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final notes

by: Annmarie Jaghab

final notes KIN 365

Annmarie Jaghab
GPA 3.91

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KIN 365
Dr. Wesley Smith
Study Guide
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This 15 page Study Guide was uploaded by Annmarie Jaghab on Tuesday December 1, 2015. The Study Guide belongs to KIN 365 at University of Miami taught by Dr. Wesley Smith in Fall 2015. Since its upload, it has received 114 views. For similar materials see KIN 365 in Physiology at University of Miami.


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Date Created: 12/01/15
1) good and bad cholesterol 2) ApoB vs APoA (good and bad?) 3) Statins (direct or indirect prevention of CVD) (Jupiter trial) 4) Dislipidemia, insulin and use of non-HDLC 5) Meilins of CAD links to lifestyle -there is no such thing as good and bad cholesterol, there are different cholesterol carriers, but only one type of cholesterol -cholesterol is important for the integrity of cell membranes -a statin drug lowers cholesterol so it lowers the integrity of the cell membrane -cholesterol is a precursor for vitamin D and then gets converted to D1 then D2 then D3 (the active form) -vitamin D is the most deficient vitamin -african Americans and the elderly are both prone to an increased deficiency of vitamin D -vitamin D has a very short half life so even if you are in the sun for a weekend, you will be deficient by the end of the week -coQ 10 is synthesized through vitamin D and CoQ10 is a carrier in the electron transport chain to get rid of reactive oxygen species, specifically superoxide -cholesterol is necessary for mylin sheath and for synthesis of hormones -cholesterol is considered bad in our environment because we evolved without cholesterol in our diet so our body got really effective at getting it from our diet and now we are provided with it at much higher levels than we had before which makes us better at using and storing it. -HDL and LDL are cholesterol transporters and transport cholesterol to the cells that need it -HDL is good and LDL is bad -when we first absorb cholesterol, we need to use bile salts in order to absorb the cholesterol and we package it into chylomicrons and the liver packages it all and lipoprotein lipase**** sucks the lipids out of the blood and deposits it in cells (like a fat vacuum). Exercise increases the expression of the enzyme, lipoprotein lipase, which means that the muscles can take the lipid from the chylomicrons and this is why exercise can lower cholesterol -VLDL is an apoB containing particle. It goes through the body and LPL throughout the body keeps taking the lipid out so it goes to an ILDL LDL -cell membranes with more lipoprotein lipase activity will result in lower cholesterol -LDL can get caught up behind the artery walls and get oxidized and become a modified LDL and become a foam cell which leads to atherosclerosis -HDL has apoA -the role of HDL is reverse cholesterol transport: remove cholesterol from arterial wall directly -trans fat would raise LDL the most (it is a partially hydrogenated vegetable oil that is unnatural because cis was made into trans) -when the trans fat gets into the LDL it hardens and makes it stiff and prevents LPL from splitting it and so the LDL levels go up -saturated fats also raise LDL because they are more solid and the LDL are more stiffened -ApoA are cardio protective because they remove cholesterol from artery walls -if you raise HDL by 4 points, your risk reduction is 32% (for every 1 point you raise HDL you lower your risk of heart disease by 8%) -when the liver is producing lipids quickly they are small but if it is slow they are large -insulin promotes high rates of fatty acid synthesis -when you have high triglycerides, it means they generate lipids at high rates so they have small LDL’s which is also correlated with insulin resistance -the larger the HDL the more protective it is against heart disease. -small dense LDL are the worst -high triglycerides are representative of a high rate of fatty acid synthesis -dislipidemia triad: high triglycerides, low HDL, and small and dense LDL -insulin promotes fatty acid synthesis -the national lipid association says that the most important marker is non-HDL cholesterol -ex. Non-HDL is total cholesterol-HDL so if 200 total and HDL is 35 you have 165 non-HDL. Over 160 non-HDL is a predictor of dislipidemia. -non-HDL does not have to be a fasted measurement -HDL have a ceiling at around 75 so over 75 they are no longer beneficial -HDL over 60 is a negative risk factor for heart disease (subtracts a