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49 Cards in this Set
- Front
- Back
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5 Mechanisms that regulate enzyme activities |
1. Long-term adaptation -changes levels -FA biosynthesis and degradation 2. Feedback Inhibition -glycolysis 3. Allosteric modificaiton -any pathway -isozymes provide tissue specificity 4. Covalent modification -glycolysis, glycogen metabolism, zymogen activation 5. Compartmentation -fatty acid synth vs. degradation (put enzymes for diff pathways in diff compartments) |
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futile cycle (substrate cycling) |
-opposing pathways active siultaneously |
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Major energy carrying molecule(s) in a cell |
1. ATP -metabolism (catabolism) = make ATP -two high-E bonds (unstable negative Os) -~7 kcal/mol of E/bond when hydrolyzed 2. Creatine-phosphate -muscles use in addition to ATP |
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anabolic vs catabolic pathways |
anabolic pathways provide storage molecules that can be metabolized to generate E when catabolic pathways are activated anabolic: use E to synthesize molecules catabolic: generate E by breaking down molecules |
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vitamins |
-essential -not altered in most rxns; exceptions: NAD in redox rxns -cofactors |
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basal metabolic rate (BMR) |
- E required to keep all organs functioning while at rest
BMR (kcal/day) = 24 x weight (kg) -Mifflin-St. Jeor equation: more exact M: BMR (kcal/day) = [10 x weight (kg)] + [6.25 x height (cm)] - [5 x age (yrs)] +5 F: BMR (kcal/day) = [10 x weight (kg)] + [6.25 x height (cm)] - [5 x age (yrs)] -161 |
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daily caloric requirement |
-BMR + E for work: --sedentary: 1.3 x BMR --moderately active: 1.6 x BMR -- very active: up to 2 x BMR - weight gain: caloric intake exceeds daily E need --stored as triacylglycerol in fat cells -weight loss: caloric intake less than daily E need --triacylglycerol use, sever cases proteins in mm. --1 lb = 3500 Cal |
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BMI |
BMI = (weight in kg)/((height in meters)^2) = 703 x (weight in lbs)/((height in inches)^2) <18.5 = unhealthy 18.6-25.0 = normal 25.1-30.0 = pre-obese 30.1-39.9 = obese > 40 = morbidly obese *take w/ grain of salt |
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mechanism that maintains constant blood glucose levels |
Liver and muscle stores glucose as glycogen when levels are high glycogen in liver is degraded to make glucose when BG levels decrease |
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why its important to maintain constant blood glucose levels |
hyperglycemia--> frequent peeing, thirst, blurred vision, fatigue hypoglycemia --> AMS, coma |
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Metabolism in fed state |
- high insulin/glucagon ratio -mainly E storage |
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Metabolism in fasting (basal) state |
-bw/n meals= BG drops -reduced insulin/glucagon - heart uses FAs and lactate - KB levels remain low |
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Metabolism in starved state (~18-24+ hrs w/o eating) |
- low BG
- low insulin/glucagon ratio |
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utility of measuring levels of metabolites (and proteins) in blood |
-Metabolic problem: clues to where problem is/what enzyme is defective 1. lactic acidosis 2. ketoacidosis 3. orotic aciduria 4. hyperammonemia 5. hyper/o-glycemia 6. hypercholesterolemia -enzymes/proteins: 1. AST/ALT- liver leakage 2. lipase- pancreatic damage 3. CPK/troponin isozymes - heart damage 4. glyosylated proteins (HbA1c)- lack of glycemic control |
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Metabolism |
1. converts nutrients into: -E -E storage molecules -critical metabolites for biochemical 2. waste product production and removal 3. precursor generation for cell growth and function 4. regulation -cellular level -whole body level (hormones) *allows scientists/physicians to understand disease at molecular level |
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Normal blood glucose level |
70-100 mg/dL |
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Nutrients |
1. Carbs (sugars) 2. Lipids (fats) 3. Protein (composed of aas) 4. Alcohol (ethanol) |
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Carbohydrates (sugars) |
-main: glucose -no essentials -4 Cal/g -stored as glycogen in muscle and liver |
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Calorie |
1 Calorie= 1 kilocalorie of E 1 kilocalorie= E needed to raise the T of 1 L of water 1 oC |
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Lipids (fats) |
-two essential: 1. linolenic acid 2. linoleic acid -9 Cal/g -storage: triglyceride in adipocytes -major E source when fasting |
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Protein |
-composed of aas (20) -9 essential aas -4 Cal/g -storage: excess aas converted to glycogen or triglyceride, nitrogen excreted as urea |
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Alcohol (ethanol) |
-7 Cal/g -storage: triglyceride |
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Why do lipids produce more E on a per C basis than carbs/proteins? |
-lipids are more reduced (=more e- available) |
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vitamin deficiency diseases |
-scurvy -Wernicke-Korskoff synrome -beriberi -rickets (D) -bleeding disorder (K) -megaloblastic anemia (B9/B12) -pellagra (B3) |
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water soluble vitamins |
B1- thiamine B2- riboflavin B3-niacin B5- Pantothenic acid B6-pyridoxine B7-biotin B9-folic acid (1 C carrier) B12-cobalamin |
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fat soluble vitamins |
A (vision) D (calcium, hormone) E (antiox) K (blood coagulation) |
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Metabolism in fed state: CHO |
