pancreas Flashcards by Yazmin Ortiz

what are the main tissues that insulin regulates (3)

liver» glucose into glycogen
muscle> glucose uptake into muscle
adipose» glucose into fat to form triglycerides

How well did you know this?

Not at all

Perfectly

what is glucagon,what does it oppose, what does it do?

-opposing hormone to insulin
- stimulates glycogen breakdown and increases glucose release from the liver

How well did you know this?

Not at all

Perfectly

what are the functions of the pancreas
- what is their percentage of pancreatic mass

exocrine(98%) and endocrine function (2%)

How well did you know this?

Not at all

Perfectly

what part of the pancreas is responsible for endocrine function

islets of langerhan

How well did you know this?

Not at all

Perfectly

what are the cell types of islets of langerhan , what is their percent make up, and function

alpha cells (20%)- secrete glucagon and increase plasma glucose and mobilize glycogen and fat

beta cells (60-75%)- secrete insulin to increase glucose uptake and deposit glycogen and fat

delta cells (<5%)- secrete somatostatin and decreases insulin and glucagon secretinf and decreases excocine gastric secretions

F cells <5% - secreate pancreatic polypeptide to decrease foood absorption

How well did you know this?

Not at all

Perfectly

synthesis and structure of insulin

pre-proinsulin has A, B ,and C Chain with A and b linked by 2 disulfied bond
signal sequence is cleaved from pre-proinsulin to form pro-insulin
cleavage of the C peptide chain to leave active insulin
insulin and C peptide stored in secretory granuels complexed with zinc for storage and release

How well did you know this?

Not at all

Perfectly

how does C peptide have a diagnostic use

in synthetic insulin there is no C peptide so it can be used to measure how much endogenous peptide is being prodcued

How well did you know this?

Not at all

Perfectly

in what cells is insulin synthesized and stored and what is its form when synthesized

in beta cells which synthesisezes pre-proinsulin

How well did you know this?

Not at all

Perfectly

what is the half life of insulin in circulation

5 min

How well did you know this?

Not at all

Perfectly

what are the normal glucose levels
- what happens as glucose increases about this range

5.5mM ( 1000mg/dL)
insulin is stimulated

How well did you know this?

Not at all

Perfectly

what is the relationship between glucagon and glucose

inverse relationship- when glucose is high glucagon is low and when glucose is low glucagon is high

How well did you know this?

Not at all

Perfectly

what is the relation ship between insulin and glucagon

as insulin rises glucagon drops

How well did you know this?

Not at all

Perfectly

what is the relationship between glucose and insulin

when glucose rises insulin rises and when it drops insulin drops

How well did you know this?

Not at all

Perfectly

what is the mechanism of insulin secretion

glucose enters beta-cells by GLUT 2 transporters
its phosphorylated and metabolized into pyruvate and further metabolized in the citric acid cycle
ATP formed by oxidative phosphorylation inhibits ATP sensitive K channels reducing K efflux
THis depolarizes the B cell and increases ca influx which stimulats the release of insulin

How well did you know this?

Not at all

Perfectly

insulin secretion is modulated by ____ and ____ signals

metabolic and hormonal

How well did you know this?

Not at all

Perfectly

what are the stimulators of insulin secretion

glucose, glucagon, amino acids, GLP1s

How well did you know this?

Not at all

Perfectly

what are the inhibitors of insulin

somatostatin and catecholamines ( alpha adrenergic)

How well did you know this?

Not at all

Perfectly

mechanism of insulin activated glucose transport

activation of insulin receptor intiates translocation of GLUT 4 containing endosome into the cell membrane,
GLUT 4 then mediates glucose transport into the cell

How well did you know this?

Not at all

Perfectly

what are the transporters that transport glucose via active transport and what is their function

SGLT 1 and SGLT 2 are involoved in active glucose transport into the the gut and kidney(renal tubules)

How well did you know this?

Not at all

Perfectly

what are the facilitated transporters of glucose and what are their function

GLUT 2 -12-20 Km - uptkae of glucose into beta cells

GLUT 4 - 5Km- insulin stiumulated glucose uptake in skeletal and cardiac muscle, adipose, and other tissues

How well did you know this?

Not at all

Perfectly

Effects of insulin on metabolic fluxes
- what are the effects of insulin on muscles, liver , and adipose tissue ( what does it stimulate and inhibit)

muscle stimulates glucose and amino acid uptake
and inhibits amino acid release
inhibits glucose release from the liver
stimulates glucose uptake into adipose and inhibits relaease from free fatty acids and ketogenesis

How well did you know this?