risk factor) -CETP (cholesterololester transfer protein) transports cholesterol from HDL to VLDL in the liver. -what raises HDL: physical activity, it is largely genetic, niacin, coconut oil -heart healthy hypothesis was that if you have high cholesterol you have more plaque in arteries and it is not as simple as that. There will no longer be a focus on cholesterol in the USDA guidelines. Cholesterol in diet does not correlate with the cholesterol in the blood. -McDonalds French fries do not have cholesterol because it doesn’t have animal products, but it can still raise your body’s cholesterol because it has saturated and trans fats -a diet high in cholesterol increases the risk of cardiovascular disease in a linear trend -so the same relationship for risk of CVD can be seen in low fiber, low plant, high animal diet -statin drugs were designed to lower cholesterol in the blood -statin drugs are isolated from a compound found in red yeast rice (natural statin) -red yeast rice is banned but it is still being sold and acts as a pharmaceutical drug -process of forming plaque in arteries: 1) LDL find their way through damaged areas of the endothelial (damage caused by sugar, free radicals, etc) 2) LDL gets modified (they get oxidized, turn rancid) 3) free radical comes in contact with the LDL and it becomes a modified LDL 4) white blood cells turn into macrophages and look for modified LDL to eat up 5) macrophage eats the LDL and becomes a foam cell which is a pus filled pocket behind the artery wall -vitamin A is a fat soluble antioxidant so the LDL is less likely to become modified when you have vitamin A in diet -when you lower inflammation there is a corresponding lower free radical generation -lowering cholesterol may help more in an indirect fashion from the anti-inflammatory effects -high sensitivity CRP is indicative of inflammation (over 10ng/dl) -jupiter trial: found that statin drugs lowered heart disease in pre- diabetic patients mainly by lowering c reactive protein not by lowering LDL (so statin drugs lower cholesterol, but not by the mechanism that people think it does) -the Jupiter trial was stopped early because the data was so sure that it didn’t even need to be continued -why is the dislipidemia triad more concerning than having high cholesterol? They have a high particle number of cholesterol -if they have dislipidemia they have? Insulin resistance -insulin resistance is tested by a HOMA score. (Glucose in blood x insulin level)/405 a score of ≥ 3.16 would be insulin resistance (you don’t need to know how to calculate this for the final exam) or they have high TG, low HDL -high triglycerides lead to an increase in visceral adipose tissue and it gets oxidized and inflamed. TNF alpha contributes to help dislipidemia because it acts as a positive feedback -visceral fat makes no leptin (very small amounts) meaning we can accumulate it quickly but also lose it quickly because it has no set point -elevated triglycerides blocks leptin across the blood brain barrier which leads to an increased cycle of obesity (block leptin in rats fat rats) -CETP: exchanges triglycerides between VDLD and HDL so when triglycerides come up HDL goes down -insulin increases fatty acid synthesis so it leads to high triglycerides -HMG coA reductase forms cholesterol and coQ 10 (electron transporter in mitochondria) -a lack of coQ 10 would lead to electron leakage in mitochondria -if someone is on a statin they should be supplemented vitamin D and CoQ10 -those on statin drugs will have more eccentric muscle damage from exercise because they have weakened cell membranes -inflammation is the most likely cause of a heart attack -one of the major promoters of inflammation is TNF alpha (an immune stimulant, a cytokine released by macrophages and visceral fat cells and numerous immune cells, kills tumors and is called tumor necrosis factor. Seems to be beneficial) -immune surveillance and cancer: inflammation and tumor growth graph is an inverted U. so high inflammation reduces tumor cell growth so those that have seasonal allergies have lower cancer levels. Low grade inflammation increases tumor growth. -TNF alpha being elevated is usually on the side of the equation with low grade inflammation (usually seen with obesity) so it is not really a good thing -TNF alpha binds to the hypothalamus and induces a fever (endogenous pyrogen) -TNF alpha reduces apoptosis -when TNF binds to the hypothalamus it promotes the release of CRH which goes to the anterior pituitary which causes release of ACTH and then to the adrenal cortex to cause release of cortisol (HPA axis) -cortisol primary role is to increase