Intestines: CHO --> glucose exported to blood Blood: glucose --> Liver, Brain, RBC, Muscle, Adipose tissue Liver: glucose --> *glycogen (storage) glucose --> *acetyl CoA --> *TG --> blood as VLDL --> FA + glycerol --> adipose tissue --> *TG (storage) glucose --> *acetyl CoA --> TCA --> CO2, ATP Brain: glucose --> acetyl CoA --> TCA --> CO2, ATP RBC: glucose --> pyruvate --> lactate Muscle: *glucose --> acetyl CoA --> TCA --> CO2, ATP *glucose --> *glycogen (for m. use ONLY) Adipose: *glucose --> *TG (storage) |
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Metabolism in fed state: TG |
Intestines: TG --> blood as chylomicrons --> FA + glycerol --> adipose tissue --> TG (storage) |
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Metabolism in fed state: Protein |
Intestines: exported to blood as aa --> liver, tissues Liver: stored? Tissues: aa <--> protein aa--> important cmpds aa --> TCA --> ATP + CO2 |
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Metabolism in fasting (basal) state: glycogen/glucose |
Liver: glycogen --> glucose --> blood --> brain, RBC Brain: glucose --> acetyl CoA --> TCA --> CO2, ATP RBC: glucose --> lactate |
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Metabolism in fasting (basal) state: lactate |
RBC: lactate --> blood --> liver --> glucose |
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Metabolism in fasting (basal) state: TG |
Adipose: TG --> blood as FA and glycerol FA--> muscle --> acetyl CoA --> TCA --> CO2, ATP FA--> liver --> ATP, Acetyl CoA --> KB --> blood --> muscle --> acetyl CoA --> TCA --> CO2, ATP glycerol --> liver --> glucose |
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Metabolism in fasting (basal) state: Protein |
Muscle: protein --> aa --> blood --> liver --> glucose, urea--> blood --> kidney --> urine |
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Metabolism in starved state: Glucose |
Liver: glycogen depleted glucose --> brain (60% normal levels) --> acetyl CoA --> TCA --> CO2, ATP glucose --> RBC --> lactate |
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Metabolism in starved state: TG |
Adipose tissue: TG --> FA --> blood --> muscle, liver TG--> glycerol --> blood --> liver --> glucose Muscle: FA --> acetyl CoA --> TCA --> CO2, ATP Liver: FA --> ATP, Acetyl CoA --> KB --> blood --> brain (40% of brains E source) --> acetyl CoA --> TCA --> CO2, ATP **brain uses KBs to decrease glucose need to decrease protein degradation in muscles |
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Metabolism in starved state: Protein |
Muscle: (occurring at reduced levels compared to basal) protein --> aa --> blood --> liver --> glucose, urea --> kidney --> urine |
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Metabolism in starved state: lactate |
RBC: lactate --> blood --> liver --> glucose |
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Carbohydrate Metabolism |
Glycolysis: -entry of sugars into met Gluconeogenesis: -synthesis of glucose from metabolic precursors Disorders: *Diabetes -hereditary fructose intolerance -lactase deficiency -glucose 6-phosphate dehydrogenase deficiency -galactosemia pyruvate kinase deficiency |
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Glycogen Metabolism |
-glycogen synthesis and degradation -storage form of glucose in liver and muscle --tissue specifc regulation, use it differently Disorders: -Glycogen storage disease |
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Generating Energy |
TCA Cycle: -central point of metabolism -generates orecursors for biosynth Oxidative phosphorylation: -generates E from transfer of e- to O2 disorders: -mitochondrial diseases (OXPHOS disorders) --> symptoms mainly in E requiring tissues = mm. and nervous system |
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Fatty Acid Metabolism |
-synth and degrad -preferred E storage form--> triacylglycerol in adipocytes -can't be used to synth carbs -become KBs in special conds disorders: -diabetes -carnitine deficiency -Jamaican vomiting disease -MCAD deficiency |
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HMP Shunt Pathway |
-alt means of glucose oxidation -converts 6 and 5 C sugars -generates NADPH --> anabolic pathwyas -direction of pathway depends on need of cell disorders: -glucose-6-phosphate dehydrogenase deficiency (most common X-linked disease in world) |
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HMP generates 5 C sugars which are need for? |
Nucleotide synthesis |
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Urea Cycle and AA Metabolism (what to do w/ N) |
-ammonia toxic to NS -aa N --> urea --> excreted - aas give rise to glucose/acetyl-CoA--> enter TCA cycle at defined points -B6, B12, folic acid have roles in aa metabolism disorders: (aa catabolic disorders) -urea cycle defects --> hyperammonemia --> irreversible mental deficiencies -PKU -MSUD -tyrosinemia -homocysteinemia -megaloblastic anemia |
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Base and Nucleotide Metabolism |
Purine and Pyrimidine Syntesis and degradation -all can be synthesized de novo -salvage pathways reduce demand on biosynthetic pathwya disorders: -excessive purine degradation --? uric acid accumulation --> gout -ADA deficiency -Lesch Nyhan syndrome -hereditary orotic aciduria |
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Cholesterol Biosynthesis |
(can't live w/o it!) -steroid hormones -required cofactors for e- transport -cholesterol metabolism and recirculation of cholesterol throughout body -LDL, HDL, VLDL, chylomicrons disorders: -heart disease |
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Enzymes |
-catalyze all rxns in metabolism -aid substrates in approaching TS = decrease E required to reach TS -do not change overall eguilibrium constant -regulated to control activity --> pathway regulation to prevent substrate cycling, pathways from occuring when don't need end proudcut, stimulate pathways when needed |
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In fed state after eating high carb meal, what pathway would be inhibited? |
gluconeogenesis |
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100 g carbs, 100 g protein, 100 g fat, 20 g alcohol = ? Cals |
1840 Cals |
