entering liver re-esterified to TGs--> these TGs accumulate as fat stores in liver -FA and TG synthesis are stimulated -TGs from acetyl-CoA and fatty acids released from adipose tissue and exported from liver as VLDL --- TNFa and other adipokines cause lipoprotein lipase to be inhibited ---accumulation of TG rich VLDL particles =DYSLIPIDEMIA -accumulation of DAG --activates PKC which interferes w. insulin signaling and contributes to insulin resistance |
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-Type 2 Diabetes Resting Muscle
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-Muscle is insulin resistant, but insulin is overproduced
--insulin levels high enough to drive most insulin dependent rxns --upregulation of enzymes involved in glycolysis due to insulin over-exposure -high flux of FA through mito leads to increase in reactive ox species which damage the mito --decrease B-ox bc decrease mito -Pyruvate produced faster than it can be used for energy production --excess converted to lactate --chronic elevation of blood lactate --hyperuricemia and lack of ketoacidosis in type II diabetes -B-ox inhibited --abnormal accumulation of TG fat stores in muscle -DAG accumulation-- PKC activation, interference with insulin signaling |
