Baillieres Clin Endocrinol Metab 1994 Jan;8(1):215-36
Somatostatin: physiology and clinical applications.
Shulkes A
Department of Surgery, University of Melbourne, Austin Hospital, Victoria,
Australia.
Somatostatin (SOM) was originally isolated as the hypothalamic inhibitor of
growth hormone release but was subsequently shown to have a widespread
distribution including the gastrointestinal tract. In fact the
gastrointestinal tract contains about 70% of the total body SOM. SOM has
inhibitory actions on gastrointestinal exocrine and endocrine secretions,
motility and blood flow. Within the gut it functions as an endocrine,
paracrine, autocrine and neurocrine factor. SOM is released by a meal, and a
number of neurotransmitters and regulatory peptides also influence SOM
release. SOM is a key component of the gastrin-acid feedback loop as luminal
acid releases SOM, which in turn has inhibitory effects on both gastrin and
gastric acid. Consistent with the diverse functions of SOM, a number of
different although related SOM receptors with distinct distribution patterns
and intracellular mediators have been cloned and sequenced. SOM is the first
of the gut regulatory peptides to have a significant therapeutic use. By
inhibiting both the target cell (e.g. parietal cell) and the release of the
active agent (e.g. gastrin) the therapeutic potential of SOM is magnified.
---More specifically, somatostatin is also the feedback hormone which shuts down insulin release. Thus, it is possible that those taking an oral somatostatin inhibitor might suffer both gastritis and hyperinsulinemia.
PHIL OSBORN SAID: "...Thus, they utterly rejected out-of-hand any arguments for the existence of a "death gene," or "aging clock." Thus, no research followup on Denkla's work..."
CYMM SAYS: Well the genes that regulate somatostatin come close to being a "death gene". Somatostatin which is upregulated as we grow older... has been called "enzymatic cyanide"; it throws a spanner into almost any bochemical works.
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