Errede Ii: Insulin Signal Pathways

Front 1

increase in glucose, changes in cell chem

Back 1

glucose trans by glut2 is metab, increase atp to adp ratio. depolarizes cell membrane / bc closing of atp-dependent k-channels
-depol leads to opening of ca2.
promooes fusion of sec vesicles iwth plasma membrane and release of insulin.

this is all in the b cells in pancreas

Front 2

exocytosis of insulin requires

Back 2

increase in intracell ca2+

Front 3

insulin axn in target cell

Back 3

-inhibit production of glucose

Front 4

in liver:

Back 4

inhibits gluconeogenesis, glyocogenolysis
stimulates: glusoce phosphorylation, glycolysis, fatty acid synthesis, glycogen synthesis.

Front 5

insulin in muscle

Back 5

uptake of glucose in these celss is the rate-limiting step of glucose metabolism.
insulin stimulates a 10 to 20 fold increase in vmax for gucose uptake by:
stim activity of glut4 glucose carriers at plasma membrane. & increase number of glut4 carriers at pm. &also increases abundance of enzymes involved with aa, tg & glucose utilization.

Front 6

insulin regulations enzyme act

Back 6

-change in act are regulated by phosphorylation status. this reg occurss through phsoph and and act of protein phosphatase ( (PP-1). catalyzes dephsoph of key metab enzymes---

Front 7

insulin in lipid metabolism

Back 7

decreases lipolysis and increases action of lipoprotein lipase (LPL), so increases triglycerides

Front 8

IRS mol and type II receptors

Back 8

IRS MOL RECRUITED TO activated receptor via PTB (phosphtyrosine binding) domain intxn (PH stabilizes intxn at pm). tyrosine phosph IRS recurits downstream signaling mol via pY-sh2 domain intxn.

Front 9

insulin activated MAPK?

Back 9

REGULATES CELL GROWTH.:
glycogen synthesis, protein synth, cell growth.

Front 10

activated PI3- insulin

Back 10

activates PKB, WHICH MEDIATES MEMBRANE TRANSLOCA OF glut4. also glyc and protein.
NOT cell growth.

Front 11

type ii diabetes

Back 11

muscle, fat and liver cells lose some of their ability to respond to insulin (mild insulin resistance)
-b cells tem increase prod of insulin to compensate for resistance., even insulin secretion fails.---resistance in liver, muscle and fat.

Front 12

molecular mechanism contributing to devel of type 2 diabetes

Back 12

impairment of insulin receptor fxn in target cells:
-receptor receptor inhib./ inhibition of IRS

Front 13

incretins

Back 13

gastrointestinal hormones, secreted into teh blood stream wihtin minutes after eating. bind to g-protein coupled receptors that stimulate cAMP production and protein kinase a........which facilitates the secretory process. also CREB FACTOR THAT REG insulin gene expression
-incretions act trhrough their g-protein coupled receptors to increase cAMP production and PKA activation

Front 14

IRS 2

Back 14

ONLY irs IS CRITICAL FOR B-CELLS TO COMPENSATE FOR INSULIN RESISTANCE.

Front 15

PRO-INFLAM CYTOKINES AND FREE FATTY ACIDS AND HIGH GLUCOSE do what to insulin and b-scell survival

Back 15

free fatty acids and cytokines stim signalingpathways that promotes serine and phosph of IRS2.
----ser phosph IRS2 IS A POOR SUBSTRATE FOR INSULIN RECEPTOR AND THE il-gfr. ...RESULTS IN CECREASED ACTIVATION OF THE PATHWAYS that control B-cell proliferation and differentiation.

Front 16

high concentration of circ glucose

Back 16

inhibits the secretion of incretins from teh intestinal mucosa. positive effects that cAMP has on b-cell mass and insulin secretion are lost.