The effects of somatostatin on hormonal and metabolic responses in chronic pancreatitis.

Abstract

Unmodified synthetic somatostatin, given as a 200-microgram intravenous bolus, plus 200 microgram infused over 3 hours, had no effect on basal plasma insulin and pancreatic glucagon-like immunoreactivity (GLI) levels, both in controls and in patients with chronic pancreatitis. Somatostatin inhibited insulin-hypoglycaemia-induced pancreatic GLI release in controls and in patients with pancreatitis, and prolonged the insulin-induced fall in blood glucose in the patients. Arginine, presumably via insulin release, caused a fall in free fatty acids (FFA) in controls, which was inhibited by somatostatin. Somatostatin abolished the rebound rise in plasma FFA in patients with pancreatitis after insulin-hypoglycaemia. This effect may be related to inhibition of pancreatic GLI release or may be a direct action of somatostatin on lipolysis.

• Authors: J L Botha, A I Vinik, D le Roith, P T Child, W P Jackson
• Journal: South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde (S Afr Med J) Vol. 51 Issue 24 Pg. 872-5 (Jun 11 1977) ISSN: 0256-9574 [Print] South Africa
• PMID: 897837 (Publication Type: Journal Article)

Chemical References

• Blood Glucose
• Fatty Acids, Nonesterified
• Insulin
• Somatostatin
• Growth Hormone
• Glucagon
• Arginine

Topics

• Adult
• Aged
• Arginine (pharmacology)
• Blood Glucose
• Chronic Disease
• Depression, Chemical
• Fatty Acids, Nonesterified (blood)
• Glucagon (blood)
• Growth Hormone (blood)
• Humans
• Insulin (blood, pharmacology)
• Male
• Middle Aged
• Pancreatitis (blood)
• Somatostatin (pharmacology)