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that (3-cells may be derived from pancreatic ductular epithelium, further emphasizing their likely communication [8]. Within the islets, there is also communication between the various cell types; glucagon from the a-cells stimulates insulin, and insulin suppresses glucagon, whereas somatostatin inhibits both insulin and glucagon.

The insulin response to glucose is age-dependent (Table 1), being highest during the pubertal growth spurt and returning toward but not quite matching prepubertal values by early adulthood. Increased growth hormone secretion during puberty is likely responsible for increased insulin secretion by inducing resistance to insulin action [9]. Placentally derived growth hormone-like hormones also are responsible for increased insulin secretion in the second half of pregnancy. Inability to compensate for growth hormone-induced IR is a likely key contributor to the increased incidence of clinically manifest DM in puberty and for gestational diabetes in women [10]. Other hormones that antagonize insulin action, such as glucocorticoids and combination estrogen-progesterone as found in oral contraceptives, also result in increased insulin secretion. Ghrelin, a gastrointestinal peptide that stimulates growth hormone secretion and appetite, and leptin, a hormone produced by fat cells, which regulates satiety indirectly, also modulate insulin secretion; ghrelin stimulates, whereas leptin lowers insulin secretion [4-6,11,12].

For any given level of glycemia, orally ingested glucose elicits a greater insulin response than when the same glycemic profile is achieved by glucose infused intravenously. This has given rise to the concept of incretins, gut-derived hormonal signals that amplify insulin response to ingested food [13]. The incretin effect, which amplifies the insulin response to glucose by some 50% to 75%, is mediated largely by two intestinal hormones, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. The incretin effect is markedly impaired in type 2 DM, mostly because of impaired glucagon-like peptide-1 secretion. Interest in restoring glucagon-like peptide 1 effects has resulted in the development of a drug recently approved by the Food and Drug Administration, exenatide, a peptide derived from lizards that activates the mammalian receptor for glucagon-like peptide-1, resulting in increased insulin secretion, suppressed

Table 1

Glucose and insulin responses to oral glucose tolerance test in prepubertal and pubertal subjects

Table 1

Glucose and insulin responses to oral glucose tolerance test in prepubertal and pubertal subjects

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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