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49 Cards in this Set
- Front
- Back
In addition to secreting insulin and glucagon, the eondocrin pancreas alos secretes which 3 hormones?
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1. Somatostatin
2. Amylin 3. Pancreatic polypeptide |
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List the different cells of the islets of langerhans and what they secrete.
Which cells are located centrally? |
a-cells: glucagon
b-cells: insulin d-cells: somatostatin f-cells: pancreatic polypeptide *B-cells are located centrally |
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Which organ is exposed to the highest concentration of pancreatic hormones?
Why? |
Liver
Venous blood from the pancreas drains into the hepatic portal V |
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The Vagal N stimulates the secretion of which pancreatic hormones?
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1. Insulin
2. Glucagon 3. Somatostatin 4. Pancreatic polypeptide |
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Sympathetic stimulation results in the secretion of which hormones?
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1. Glucagon
2. Pancreatic polypeptide |
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Sympathetic stimulation results in the inhibition of which hormones?
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1. Insulin
2. Somatostatin |
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Describe the 2 storage pools of insulin granules.
What type of release pattern results from these separate stores? |
5% stored in readily releasable pool
95% stored in reserve pool and need to be chemically modified/physically translocated to be used *Biphasic pattern of insulin release in response to stimulation of the B-cell by glucose |
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List the 3 locations of insulin degradation?
Which one is the major site of degradation? |
1. Liver <--major site
2. Kidneys 3. Peripheral tissues |
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Why is C-peptide used as an index of the secretory capacity of the endocrine pancreas rather than insulin?
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C-peptide has a longer half life (it is not degraded in the liver, like insulin)
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When do the 2 identifiable rhythyms of insulin release occur? (describe in period of minutes)
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First phase: 5-10 minutes
Second phase: 60 - 120 minutes |
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Which nutrients stimulate the release of insulin?
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1. Glucose
2. Amino acids |
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Which hormones regulate the release of insulin?
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1. Insulin (+)
2. GLP-1 (+) 3. Somatostatin (-) 4. Epinephrine (-) |
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Which neurotransmitters regulate the secretion of insulin?
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1. Norepinephrine (-)
2. Acetylcholine (+) |
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How is the regulation of K+ channels by ATP mediated?
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sulfonylurea receptor
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What is the major pathway in the mediation of insulin-stimulated glucose transport and metabolism?
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PI3-K activation
(phosphoinositide-3-kinase) |
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How can exercise stimulate glucose transport independent of PI3-K?
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Pathway involving 5'-AMP-activated kinase
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List 4 hormones/neurotransmitters that amplify insulin secretion.
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1. CCK
2. ACh 3. GLP-1 4. Gastrointestinal peptide |
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What is the effect of catecholamines on insulin secretion?
What type of mechanism is used? |
Inhibition
G-protein coupled receptors (also used by somatostatin) |
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Describe the immediate, early, moderate, and delayed effects of insulin.
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1. Immediate --> glucose transport
2. Early --> regulation of metabolic enzyme activity 3. Moderate --> enzyme synthesis 4. Delayed --> growth and cellular differentiation |
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Which proteins facilitate the interaction of the insulin receptor with intracellular substrates by serving as a scaffold for recruitment of proteins?
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IRS proteins
(insulin-receptor substrates) |
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Describe the insulin receptor.
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Heterotetrameric (2a, 2beta chains) linked by disulfide bond
a-chain = insulin binding b-chain = tyrosine kinase activity |
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Describe the 2 major pathways activated by insulin binding to its receptor.
What are the different roles of these pathways? |
1. PI3-K --> metabolic activity
2. MAPK --> proliferation, differentiation |
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How is the number of insulin receptors modified?
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1. Exercise
2. Diet 3. Insulin 4. Other hormones |
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How does chronic exposure to high insulin, obesity, and excess growth hormone effect the number of insulin receptors?
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Results in downregulation of insulin receptors
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How does insulin stimulate lipogenesis?
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Activation of acetyl-CoA carboxylase
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What type of physical conditions cause elevated insulin levels?
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1. High waist circumference/ high waist-to-hip ration
2. Excess visceral fat 3. High BMI 4. Sedentery lifestyle 5. High energy intake |
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What are the consequences of the proliferative effects of chronic hyperinsulinemia?
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(influence vascular smooth muscle cells)
1. Hypertension 2. Atherosclerosis 3. Cardiovascular disease 4. Dyslipidemia |
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Proglucagon is expressed in which 3 organs?
Which main products of proglucagon are expressed in these tissues? |
1. Pancreas --> glucagon
2. GI tract --> GLP-1 3. Brain |
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Where is GLP-1 produced and what influences its production?
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Produced in the small intestine in response to high conctration of glucose in the intestinal lumen
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What is the effect of GLP-1 on insulin?
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Amplifies insulin release
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What is the effect of somatostatin on insulin and glucagon release?
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Inhibits both
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What are the principle target tissues for glucagon?
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1. Liver
2. Adipose tissue |
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What is the MAIN physiologic effect of glucagon?
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Increase blood glucose by:
Stimulating de novo hepatic glucose via gluconeogenesis and glycogen breakdown |
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What is the effect of glucagon on adipocytes?
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Activation of hormone sensitive lipase
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What type of meals stimulate the release of somatostatin produced by d-cells of the pancreas?
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1. High-fat
2. High-protein 3. High-carbohydrate |
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What hormone inhibits somatostatin?
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Insulin
(d-cells located in periphery of b-cells) |
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What stimuli result in the release of pancreatic polypeptide?
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1. Food
2. Exercise 3. Vagal stimulation |
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Where is amylin stored?
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In b-granules along with insulin and C-peptide
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How does a meal affect plasma amylin concentrations?
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Increases plasma amylin
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What is the function of amylin?
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Works with insulin to regulate plasma glucose concentrations:
1. Inhibits post-prandial secretion of glucagon 2. Slows gastric emptying |
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What concentration of amylin would you expect to find in a patient with Type 1 diabetes?
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Low or absent
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What is the most common pancreatic hormone-producing tumor?
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Insulinoma
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What is the effect of a lack of insulin on circulating fatty acids and amino acids?
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Increases level of circulating fatty acids and amino acids
(decreased inhibition of lipolysis and proteolysis) |
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What is the earliest phyhsiologic indication of B-cell dysfunction in Type 2 diabetes?
What is the consequence of this defect? |
Delay in the acute insulin response to glucose
*Results in exessive rise in blood glucose, which then produces a compensatory and exaggerated second-phase hyperinsulinemic response |
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What are the 3 main pathologic defects in Type 2 diabetes?
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1. Excessive hepatic glucose production
2. Defective B-cell secretion 3. Peripheral insulin resistance |
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Can exercise decrease insulin resistance in patients with Type 2 diabetes?
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Yes
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What measurement is used to moniter glycemic control in patients with known diabetes?
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Hemoglobin A1C
(glycosylated hemoglobin) |
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Which diabetic treatment increases tyrosine-kinase activity in insulin receptors?
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Biguanides
(enhance insulin-mediated glucose uptake in skeletal muscle and adipocytes) |
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Which diabetic treatments delay the intestinal absorption of glucose?
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a-glucosidase inhibitors
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