All of the hormones secreted by the endocrine pancreas regulate metabolic functions either systemically, regionally (in the gastrointestinal tract), or locally (in the islet itself).
Insulin is the most abundant endocrine secretion. Its principal effects are on the liver, skeletal muscle, and adipose tissue. Insulin has multiple individual actions in each of these tissues. In general, insulin stimulates
• Uptake of glucose from the circulation. Specific cell membrane glucose transporters are involved in this process.
• Storage of glucose by activation of glycogen synthase and subsequent glycogen synthesis.
• Phosphorylation and use of glucose by promoting its glycolysis within cells.
In addition to its effects on glucose metabolism, insulin stimulates glycerol synthesis and inhibits lipase activity in adipose cells. Circulating insulin also increases the amount of amino acids taken up by cells (which may involve cotransport with glucose) and inhibits protein ca-tabolism. Insulin appears to be essential for normal cell growth and function, as demonstrated in tissue culture systems.
Glucagon, secreted in amounts second only to insulin, increases blood glucose levels
The actions of glucagon are essentially reciprocal to those of insulin. It stimulates release of glucose into the bloodstream, and stimulates gluconeogenesis (synthesis of glucose from metabolites of amino acids) and glycogenosis (breakdown of glycogen) in the liver. Glucagon also stimulates proteolysis to promote gluconeogenesis, mobilizes fats from adipose cells, and stimulates hepatic lipase.
Somatostatin inhibits insulin and glucagon secretion
Somatostatin is secreted by the D cells of the islets. It is identical with the hormone secreted by the hypothalamus that regulates somatotropin (growth hormone) release from the anterior pituitary gland. Although the precise role of somatostatin in the islets is unclear, it has been shown to inhibit both insulin and glucagon secretion.
The molecular characteristics of the major and some minor islet hormones are summarized in Table 17.4.
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