glucose output from the liver so it could cause central obesity (cortisol is an anti-insulin) -physical inactivity disease zone: inactive abdominal adiposity macrophage infiltration of visceral fat chronic systemic inflammation insulin resistance, atherosclerosis, neurodegeneration, tumor growth -TNF alpha is a major cytokine produced by foam cells that activates acetyl coA carboxylase thereby inhibiting fatty acid synthesis and lead to increased fat accumulation which could cause insulin resistance and increase partitioning of fatty acids into the DAG state (intramuscular DAG is bad and acts as a second messenger to turn off insulin and can be a direct mechanism of skeletal muscle insulin resistance because of that) -the mitochondria cannot use the DAG one fatty acid at a time and oxidize them -those who are insulin resistant are less efficient at burning fat (DAG cannot be incorporated into the fat burning process) -TNF alpha increases hormone sensitive lipase for subcutaneous fat -TNF alpha increases FABP and increases CD36 and FAT for visceral fat -so essentially TNF takes fat and turns it from subcutaneous fat to visceral fat -TNF alpha fluctuates and is not as stable as C reactive protein, and this is why we measure c reactive protein -study took active college students over 2 weeks and told them they could only take 1500 steps a day and their BMI went down and there was less body fat via skin fold but they had a 7% increase in visceral fat and an elevation in inflammation (shows that there was migration of fat from subcutaneous to visceral stores from the inflammation) -IL6 has a negative feedback with TNF alpha because as TNF alpha goes up IL6 brings it back down -exercise is potently anti-inflammatory -during exercise, inflammation is only increased locally to the working muscle, but systemically, inflammation is lowered partly from the release of IL6 -weight loss is anti-inflammatory through adipokines such as adiponectin and possible less resistin. Visceral fat is the fat that gets most inflamed so a reduce in visceral fat would be best -a diet high in processed foods is high in omega 6 which increases inflammation -a diet high in plants is anti-inflammatory -TNF and the HPA axis -TNF alpha and body fat storage patterns -TNF alpha and acetyl coA carboxylase leading to DAG and insulin resistance -ambulance analogy -the cliff or the ambulance: for example if people are falling off a cliff the problem could be stopped by erecting fences or having an ambulance at the bottom. So by prevention you are also saving. People are profiting by the ambulances at the bottom -TNF alpha acts as an immune initiator -(subcutaneous/fat mass) ratio should be high, meaning you have less visceral fat -fat cell changes most 0-1 year old then 3-5 years old and then adolescence. So set point is being determined at childhood. -paleolithic era at 2.5 million years ago-10,000 years ago -about 75% of the Paleolithic diet was fruit (intrinsic sugar, has fiber in it and is not thought to contribute to cardiometabolic syndrome) -seasonal insulin resistance theory: fruit is mainly ripe during the fall months. The increase consumption of fructose would increase adipose tissue to prepare you and insulate you for the winter months. -paleo diet had 16-25% of monosaturated fat from wild meat, bone marrow and nuts (omega 9’s) -the Mediterranean diet is also high in monosaturated fat -paleo is low in cholesterol -plant sterols and fibers help reduce the cholesterol in the intestine -we are genetically predisposed to absorb all the cholesterol we get and hold on to it. -through the diet we have a positive feedback system with cholesterol because bile salts come from cholesterol and bile helps break down fat (so high fat diet makes you better at absorbing fat) -70% of the western diet was not available in the paleolithic diet: dairy, refined sugars, cereal grains, refined vegetable oils, alcohol. -resistance starch: increases the microbiota in the gut (acts as a probiotic to increase the good bacteria in the gut). Ex. Green bananas are a very good source. Mango is also a good source -protein diets are cautioned because it can lead to bone loss from inadequate calcium intake, but when you’re eating plants and getting vitamin D you are getting an increase in non-heme iron absorption -anthocyanins help convert alpha linolenic acid (omega 3) to EPA and DHA (synergistic effect) -corn and soy are our most abundant sources of omega 6 -fiber found mainly in largely viscous fruit fibers lowers glycemic index and forms short chain fatty acids -fiber increases microbial organism activity -best time to consume