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Study guide for Exam 2: HNF 4611. How is glucose absorbed in the small intestine? With high [glucose] in the intestinal lumen, which pathway is dominant? - Glucose alone cannot cross cell membranes, it needs a carrier. - GLUT1 (RBCs), GLUT2 (liver, pancreatic B-cells, small intestine), GLUT3 (neurons), GLUT4 (muscle and adipose tissue)- 3 ways of glucose absorption in the small intestine:  sodium-glucose cotransporter (secondary active transport) When glucose (and fructose) in lumen is high: GLUT2 (facilitated diffusion) Fructose- GLUT 5 o To go out of the small intestine: glucose & fructose- GLUT22. How does insulin regulate intestinal glucose absorption? Through which transporter?- When insulin is released GLUT2 is inhibited- you already have enough glucose so you donot need to take in more. - Note: Insulin binds to receptors on muscle and adipose tissue only.- With glucose injection, you have less insulin produced because you are bypassing absorption; thus, more glucose is absorbed through GLUT2 due to the lack of inhibition.3. Understand the concept and the meaning of Km. How do the Kms of GLUT1, 2, and 4 compare to each other? What’s the physicological importance of that?- The > the Km, the < the affinity - The < the Km, the > the affinity - Glut 1 and 3 responsible for basal uptake in many tissues have a very low km (higher affinity)- Glut 2 in the liver, enterocytes, and pancreatic B-cells has a very high Km (lower affinity) - Glut 3 in the brain has a very low Km (high affinity) - Glut 4 in muscles and adipose tissue has a physiological Km, regulated by insulin.4. Does the liver absorb dietary glucose, fructose, and galactose from the portal vein differently? - Liver is the first organ after intestinal absorption, except for fats- Fructose and galactose are removed by the liver-o If too much fructose/galactose is consumed, the liver cannot process it all and it turns them into fat- Some glucose is removed by the liver (but GLUT2 has a high Km, low affinity)- Increase in blood glucose leads to insulin secretion5. What tissues have GLUT4? How is GLUT 4 regulated? By making new GLUT4 or by regulating its location in the cells?- GLUT 4 is present in muscle and adipose tissue - This transporter has a physiological Km. - GLUT 4 is regulated by insulin- insulin triggers translocation of GLUT4 from the vessels in the cell to the membrane6. What is diabetes? What is the difference between type I and type II?- Diabetes- Impaired fasting glucose. Impaired glucose tolerance. Lots of glucose in the blood. - Type I diabetes- An autoimmune disease that destroys pancreatic B-cells. This causes a lack of insulin secretion. The actions of glucagon and glucorticoids are not inhibited. Thebody keeps making glucose because it cannot absorb any from the blood. This leads to hyperglycemia, ketoacidosis, urination, and electrolyte imbalance. - Type II diabetes- tissues and organs are not responsive to insulin. Genetic predisposition coupled with environmental factors. Starts with insulin resistance in the muscle, which slows uptake via GLUT4. Increase in insulin secretion (but no glucoseuptake). Liver and adipocytes ARE RESPONSIVE, so adipocytes take in glucose and convert in to fat. 7. Know the conversion of [glucose] between mM and mg/dL. 5mM = 90 mg/dL. Remember the numbers unless you really know how to calculate them. - 10mM glucose=180 mg/dl- 5 mM glucose= 90mg/dl 8. Know how diabetes and prediabetes are defined based on the results of oral glucose tolerancetest. - Diagnosis of diabetes- impaired fasting glucose- 126 mg/dl or >. Impaired glucose tolerance- if plasma glucose is 200 mg/dl or > at 2 hours. - Prediabetes- Fasting plasma glucose between 100mg/dl and 125 mg/dl. Plasma glucose 2h post glucose consumption between 140mg/dl and 199 mg/dl. 9. What does HBA1C measure? Is it an indicator of a long-term or short-term glucose level? Why? - HBA1C measures glycated hemoglobin. This does not require fasting since it is based on free glucose in the blood. This is an indicator of long-term glucose level. 10. Is there an association between type II diabetes and obesity? - Yes, because the muscle is not responsive to insulin, the body keeps making insulin in hopes of increasing glucose absorption in the muscle. However, the liver and adipocytes are responsive to insulin, so the adipocytes increase lipid storage convert it to fat. - Prolonged increase in blood insulin leads to resistance in the liver. This makes it harder to control gluconeogenesis as insulin cannot inhibit this process. You get further increase in blood glucose, and more insulin secretion. - This leads to more obesity (adipocytes are still responsive to insulin and store fat)11. Describe the etiology of type II diabetes? In other words, insulin resistance in what tissues leads to type II diabetes? - Insulin resistance in muscle leads to type II diabetes. Eventually liver is resistant too. Adipocytes are not resistant, they are stimulated by insulin and take in glucose (and make fats)12. What are the a few key things to do to prevent or delay the onset type II diabetes? - The key is to prevent/limit muscle resistance - Prevent onset of obesity- Exercise (makes muscles more responsive to insulin)- Consume complex carbohydrates, legumes, whole grains. Low glycemic index foods withample dietary fiber. 13. What are the two systems that metabolize alcohol in the liver? - Alcohol metabolism in the liver:o Ethanol + NAD acetylaldehyde + NADH o Acetylaldehyde + NAD acetate + NADH o Acetate + CoA Acetyl CoAo 2 NADH produced, 1 acetyl CoA formed- Microsomal ethanol oxidizing system (MEOS)o Occurs in microsomeso Active when high alcohol intake o Yields H2O rather than NADH .14. How does alcohol alter the NADH/NAD ratio in the liver? What is the adverse consequence of that? - The metabolism of alcohol increases the NADH/NAD ratio, since more NADH is produced. - The high NADH ratio prevents the conversion of lactate to pyruvate (which forms NADH); thus, gluconeogenesis is inhibited- hypoglycemia occurs.15. Where is the hormone sensitive lipase? In what tissue? Inside or outside of cells? What does this enzyme do? How is it regulated? - The hormone sensitive lipase is located in adipose tissue. - It hydrolyses triglycerides to yield nonesterified fatty acids (NEFA)- Hormone sensitive lipase is activated by glucagon and epinephrine and inhibited by insulin acting on their respective cell membrane receptors -


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MSU HNF 461 - Study guide for Exam 2

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