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Study Guide - Metabolism (Week 3).pdf

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Study Guide Metabolism (Week 3) A. State the fates for the energy released from breaking the phosphate bonds in ATP 1. Energy to drive chemical reactions 2. Heat B. State the general pathways by which AT...

Study Guide Metabolism (Week 3) A. State the fates for the energy released from breaking the phosphate bonds in ATP 1. Energy to drive chemical reactions 2. Heat B. State the general pathways by which ATP can be produced 1. Combusion of carbohydrates i. Glycolysis ii. Citric acid cycle 2. Combustion of fatty acids i. Beta-oxidation 3. Combustion of proteins (after being broken down into amino acids) C. Describe the role of phosphocreatine for energy transfer 1. Reversible reaction used to generate ATP 2. Phosphocreatine + ADP ↔ ATP + Creatine i. Moves rightward whenever ATP levels become ever so slightly depleted (a) Maintains high ATP levels in cell (a) Acts as ATP “buffer” ii. Moves to the left when ATP demand is low (a) Phosphocreatine is resynthesized 3. “Immediate” source of chemical energy 4. Also known as “creatine phosphate” D. State the end products of glycolysis 1. 2 molecules of pyruvate 2. ATP i. 2 ATP if glucose is used ii. 3 ATP if glycogen is used (a) Thus, glycogen is a better source of energy than glucose! E. State the sources of anaerobic ATP availability/production, and how long they can sustain exercise independently of oxidative metabolism 1. Existing ATP in cell – ~1 second 2. Phosphocreatine – 5-10 seconds 3. Glycolysis - ~30-60 seconds F. Rank and briefly describe the amount of energy sources in the body 1. Most = fat mass 2. Glycogen = storage form of glucose i. Found in liver, skeletal muscle, and kidney 3. Glucose = found in blood stream 4. [Protein = abundant, but not typically used for ATP production G. Briefly describe blood glucose regulation 1. Glycogen – production of glycogen from glucose i. Turned on by insulin 2. Glycogenolysis – breakdown of glycogen 3. Gluconeogenesis – formation of new glucose from amino acids 4. Controlled by various hormones i. Insulin (a) Takes glucose from blood and puts it into skeletal muscle, adipose tissue, and liver (a) This lowers blood glucose levels (b) This allows glucose to be saved in the form of glycogen for later usage (b) Promotes glycogen formation (c) Turns off gluconeogenesis ii. Glucagon and epinephrine GENERALLY do the opposite (a) Turn on glucose production in the liver H. Describe Diabetes Mellitus 1. Excess blood glucose i. Causes blood to accumulate in urine (a) Causes urine to taste sweet (a) Due to glucose being filtered out and not reabsorbed in the kidneys (b) Because glucose is osmotically active, this causes water to be lost via urine (a) Polyuria = excess urine (b) Polydipsia = excess thirst 2. Type I diabetes mellitus i. Formerly known as “juvenile diabetes” ii. Primary pancreatic dysfunction – cannot produce sufficient insulin (a) Often immune-mediated 3. Type II diabetes mellitus i. Plenty of insulin is produced, BUT… ii. Cellular receptors are less sensitive to the effects of insulin (a) Glucose not able to enter skeletal muscle and adipose tissue (b) Blood glucose levels rise I. Briefly describe how diabetes mellitus leads to atherosclerosis 1. Excess glucose causes endothelial damage 2. Leads to atherosclerotic plaques i. Blood vessels do not function as well ii. Impaired blood flow to target organs (a) Impaired function of those organs (a) Heart disease (b) Retinopathy (c) Kidney failure iii. Increased heart attack (myocardial infarction) and stroke risk J. Briefly describe HbA1c test and the advantage of it over fasting blood glucose 1. Hemoglobin A1C is glycosylated hemoglobin i. Hemoglobin which has been exposed to glucose 2. Greater HbA1c indicates average blood glucose level across many weeks i. More informative than a single fasting blood glucose value ii. May reflect impaired glucose tolerance following eating, even if fasting blood glucose is normal K. Briefly describe “pre-diabetes” 1. Fasting blood glucose is above normal (>100mg/dL), but below diabetes threshold (e.g.,

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