probiotics is around a meal EATING FOR MS VIDEO by Dr. Terry Wahls: -need B vitamins, antioxidants and sulfur for mitochondria -recommended 9 cups of vegetables, 3 cups are in each plate so 3 plates, 1 plate GFV, 1 plate brassicas, 1 plate of seaweed and color -the diet is basically plants and a side of grass fed meat -resveratrol: found in grapes, peanuts, and berries. Mostly in red wine. Seen to have anti carcinogenic effects, suppresses blood vessel growth, anti-inflammatory -carotenoids: major anti-inflammatory -Quercitin: major flavanoid, adenosine antagonist (like caffeine, found that eating an apple woke people up to the same degree as a cup of coffee), anti-inflammatory -the strongest carcinogen in the human body: IGF1 -Laron syndrome: congenital dwarfism resulting from a mutation in the hepatic GH receptor. They do not develop cancer, T2DM or acne. The consumption of the Western diet promotes IGF signaling (mainly dairy). Paleo diets are helpful to counteract it. -obesity insulin resistance increased IGF1 and IGF1 receptor carcinogenesis -effects of a low fat, high fiber diet and exercise program on breast cancer risk factors in vivo and tumor cell growth and apoptosis in vitro. They dripped the blood of the people on the cancer cells to see if apoptosis occurred. -hyperinsulemia lowers SHBG and IGF1 binding protein which leads to higher levels of IGF1 -well done meat intake is positively associated with Breast Cancer risk, while fruit and vegetable intake negatively associated -in a two week intervention from this plant based diet, there was a much higher rate of apoptosis (eating a high plant based diet and restricted animal protein to prevent cancer?) -IGF1 binding protein went up meaning they could take free IGF1 -when you weight train, IGF1 gets directed into the muscle and it’s no longer freely circulating in the blood (so weight training to prevent cancer?) -one way to measure apoptosis would be dUTP (marker of DNA damage) -fleshy foods like meat are similar to human tissue so when you have dairy proteins, you have higher IGF1 levels because BCAA’s can cross the blood brain barrier and so IGF goes up because the body assumes you need to fix broken down muscles even though you’re not working out -immune surveillance: natural killer cells have one job to hunt cancer cells and destroy them. When you exercise, natural killer cells get activated. -NEUGc compound can elicit an immune response (only made by animals, humans don’t make it so the only way we can get it is by eating meat). NEUGc can be activated and incorporated in cell membranes. -in the presence of NEUGc there were much higher levels of inflammation -cells use lysosome transporters -NEUGC caused angiogenesis -gave them anti-inflammatory chemicals such as an NSAID cox2 inhibitor and found that the tumor weight went down by half -NUGc is found in flesh meaty foods (even dairy) -cancer cells have high levels of NUGc in their membranes -it has been shown that when you have NUGc in cancer cells it produces a low grade antibody response against NUGc -the inflammatory response to NUGc enhances angiogenesis and tumor growth eat to starve cancer TED talk -soy actually decreases cancer risk because it is anti-angiogenic -food synergy even seen in combining teas -adipose tissue feeds cancer cells (if you give an obese rat an angiogenic treatment, it loses weight) -HIF vs NonHIF Angiogenesis: HIF related ones: 1) exercise associated cardioprotection (collateral circulation we develop extra blood vessels) GOOD 2) increased AVO2 difference GOOD 1) Retrolentral Fibroblastoma (risk of blindness in infants)BAD 2) Wet age related macular degeneration (due to poor circulation in eye and activation of HIF) BAD -HIF related diabetic blindness -drop in oxygen availabilityhypoxia induced factors surviveVEGF causes greater amounts of blood vessels Non-HIF ones: -leptin and angiogenesis -cancer develops blood vessels via non-HIF factors which are fragile and poorly constructed blood vessels whereas the ones made by normal hypoxia will help the bad vessels from growing -inflammation (NFKB, ROS) and angiogenesis (scar tissue) blood Q and fibrin. Blood flow and WBC’s -obesity relation to angiogenesis: for every pound of fat in the human body you need more blood vessels so leptin would increase blood vessels and promote angiogenesis -nutrient synergy: -vitamin E supplementation: more studies show bad than good -vitamin C alone not so good -vitamin C and E together has a good effect on preventing cancer -tomatoes greatly reduce the effect of prostate cancer -lycopene by itself won’t reduce cancer -EGCG: a hepatotoxin, very bad for