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Alcohol Metabolism/Integration of Pathways

by: Channelle Brown

Alcohol Metabolism/Integration of Pathways HUN3224

Marketplace > Florida State University > Nutrition and Food Sciences > HUN3224 > Alcohol Metabolism Integration of Pathways
Channelle Brown

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About this Document

The information in these notes will be included on the cumulative final exam. Includes visual aids as well. (some of the slides are up in their entirety on Blackboard but I took extra notes as wel...
Intermediary Metabolism
Dr. Farrell
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This 16 page Bundle was uploaded by Channelle Brown on Saturday April 23, 2016. The Bundle belongs to HUN3224 at Florida State University taught by Dr. Farrell in Spring 2016. Since its upload, it has received 24 views. For similar materials see Intermediary Metabolism in Nutrition and Food Sciences at Florida State University.

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Date Created: 04/23/16
Alcohol Metabolism  Commonly associated with vitamin/mineral deficiency  Not a macronutrient because it is a toxin  Still has calories  Dietary guidelines o If you choose to drink, guidelines (moderate):  Equal to or less than 2 drinks/day – men  Equal to or less than 1 drink/day – women o 1 drink provides ½ oz. of ethanol  12 oz. beer  10 oz. wine cooler  1.5 oz. liquor (80 proof)  1 oz. liquor (100 proof)  5 oz. wine o Flavored alcohol – more flavoring/calories, less alcohol o Ethanol: combo of carbs and alcohol  Carbs are fermentedyeast gives off alcohol o Alcohol = 7kcal/g  TopHat: Per gram, does alcohol provide more calories than fat? o Answer: fewer than fat (9kcal/g), more than carbs (4kcal/g)  How many calories of EtOH in a 12 oz. beer is 5% ABV (alcohol by volume)? o 0.8 g/mL x ABV% x volume of beverage (mL) = g of alcohol o E.g. – 0.8 g/mL x 0.05 x (12 oz. x 30 mL) = 14.4 g EtOH o 1 oz.=30 mL o Budweiser 5%, 145 calories o Budlight 4.2%, 110 calories (lower caloriesless ethanol)  Alcohol Metabolism o 3 systems  Alcohol dehydrogenase (ADH)  Located in gastric mucosal cells in : o Gut (stomach) o Hepatocytes (liver)  ADH levels: o Men > women (why women die of alcoholism more than men) o Asian, natives, etc. < Europeans (why Asians get ‘Asian flush’ when drinking too much; not an allergy, just an intolerance) o Without ADH, it’s harder to break down alcohol  Function: o Converts an –OH into an aldehyde o Requires NAD  Men/Europeans: can consume more alcohol since they break them down faster o Reactions:  Ethanolacetaldehyde (still toxic)  Increases inflammation in GI tract those with IBS, problems with tract, etc. should avoid alcohol  Retinolretinal (vitamin A)  Can affect vision  More retinol used to metabolize alcohol so not as much goes to vision/eyes o *amount of enzymes produced varies o When we don’t have enough NAD to break down all EtOH(in blood) intoxication  TopHat: Where does alcohol metabolism begin? o Answer: stomach  Acetalydehyde Dehydrogenase  Located in liver  Function o Acetaldehydeacetate o Requires NAD  Makes energy o Goes into Krebs cycle  Problems: o Saturation of enzymesgoes to brain (we use all ADH and cannot break acetaldehyde downgoes to bloodintoxication/inflammation) o Depletion of NAD= decreased B vitamins  Deficiency found commonly in alcoholism  Microsomal ethanol oxidizing system (MEOS)  Location: smooth endoplasmic reticulum in hepatocytes (liver) o This is why you cannot get rid of intoxication at whatever time you want; liver metabolism is timed  SERworks like ETC o Utilizes riboflavin (FAD and FADH) and niacin (NADPH) o Cytochrome p450 (protein)  End products: o Water, NADP o Acetaldehyde  Inducible o We can change it if we drink more alcohol o Increased SER funtioning o Increased P450  Metabolizes xenobiotics o Why we don’t take medications and alcohol together  Medications can change the metabolism of other drugs  DrugsMEOS pathway  Especially prescription painkillers  It can double the effects and make it work faster/worse  MEOS pathway is smaller for people who don’t drink as often  Large MEOS when people consume a lot regularly (alcohol is metabolized faster) o MEOS=contributes a lot to tolerance o This pathway is very sensitive o “spillover pathway” o Dependent on ADH o Large personlarge blood volumethey can consume more (EtOH is more spread out throughout body)  Amount of fat free mass and fat mass doesn’t seems to make a difference since this pathway deals with hepatocytes in the liver o In alcoholics and those who regularly drink, MEOS will be induced before ADH is completely saturated; the body knows more drinks are coming  Catalase  Utilizes hydrogen peroxide  <2% EtOH oxidation  Acetate  About 20-30% stays in the liver o Acetateacetyl CoA o De novo fatty acid synthesis o Fatty acids: stay in liver, enter blood via VLDL  About 70-80% enters blood stream o Signals decreased fatty acids from adipose o Fatty acids that are released travel to liver  Enters muscle tissue o Acetateacetyl CoA o Oxidized to energy o Other Metabolic Changes in Response to Ethanol  Body slows other metabolic