I've read the following facts about pancreatic somatostatin released from delta cells of the islets of Langerhans:

  1. Blood glucose, fatty acids, and plasma amino acids stimulate somatostatin
  2. Somatostatin inhibits glucagon, insulin, and overall GI secretion
  3. The 'net action' of somatostatin is to "delay nutrient absorption in the GI tract and thus prolong the intestinal absorption of food after a meal."

I'm very confused about this 'net action.' If glucose activates both insulin and somatostatin, yet somatostatin inhibits insulin, what inhibits somatostatin's action and allows insulin to do its thing? In other words, how is somatostatin regulated? And especially, when does insulin come into play if not when blood glucose levels are increased?

To drive the point home, what gastrointestinal physiological abnormality would result from a person lacking pancreatic somatostatin? I understand somatostatin's inhibition of GH on the endocrine system and how that can lead to acromegaly, gigantism, etc, but I haven't been able to find any literature on pancreatic mutants or knockouts, and I have no clue what the effect would be in the GI. Would such a mutant defecate excessively and have poor nutrient absorption...?


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