you in supplement form -green tea: has a lot of benefit -ALA (alpha linoleic acid: comes from chia and flax but only 16% gets converted into DHA and EPA. Associated with anti-inflammation, decreased blood pressure and decreased CAD) -ALA plus anthocyanins results in 80% conversion into DHA and EPA which decreases inflammation, BP and CAD (so nutrient synergy ex. Berries and chia seeds in smoothie together) Nutrition and Health: -basic ROS cascade: when LDL become oxidized the inflammatory mediators create even more inflammation -free radicals generated from metabolism -in your body peroxisomes form hydrogen peroxide (bleach) to kill bacteria -Reactive nitrogen species: nitric oxide generated by endothelium which dialates arteries. Reacts with superoxides and makes peroxynitrate reactive oxygen cascade: -oxidative stress is promoted from unloading, aging, chronic inflammation, strenuous exercise, radiation -showed in a NASSA experiment that antioxidants could slow deterioration in zero gravity space -chronic inflammation increases ROS -2-5% of all oxidative phosphorylation results in ROS (mostly superoxide) -exercise increases free radicals but it also has many positive adaptations by increasing free radical defenses -if on a statin drug, you have less coQ10 so more protons would leak from the mitochondria -NADH oxidase also increases free radicals in sarcoplasmic reticulum -superoxide is turned into hydrogen peroxide by cu-zn SOD or Mn SOD -maganese superoxide dismutase (SOD) is in the mitochondria and neutralizes the hydrogen peroxide radical -aerobic exercise increases the amount of superoxide dismutase -if 2 O2reacts with iron, it forms OH- (a hydroxyl radical that damages proteins) which can lead to lipid peroxidation (oxidation of fat promotes inflammation) -MDA is a marker of lipid peroxidation, MDA binds to the DNA and is a DNA adjunct which causes defects leading to cancer -catalyse is an antioxidant enzyme that can take 2 H O2an2 turn them into water and oxygen -GPX (glutathione peroxidase): glutathione comes from selenium (comes from brazil nut) which results in hydrogen peroxide turning into 2 water molecules -thousands of phytochemicals but the water soluble ones: resveratrol, flavanoids, EGCG, sulphorophane, gingerol -found that treatments with antioxidant supplements actually increased mortality and decreased the expression of GPX and other antioxidant enzymes -fatigue index: decreases over time as force production decreases, but when vitamin C and E were put in the test tube there was a 40% improvement in reducing fatigue (done in a test tube in vitro so you can’t really say much from that) -gogi berries have a very high antioxidant amount -acai berries have the most antioxidants -some amount of free radicals is actually helpful because they bind to reanadine channels in the SR and it leads to greater calcium permeability (more Ca comes out of SR) -when oxidative stress exceeds buffering capacity is when oxidative stress becomes bad. (inverted U graph between force production and H2O2 production) -cross bridges between myosin and g actin get weakened from the free radicals -when we have mutation from DNA damage we have formation of malignancy -to destroy cancer: have Natural Killer Cells destroy them, tumor suppressor gene p53, cut off blood supply -inflammation as well as IGF-1 speeds up the process of going from a normal cell to a malignant cell -NfKB in skeletal muscle is good because it leads to hypertrophy. In other tissues, NfKB can actually turn off p53 and cause cancer -the anti-cancer diet: over 10 servings of vegetables a day. At least 4 servings of fruit a day. No refined sugar (cancer cells only use sugar for fuel). High fiber diet. Adequate caloric intake but not excessive. Lower caloric intake leads to lower metabolism which results in less free radicals nutrition and weight loss -Pima Indians are an example of a group of people who jumped through evolution very quickly. Were in Mexico as hunters and gatherers and the ones that move into the US are given food at liberal. 