processes to metabolize alcohol  Gluconeogenesis decreases (hypoglycemia)  Protein synthesis decreases  Krebs cycle slowsfatty acid synthesis  Fatty acid synthesis increases  Ketone formation increases  NADH: NAD ratio increases  Running out of NADcannot metabolize alcohol  Why we make lactate from pyruvate to make more  There is a lot of disregulation when we consume alcohol  Organ specific  GI tract o Stomach increases HCl secretions o Acetaldehydetoxic (especially to mucosal cells)  Decreases intestinal absorption of almost all vitamins, especially B vitamins o Increases in iron absorption (in liver)where “stop” mechanism is  Damaged liverunregulated amount of iron comes intoxicity o Risks of GI tract cancers increases  Kidneys o Increased excretion of:  Mg, K, Ca, Zn (electrolytes) o Decreases ADH production  More fluid loss because of increased urine excretiondiuresis  Brain o Decreased oxygen o Can shut down if too loss EtOH, loss of consciousness  Protective mechanism so that the body can’t consume anymore  Passing out – due to how the body metabolizes  Liver o Fatty liver – fat builds up  After a day of drinking, you can see fat on the liver  It will eventually go away  Can be seen with alcoholics or nonalcoholics o Hepatic disease (cirrhosis)  Scar tissue builds up on liver o Lactic acidosis o Remember: the liver is the main storage site for vitamins and converts vitamins to metabolically active forms o Vitamin and Mineral Changes with EtOH  Fat soluble  Vitamin E o Antioxidant – protects cell and organelle membranes o Depleted with chronic EtOH (cell damage)  vit. E is used  Vitamin A o EtOH consumption=decreased levels of vitamin A o Retinolretinal via retinol dehydrogenase  The retinol dehydrogenase is “stolen” by EtOH  Low vitamin A, less retinol o Supplementation may lead to toxicity due to decreased liver function (too much of a good thing can be bad)  Water soluble – B vitamins  When drinking lots of alcohol, the body can’t use B vitamins so they go through the urine and leave the body  B1 = Wernicke-Korsakoff syndrome o Psychosis o Can be seen in those even after the quit drinking alcohol o ‘leftover alcoholism’ o Thymine deficiency = effects of drunkenness, ataxia, shifting eyes, short-term memory loss  Folate (B9) o Responsible for cell division/differentiation  Niacin and Riboflavin  Biotin (B7) and Pantothenic Acid (B5) o Decreased intestinal transporter  Vitamin C  Antioxidant, carnitine  Why? o Intestinal transport? Cellular transport? Decreased conversion of vitamin to active form (liver)? Increased utilization of vitamin?  Iron  Increases iron absorption  Liver usually puts a stop on iron absorption (regulates it), but if the liver is damaged, iron comes in unregulatedtoxicity o Toxicity can be seen in alcoholics who continue to eat heavily o Can also lead to hemochromatosis (iron overload) o Hangover  Dehydration  Increased fluid output with more EtOH consumption  Low blood sugar  Body metabolizesglucose into liver  Treatment/prevention?  CHO containing food?  B. vitamin before drinking? o Not really effective unless you already have a deficiency in B vitamins o If you don’t have a deficiency, you will just urinate them out  OTC analgesics? o Can help the symptoms (e.g. – headache, sore muscles from increased lactate, etc.) o They are metabolized through the liver so just be careful about the amount taken  Antioxidants? o Won’t really hurt TopHat: Why might alcoholics have iron toxicity? Answer: Decline in liver function results in increased iron absorption. TopHat: Chronic alcoholics have what kind of malnutrition? Answer: Kwashiorkor – with alcohol, there are plenty of calories but there’s low protein and distended fatty livers Integration of Cycles (*the Energy Expenditure lecture part of the slides is already all up on Blackboard)  Krebs cycle o Amphibolic pathway o Central to metabolism o Involved in both catabolism and biosynthesis of carbs, fats, and protein  Acetyl CoA o Pyruvate dehydrogenase reaction is not reversible  Reaction: pyruvateacetyl CoA o Must be used for energy, fatty acid synthesis, cholesterol synthesis, ketogenesis  Fed vs. Fasting o Occurs in shifts o Not clear cut o Fed  Primary hormone: insulin o Fasting  In stages and depends on the individual  Glucose-dependent tissues – erythrocytes, brain/central nervous system  We have to eat in order to get glucose; it is limited  Initially:  Glucose levels drop (below 60=BAD)  Glycogen stores are broken down o GlycogenG6P (only in liver)  Circulating amino acids are used for gluconeogenesis  We have lots of fat stored o Fatty acid are released in higher quantities  Few days:  Glucogenic amino acidskeep glucose levels up  Glycerol can also be turned into glucose  Fatty acids in other parts of body, metabolized into ketones  Early weeks:  Body conserves energy  Lowers body temperature, blood pressure, and kidney function  Minimal gluconeogenesis, spares body protein  About 10 daysbrain/CNS have to adapt to ketones o Ketone production increases o Some parts of brain only uses glucose  Minimal Krebs cycle as well  TopHat: What is happening to BMR at this point?  