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Phys Spring 4 Lec 7
Pancreatic Hormones
| Question | Answer |
|---|---|
| What are the cells of the pancreas? What structure are these cells a part of? | Beta cells (60%), alpha cells (25%), delta cells (10%); Islet of Langerhans |
| What do beta cells secrete? | Insulin |
| What do alpha cells secrete? | Glucagon |
| What do delta cells secrete? | somatostatin |
| Discuss the structure of the pancreas | Islets of Langerhans are supplied w/capillaries, which carry the secretions --> portal vein --> general circulation |
| What is the half-life on insulin in the circulation? | 6 minutes |
| Where is insulin metabolized? | Liver |
| Discuss the action of insulin at the insulin receptor | Insulin binds to receptor --> alters internal kinase --> initiates phosphorylation cascade --> GLUT-4 glucose transporters are moved to cell surface --> glucose uptake inc w/in seconds |
| Discuss the 3 mechanisms of insulin resistance | 1. Blockage of insulin binding to receptor; 2. Alteration of an intracellular link b/n insulin binding and the insertion of GLUT into cell membrane; Inc speed of internal degradation of the insulin-receptor complex |
| Discuss the 3 effects of insulin on CHO metabolism | 1. Inc glucose uptake into muscle & adipose tissue; 2. Inc glucose uptake into liver; 3. Inhibit gluconeogenesis in the liver |
| How does insulin affect muscle glucose storage? | In muscle, unused glucose is stored as glycogen. W/on insulin, muscle is almost impermeable to glucose. |
| TRUE or FALSE: The nervous system requires insulin for glucose transport | FALSE |
| How is glucose stored in the liver? | Stored as glycogen, and excess glucose is converted to FA |
| Discuss the effects of insulin on fat metabolism | Increases: glucose uptake into adipose, FFA absorption into adipose, and triglyceride (TG) synthesis in the liver; Reduces lipase action in adipose |
| What is glucose used for in adipose? | conversion of glycerol --> triglycerides |
| How are triglycerides (TG) transported from the liver to adipose? | By VLDLs & LDLs |
| What are the 4 effects of insulin DEFICIENCY on fat metabolism? | 1. Adipose tissue lipase is activated --> plasma FFA levels inc; 2. FFAs used for energy (normal); 3. Excess FFA inc cholesterol & TG synthesis in liver; 4. Excess FFA are broken down into acetoacetic acid --> leading to acidosis & conversion to ketones |
| Discuss the effects of insulin on protein metabolism | Inc: transport of glucose & AAs into muscle, and action of ribosomes in protein synthesis; Dec: catabolism of proteins by lysosomes, and gluconeogenesis by liver (so AAs are available for protein synthesis) |
| Describe the synergy between insulin & GH | Inc the rate/amount of weight gain |
| What are the 4 effects of insulin DEFICIENCY on protein metabolism? | 1. Protein synthesis stops, catobolism of proteins inc, plasma AA levels inc; 2. Excess AAs are used for energy or gluconeogenesis; 3. Urea levels inc in urine; 4. Muscle wasting, weakness, & organ dysfxn are all severe effects of diabetes |
| What stimulates insulin secretion? | 1. Inc plasma glucose; 2. Inc plasma AAs; 3. CCK, glucagon, incretins; 4. B-adrenergic & cholinergic stimulation |
| What inhibits insulin secretion? | 1. Dec plasma glucose; 2. somatostatin; 3. a-adrenergic stimulation (esp. during exercise) |
| What is the Incretin Effect? | Oral glucose induces a much greater insulin response than does the same amount of IV glucose. The GI tract secretes incretins, which inc insulin response |
| What is GLP-1? What is its fxn? | It is an incretin - Glucagon-like intestinal peptide. It is secreted into circulation to enhance insulin secretion |
| How is GLP-1 made? | The L cells of the GI tract produce proglucagon, which is then cut to produce GLP-1 |
| What is the fxn of glucagon? | Inc breakdown of liver glycogen & gluconeogenesis, inc rate of AA uptake into liver cells (for gluconeogenesis), and activates enzymes of gluconeogenesis |
| What stimulates glucagon secretion? | Hypoglycemia, inc plasma AAs,and exercise |
| What inhibits glucagon secretion? | Somatostatin, Insulin, Glucose |
| Relate glucagon levels to levels of plasma glucose | As plasma glucose dec, glucagon inc |
| What stimulates somatostatin secretion? | Inc blood glucose, inc plasma AAs & FFAs, inc CCK and other GI hormones |
| What inhibits somatostatin secretion? | Secretion of insulin, glucagon, dastrin, & GH; gastric & intestinal peristalsis |
| What is the fxn of somatostatin? | To slow down the entire digestive process |
| What controls glucose use in hypoglycemia? | Cortisol & GH decrease glucose use by most cells |
| Where is most glucose stored? | Liver |
| How are glucagon & insulin related? | Inversely proportional: Insulin acts in response to high blood glucose to reduce it, and glucagon acts in response to low blood glucose to increase it |
| What are the effects of hypoglycemia? | Headache, weakness, shaking, cold sweat, seizures, loss of consiousness, coma (glucose is required by the brain) |
| What are the effects of hyperglycemia? | 1. Osmotic & dehydration damage to tissue --> loss of body water in urine; 2. Inc risk of heart attack, stroke, and blindness --> glycation of proteins on endothelial cell walls |
| Discuss Type I diabetes | AKA insulin-sensitive, juvenile onset; 1. autoimmune dz d/t viral infection; 2. destruction of pacreatic B-cells; 3. Plasma insulin levels low/absent; 4. high plasma glucose |
| Discuss Type II diabetes | AKA insulin-insensitive, adult onset; 1. Dec sensitivity of target tissue to insulin --> "insulin resistance"; 2. High plasma glucose AND insulin --> B-cells constantly responding to excess glucose |
| What are acute complications of untreated type I diabetes? | 1. High glucose levels cause osmotic diuresis & dehydration; 2. Excess use of FA for fuel produces ketone bodies and results in metabolic acidosis; 3. w/o tx, will lead to death w/in months |
| What are the chronic complications of Type II and long-term type I? | Ongoing & inc damage to blood vessels, peripheral nerves, eye, and kidneys, primarily as an effect of high blood glucose via glycation |
| What is glycation? | The aldehyde group of a glucose attached to available NH2 on an AA sidechain (no enzyme required). Rearrangement follows, leaves attached glucose w/aldehyde available to attach another NH2. Cross-linking occurs --> stiffening of protein |
| Discuss the HbA1c test | Glycation occurs in RBCs. HcA1c measures the % of glycated Hb, which is an index of the avg glucose levels during the previous few months. An HbA1c score of 6 corresponds to an avg 115mg glucose/dL |
| What does glycation do to blood vessels? | 1. Stiffens blood vessel proteins --> dec compliance --> HTN --> local injury & atherosclerotic deposits; 2. Thickening of basement membranes of ECs --> less O2 & nutrient transport --> local necrosis & neuropathy |
| What does glycation do to nerve tissue? | Long-lived neurons accumulate glycation damage --> peripheral neuropathy --> major cause of non-traumatic limb amputation |
| What does glycation do to connective tissue? | Long-lasting connective tissue accumulates glycation damage |
| How is blindness caused by diabetes? How often does this occur? | Damage to lens proteins + retinal blood vessels + neurons --> adult-onset blindness. All type I pts and most type II pts have at least some retinal damage. |
Created by:
hclark86
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