95% of pima Indians in the US have metabolic syndrome. They have the highest rates of diabetes and CVD. Study by Odea took 10 pima Indians to the coast line to live with people who foraged for food and they reversed their risks -obese sibling you have a 42% increased risk of obesity and obesity related disease (shows the genetic component). Compared to an obese friend/spouse, you have an increase risk of obesity by 171% (shows the effects of lifestyle) -over 1/3 of American’s are considered obese -developing countries: malnutrition (anemia and vitamin deficiency). Kwashikor so malnourished that plasma protein goes down and the water leaves the plasma and goes into the tissue spaces near the stomach -developed countries: chronic disease “syndrome x” abdominal obesity and diabetes -visceral adipose tissue is the easiest to lose because it does not produce leptin and therefore doesn’t have a set point -intermittent fasting works because you are depleting glycogen stores for a day as if you are exercising -you cannot spot reduce fat but to decrease visceral adipose tissue: 1) increase physical activity (the muscle glycogen is only used for muscles to work because they cannot be turned back into sugar since they do not have glucose 6 phosphatase) (PAL=TDEE/BMR) 2) lower carbohydrate levels (45% can use intrinsic sugars only (natural sugars that we need to free). Carb level should be linear with activity) 3) stress reduction (20 minutes) 4) sleep (6 to 8 hours of quality sleep per night) (lowers cortisol and lowers grehlin [makes you hungry] and higher CCK [makes you full]) -when you process the carbs it takes the germ and the endoperm with the fiber out and all you are left with is the sugar and the gluten. True whole wheat bread is sprouted grain bread (when you put white bread it water it turns mushy because the sugars dissolve whereas when you put whole wheat bread in water it doesn’t dissolve as much) -300% more glucogenogenesis and glucose output in people with metabolic syndrome (proves cortisol is partly responsible for obesity) **-metformin is a biguanide type medication (combats metabolic syndrome) that decreases ATP and increases AMP, metabolized in the liver, lowers gluconeogenesis by 1/3, thus reducing hepatic glucose output by 1/3, and increases AMP kinase -changes in sex hormones with those who are obese. Breast growth in men. Polycystic ovarian syndrome in women. -similar dopamine activation from sugar as there is to cocaine. Did a study with rats, half had cocaine and half had sugar and alternated and when they got to choose, 80% picked sugar -Liver fuel overload: 1) fructose: has a lower glycemic index, 100% of the time it goes to the liver 2) inactivity and stress 3) alcohol Increased Glucose Output Insulin has to increase -pyloric sphincter of the stomach duodenum (pancreas is positioned inside that folding)17 feet of the intestine -so when you have a free sugar it gets absorbed in the pancreas right away from the duodenum -glucose goes through a GLUT 2 transporterglycolysis occurs proinsulin gets cleaved into c-peptide and insulin -c-peptide can tell you if you are hyperinsulemic -type ½ diabetes: pancreas cells begin to die so a type 2 diabetic can turn into a type 1 diabetic -physical inactivity and stresscortisol/glucagonliver fuel overload increased glucose outputpancreas is stimulatedincreased insulin production fatty acid synthesis and reduced fatty acid oxidation[artery diseases such as heart disease. Leptin resistance which leads to increased obesity], visceral fat storage (NAFLD)[cancer and heart disease], obesity[diabetes], increased sodium retention [hypertension] -high levels of insulin turns on lipoprotein lipase and fatty acid binding protein -rat obesity is usually studied to look in depth at obesity but when they were put on a high sugar diet the rats just became more active -inactivitymitochondrial impairmentsmuscle lipid accumulationinsulin resistanceincreased insulin production fatty acid synthesis and reduced fatty acid oxidation[artery diseases such as heart disease. Leptin resistance which leads to increased obesity], visceral fat storage (NAFLD)[cancer and heart disease], obesity[diabetes], increased sodium retention [hypertension] -grew satellite muscle cells of obese and lean subjects and the lean ones could burn fat better when grown in a pitri dish so this is evidence that obesity is linked to mitochondrial impairments -the inability to burn fat makes the muscle cell resistant to insulin -intramuscular triglycerides are in runner so they can use it as a source of fat oxidation -A1c are glucose damaged red blood cells -if C-peptide levels are greater than 2.1ng/dl in T2DM, it indicates hyperinsulemia usually -when glucose enters the pancreas it is split into pro-insulin and c- peptide -insulin is supposed to do glucose disposal and c-peptide is supposed to do repair of glucose damage by being an antioxidant and repairing damaged tissues -when C-peptide levels are critically low, they may not be producing enough insulin meaning that there is apoptosis of the beta cells of the pancreas and a type 2 diabetic can turn into a type 1 because of life style factors -metformin decreases glucose output by 1/3. They suggest