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Sensitivity to beta-endorphin as a cause of human obesity.

作者信息

Giugliano D, Salvatore T, Cozzolino D, Ceriello A, Torella R, D'Onofrio F

机构信息

Istituto di Medicina Generale, Terapia Medica e Malattie del Metabolismo, Prima Facoltà di Medicina, Università di Napoli, Italia.

出版信息

Metabolism. 1987 Oct;36(10):974-8. doi: 10.1016/0026-0495(87)90135-1.

DOI:10.1016/0026-0495(87)90135-1
PMID:2958673
Abstract

Naloxone, an opiate antagonist, was given as an intravenous bolus (5 mg) in both lean and obese healthy subjects. In lean people, there was a slight trend for insulin and C-peptide concentrations to decrease below baseline values with no glucose change. Obese subjects showed an exaggerated suppression of insulin and C-peptide and a slight decrease of glucose. Glucagon was suppressed in both groups. An infusion of human beta-endorphin (0.05 mg/h) produced only minor changes in plasma glucose, insulin, glucagon, and C-peptide concentrations in lean subjects, but caused marked increments in obese. Glucagon rose in both groups, but its response was greater in obese subjects. A ten-day treatment with naloxone (1.2 mg twice a day) did not change the metabolic and hormonal responses to an oral glucose load (75 g) in lean but significantly inhibited the insulin and C-peptide responses to glucose in obese people. These results suggest that an increased opiate drive to the pancreatic beta-cell and an increased responsiveness of insulin to beta-endorphin are present in human obesity.

摘要

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