HNF 461 10 7 13 Lecture 15 Outline of Last Lecture I Glucose Uptake General Information II Glucose Transporters a GLUT 1 5 b Km Levels III Monosaccharide Absorption a Glucose Galactose b Fructose IV Regulation of Glucose Transport V Monosaccharide Transport Uptake a Role of Insulin VI Fate of Glucose Outline of Current Lecture I Type I Diabetes II Clinical Glucose Units III Diagnosis of Diabetes IV Prediabetes V Management of Diabetes VI Type II Diabetes a Progression b Management Treatment VII Hypoglycemia a Preprandial b Postprandial VIII Alcohol a Metabolism These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute b Microsomal Ethanol Oxidizing System c Consequences Current Lecture Diabetes Hypoglycemia and Alcohol 1 Type I Diabetes a Autoimmune disease that destroys beta cells in pancreas so cannot produce insulin b Actions of glucagon and glucocorticoids are unopposed c Can cause hyperglycemia ketoacidosis and excess urination which can cause dehydration electrolyte imbalance and net loss of nutrients 2 Clinical Glucose Units IMPORTANT TO KNOW THESE NUMBERS a 180 grams per mole b 10 mM glucose 180 mg dL c 5mM glucose 90 mg dL d 1 dL 100 mL 3 Diagnosis of Diabetes a Fasting Glucose Levels glucose levels are 126 mg dL or higher b Impaired glucose tolerance after meal if 2 hrs after meal glucose levels are 200 mg dL or higher 4 Prediabetes a Fasting plasma glucose levels between 100 125 mg dL b Plasma glucose 2 hrs post eating between 140 199 mg dL c If prediabetic there is a high chance that the disease will progress to diabetes in the next 10 years 5 Management of Diabetes a Monitor blood glucose b Monitor glycated hemoglobin measures how much sugar is bound to the protein 6 Type II Diabetes Caused by genetic and environmental factors obesity increases risk too a Progression i Starts with insulin resistance in the muscle so muscle is not responsive to insulin Increases blood glucose levels so liver produces more insulin adipocytes are still responsive to insulin so they take up more glucose increased lipid storage ii Liver becomes resistant to insulin more glucose accumulates in the blood which increases insulin production but eventually beta cells will fail due to over production of insulin b Management Treatment i Prevent limit muscle insulin resistance ii Weight control iii Exercise muscle cells can become responsive to insulin iv Consumption of complex carbohydrates legumes whole grains foods with low glycemic indexes and with ample dietary fiber 7 Hypoglycemia lower glucose levels than normal a Preprandial fasting levels of glucose are low b Postprandial reactive hypoglycemia too much insulin is produced post meal so too much glucose is absorbed into the cells lower glucose levels in blood 8 Alcohol provides empty calories provide only energy and no extra value nutrients a Metabolism Two oxidative reactions i Ethanol is oxidized to acetaldehyde by ADH requires NAD which is oxidized to NADH ii Acetaldehyde is oxidized to acetate by ALDH requires NAD which is oxidized to NADH iii Acetate can be converted to acetyl CoA which will participate in the TCA cycle b Microsomal Ethanol Oxidizing System i Occurs in microsomes where enzymes are present that can metabolize high levels of alcohol ii Yields H2O instead of NADH so contributes to less energy for the body c Consequences i Acetaldehyde may bind to proteins toxic to proteins ii Production of NADH will increase the NADH NAD ratio iii Can cause hypoglycemia lactate cannot be converted to pyruvate and lack of pyruvate leads to lack of pyruvate glucose conversion iv Fatty acid oxidation inhibited in the liver buildup of fatty acids in liver can become insulin resistant v Metabolism of vitamin A and drugs will decrease because they use the same enzymes that metabolize alcohol
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