being on a Theraputic Lifestyle Diet which is low fat -no difference in retention between exercise and metformin in the diabetes prevention program (both 74% retention). Lifestyle was 40% more effective than medication -5 things that make up metabolic syndrome: (2400 increased risk of type 2 DM) 1) High triglycerides (over 135mg/dl) 2) high waist circumference (40in males and 35in females) 3) low HDL (less than 40mg Dl) 4) high systolic blood pressure (greater than 135) 5) high serum blood glucose (over 100) NEED 3 OF THE FIVE SYMPTOMS TO CLASSIFY METABOLIC SYNDROME -ectomorph: burns fat very fast so has trouble gaining weight -endomorph: has trouble losing weight -fatty acid oxidation vs lipolysis: lypolysis is breaking the ester bond in fats into fatty acids and glycerol via hormone sensitive lipase (which is turned on by Growth hormone, epinephrine, and nor epinephrine) -glycerol is the best marker of lypolysis -free fatty acids circulate bound to albumin and enter myocytes via diffusion or protein mediated transport -protein mediated sarcolemmal transport most important in active tissue -activated by AMPK: FAT/CD36, FABP, FATP-6 -long chain fatty acids need transporters to get in (FATCD 36) -increase fatty acid uptake is associated with high intramuscular triglyceride levels which leads to an increase in sarcolemmal without increases in total FAT/CD36 -glycerol is the best marker of lipolysis -ATP/AMP ratio is important because as soon as ATP is used it turns into ADP and AMP kinase takes 2 ADP and makes ATP AND AMP. -energy crisis: ATP levels go down and AMP levels go up -very high levels of glycogen saturation (in people who do not use their muscles) will create high ATP and low AMP ratio -FFA turns to long chain fatty acids which turn into DAG which turns off protein kinase C which can turn off the insulin cascade -in obesity there is a low level of fat burning enzymes (CAT, B-HAD, cytochrome C oxidase, citrate synthase) -in obesity cells are more glycolytic and there are 35% smaller mitochondria -obese subjects have higher RQ -obese have high levels of LCFA-CoA, DAG, and ceramide -found that in obese patients, fat oxidation went up from long slow distance training but not from high intensity interval training -1/2 people over 50 have metabolic syndrome -if someone is insulin resistant they are also IGF1 resistant and will have trouble growing muscle -prader willi: uninhibited release of ghrelin. So they are always hungry and their metabolic rate is lower from neuropeptide y. Genetic mutation that leads to obese children -set point is determined right after adolescence -the thirsty genotype: natural selection has favored those who can lay down extra body tissue when there will be famine -catabolic hormones: raise metabolic rate and make you full (cocaine and amphetamine, POMC and CART) -anabolic hormones: lower metabolic rate and make you hungry (NPY and AgRP) -triglycerides and leptin: TAG’s would be elevated in the bloodstream when you’re starving because cortisol is released which would increase TAG because you want to burn fat for fuel. TAG acts to block leptin receptors. -but a high level of TAG would lower metabolism and if you’re dislipidemic it becomes a positive feedback cycle -extra TAGs get deposited in skeletal muscle which leads to insulin resistance -so people with dislipidemia are much more susceptible to gaining weight -canabanoids are small lipids which give the “exercise high” -after exercise there is a “reward quest” style of hunger -abdominal cells produce cortisol on top of the cortisol you already release from the hypothalamus -losing weight gives you a pseudo prader willi syndrome -eccentric damage causes decreased uptake so long slow distance training is more beneficial in terms of improving insulin sensitivity -supplements for weight loss have: caffeine, white willa bar (aspirin, adenosine antagonist so it prolongs caffeine effects), ephedra (stimulant effect similar to cocaine) -weight loss from supplements is not sustained -only approved FDA drug for weight loss is “Alli” and many counterfeit strains are made -for females, if waist is 85% of hip they are at risk for insulin resistance. For men if it is greater than 100% they are at risk -gynoid obesity (thighs, buttocks, hips) is harder to get rid of -fat cell number is harder to decrease than cell size -caloric surplus is always needed even in obese children, they are growing and the surplus is what grows lean body mass -intermittent fasting: eating normally for 5 days of the week and eating 500calories for 2 days women (600 men) -


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