Not at all

Perfectly

what is glucagon synthesized by and when is stimulated

synthesized by alpha cells and stiumulated when glucose is low

How well did you know this?

Not at all

Perfectly

what is the half life of glucagon and what is it degraded by

5-10 min - degraded by the liver

what gene is glucagon synthesized by and in what form is produced

GCG gene produced as a pre-prohormone which is cleaved in alpha cells to yield glucagon

what does the GCG gene also give rise to and what is its function

GLP-1 glucagon like polypeptide -is it incretin and enhances the secretion of insulin and increases glucose uptake from the blood

what are the stimulators of glucagon secretion

what are the inhibitors of glucagon

effects of glucagon on metabolic fluxes - what are the effects of glucagon on the liver and adipose tissue

- stimulates the generation of glucose from glycogen and amino acids in the liver - and mobalization of fatty acids in fat

by what cells is somatostatin produced by

delta cells in tha pancreas

what is somatostatin release stimulated by

stimulated glucose and amino acids ( same as insulin)

what is the affect of somatostatin on the islets and GI

inhibts the release of islet hormones such as insulin and glucogon - in the gi tract it decreases glucose absorption and decreases blood flow

how do epinephrine and norepinephrine affect glucose metabolism

- epinephrine stimulates glucose production by increasing gluconeogenesis iin the liver and glycogenolysis in the liver and muscle - inibits the action of insulin - lipolyisis and ketogenesis are stimulated INCREASE BLOOD GLUCOSE

what is the major effect of cortisol on metabolism

stimulates mobilization of amino acids and their conversion to glucose

how does cortisol do to insulin and adipose tissue

- inhibts glucose uptake by insulin and can cause mobilization of fat or facilitate fat storage

what is cortisol describes as since it increases glucose

hypeglycemic but doesnt stimulate glycogen deposition

what is the endocrine hormone of adipose tissue -what is the amount of secretion proportional to

leptin and is secreted propotional to the amount of adipose tissue

what is the function of leptin

reports the size of adipose mass to the hypothalamus

what happens with exxcessive food intake

increase adipose mass, leptin increases and leads to a series of behavorial and metabolic changes

what are the effects of leptin

- reduced appetite, incresased energy expenditure, thermognesis etc

what does mutation of leptin do to the mouse

eats too much and gets fat

what is the most common cause of hypoglycemia and convulsions

overdose of insulin

why is the brain sensitive to hypoglycemia

- it has little stored carbs and depends on glucose for energy

what are the symptoms of hypoglycemia

cognitive dysfunction lethargy coma convulsions brain damage

what is Diabetes mellitus caused by

defieceny in the effects of insulin

what is type 1 diabetes -what is it called - what is it caused by

insulin dependent mellitus - due to primary failure of insulin secretion by the endocrine pancreas

what is type 2 diabetes -what is it called and what is it caused by

non insulin dependent diabetes, due to loss of insulin sensitivity of the tissues which is acompannied by reduced inuslin secretion

what is DM charecterized by and what is the cause of these effects

- polyuria (excessive urine output), - polydipsia (excessive thirst), - polyphagia (excessive eating), - hyperglycemia, - glucosuria (glucose in urine) The primary cause of these effects are failure of glucose uptake

when does type 1 diabetes (IDDM) present and what is the casus - what is the treatment - what are the levels of plasma insulin - what happens to weight

presents early in life so called juvenile onset diabetes - caused by loss of pancreatic beta cells other cells remain intact - insulin is low -weight loss administer insulin

when does type 2 diabetes present - what is the cause - what are the insulin levels - weight - treatment

presents later in life >40 adult onset diabetes - caused by the development of insulin resistance - may over stimulate beta cells to compensate for low insulin - insulin can be low or near normal - cant administer insulin - patients are generally obese - Treatments include sulfonylureas, metformin and diet

diagnosis diabetes mellitus with the glucose test

- when glucose is given plasma glucose increases greater than normal and doesnt decrease for a ling time

how can you measure blood glucose with HbA1c

- measures how much glucose is covalently bound to hemoglobin - can measure a 3 month time window and how much glucose was consumed

what is a normal and prediabetic,diabetic A1c

normal 4.5-5.6 pre- 5.7-6.4 diabetic- >6.5

metabolic syndrome - what are the metabolic risk factors

Abdominal obesity * High plasma triglycerides * Low HDL- and high LDL- cholesterol * High fasting blood glucose * Insulin resistance * Elevated blood pressur

what diseases are increased with metabolic syndrome

* Type 2 Diabetes * Coronary Artery Disease * Stroke