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Insulin, Glucagon And Somatostatin Essay

1174 words - 5 pages

Insulin, Glucagon and Somatostatin

The principal role of the pancreatic hormones is the regulation of
whole-body energy metabolism, principally by regulating the
concentration and activity of numerous enzymes involved in catabolism
and anabolism of the major cell energy supplies.

The earliest of these hormones recognized was insulin, whose major
function is to counter the concerted action of a number of
hyperglycemia-generating hormones and to maintain low blood glucose
levels. Because there are numerous hyperglycemic hormones, untreated
disorders associated with insulin generally lead to severe
hyperglycemia and shortened life span. Insulin is a member of a family
of structurally and functionally similar molecules that include the
insulin-like growth factors (IGF-1 and IGF-2), and relaxin. The
tertiary structure of all 4 molecules is similar, and all have
growth-promoting activities, but the dominant role of insulin is
metabolic while the dominant roles of the IGFs and relaxin are in the
regulation of cell growth and differentiation.

Insulin is synthesized as a preprohormone in the b cells of the islets
of Langerhans. Its signal peptide is removed in the cisternae of the
endoplasmic reticulum and it is packaged into secretory vesicles in
the Golgi, folded to its native structure, and locked in this
conformation by the formation of 2 disulfide bonds. Specific protease
activity cleaves the center third of the molecule, which dissociates
as C peptide, leaving the amino terminal B peptide disulfide bonded to
the carboxy terminal A peptide.

Insulin secretion from b cells is principally regulated by plasma
glucose levels, but the precise mechanism by which the glucose signal
is transduced remains unclear. One possibility is that the increased
uptake of glucose by pancreatic b-cells leads to a concommitant
increase in metabolism. The increase in metabolism leads to an
elevation in the ATP/ADP ratio. This in turn leads to an inhibition of
an ATP-sensitive K+ channel. The net result is a depolarization of the
cell leading to Ca2+ influx and insulin secretion.

Chronic increases in numerous other hormones (including GH, hPL,
estrogens, and progestins), up-regulate insulin secretion, probably by
increasing the preproinsulin mRNA and enzymes involved in processing
the increased preprohormone. In contrast, epinephrine diminishes
insulin secretion by a cAMP-coupled regulatory path. In addition,
epinephrine counters the effect of insulin in liver and peripheral
tissue, where it binds to b-adrenergic receptors, induces adenylate
cycles activity, increases cAMP, and activates PKA. The latter events
induce glycogenolysis and gluconeogenesis, both of which are
hyperglycemic and which thus counter insulin's effect on blood glucose
levels.

Insulin secreted by the pancreas is...

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