Answer: decreases but it depends (no right answer) o Depends on person and how long they’ve been fasting o Too efficient: ketosis o But body is trying to offset ketosis: body functions decline, making our body survive through starvation periods  Several Weeks:  Immune system declines  Fat stores are nearly depleted  Body begins to use lean body mass for energyPEM (protein malnutrition)  Near death (about 2 months)  Organs broken down for energyorgan failure  Even if that individual survives, there will be some permanent damage to organs  Women can survive longer than men since they have a higher percentage of essential fat  It can depends on activity level  Refeeding Syndrome (AKA hypophosphatemia=low phosphate levels) o At-risk  Severely malnourished  Anorexics  Morbidly obese after massive weight loss  The body still thinks it’s starving o What is it?  Abnormal metabolism resulting from an abrupt shift from fat to carbs as a substrate when a person is aggressively fed after a period of starvation; can be deadly (research: concentration camp survivors) o Symptoms/complications  Hypotension  Edema  Respiratory failure (due to the body straining)  Myocardial dysfunction (due to body straining)  Muscle weakness  Tachycardia  Dizziness o Why?  Starvation  Body uses fat for energy  Glucagon=main hormone  Begin to aggressively refeed  Increased insulin to cover CHO influx  Decreased glucagon o Decreased gluconeogenesis, fatty acid mobilization  Increased insulin levels induce glucose uptake into cells  At the same time:  Phosphorous in blood – driven into cells/tissues  Decreased phosphorous in bloodstreammuscle weakness  K, Mg, pulled into cells o Decreased serum electrolytes  body begins to retain fluid in extracellular spaceedema o Organ Specific  Heart: increased cardiac workload  Gut: atrophy with starvation o Treatment  Initially: restrict CHO and gradually increase  Increase protein to restore lean body mass  This won’t cause a big shift to insulin like carbs do  Maintain fluid balance  (clinically) monitor lab electrolyte values o K, Mg, Na, Phosphorous  Metabolic Syndrome o Cluster of symptoms (3 out of 5)  Elevated waist circumference  Equal to or > 40 in – men  Equal to or > 35 in – women  Elevated triglycerides  Equal to or > 150 mg/dL  Low HDL levels  <40 mg/dL – men  <50 mg/dL – women  High blood pressure  SBP: equal to or > 130 mmHg  DBP: equal to or > 85 mmHg  Increased fasting glucose  Equal to or > 100 mg/dL o Values vary in different areas of the world. The U.S. has stricter values than others. o TopHat: Diabetes is a diagnostic criteria for metabolic syndrome.  Answer: False. It is not linked to this syndrome. o Insulin resistance  Hyperinsulinemia  More insulin released from pancreas to regulate blood glucose  Increased insulin and glucose levels (neither are being used)  Tissues  Muscle (GLUT4 dependent) – insulin no longer stimulates glucose uptake  Adipose tissue – unregulated free fatty acid release  Liver (not GLUT4 dependent) – retains insulin sensitivity; picks up all glucose o Insulin stimulates triglyceride synthesisfat (adipose tissue) o Increased VLDL and serum triglycerides stay in liverfatty livernonalcoholic fatty liver disease  Kidney – retains insulin sensitivity, tries to take care of glucose o Increases sodium retentionhypertension o Treatment  Medications for symptoms: polypharmacy (multiple meds can cause even more problems because of side effects, etc.)  Weight loss  Diet – low fat is not beneficial if they are high simple carbs  Exercise o Physical Traits/Symptoms  Acanathosis nigricians – darkening around the neck/other body folds and creases  Lipodystrophy and more fat around the neck area  Excess adipose tissue that is visceral fatmore dangerous since it is putting pressure on organs o TopHat: How does exercise help with insulin resistance?  Answer: helps move glucose into GLUT4 mediated cells  Diets o Low fat  High CHO and low protein  Low protein – cannot maintain lean body mass  About 10% fat (normal intake – about 30%)  Examples: Dean Ornish (vegetarian), Pritikin (lean meat)  Advantages: decreased saturated fat  Metabolism: increased CHOincreased insulinstorage o Depending on calories consumed, you can still see weight gain o Low fat foods use sugar to replace the fat o Low CHO diets  Tend to be high in protein and fat  Some as low as 5% CHO (tricks body into ketosis)  Examples: Atkin’s, Southbeach, Sugar Busters  Advantages: protein sparing (keep LBM), no calorie counting since ketosis is less efficientweight loss  Metabolism:  Initially: increased glycogenolysis  Over time: lipolysis, beta-oxidation, ketogensis o Paleo diets  Different kinds for men, women, and active people  High in protein and veggies, low in fruits and fat/oils o All of these diets could have been somewhat healthy if marketing/food companies didn’t catch on o Eat real, whole foods and have a balanced diet *We did not go over muscle/exercise for the exam. Final Exam Info: o 75-80 questions o 27% of grade o Comprehensive from each section o Do not need a calculator o She likes integration of cycles/combined questions Alcohol Metabolism/Integration of Pathways – Diagrams/Charts


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