Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 1990 Feb;22(2):96-100.
doi: 10.1055/s-2007-1004859.

Beta-endorphin, insulin, ACTH and cortisol plasma levels during oral glucose tolerance test in obesity after weight loss

Affiliations
Comparative Study

Beta-endorphin, insulin, ACTH and cortisol plasma levels during oral glucose tolerance test in obesity after weight loss

C Giovannini et al. Horm Metab Res. 1990 Feb.

Abstract

In order to clarify a possible relationship between opioid peptides and glucose homeostasis in obesity we studied Beta-Endorphin (B-Ep), ACTH, cortisol and insulin plasma levels in response to an oral glucose tolerance test (OGTT) in 8 subjects after a hypocaloric diet for 90 days. We obtained through this treatment a weight loss superior to 30% of the initial weight excess (WE) compared with ideal body weight. Moreover, we compared the obtained results with our preliminary study that was performed with the same protocol but without caloric restriction. B-Ep was measured by RIA after silicic acid extraction and G75 Sephadex column chromatography. ACTH, insulin and cortisol were measured directly on plasma by an RIA method. Basal and during OGTT-induced levels of glucose, insulin, ACTH and cortisol decreased in comparison with the values obtained before diet. Conversely, B-Ep remained higher than normal both in the basal condition and during OGTT, and showed values consistently similar to those before diet. These data show that hyperinsulinemia is corrected by weight loss, while hyperbetaendorphinemia remains unchanged. Accordingly, it can be suggested that no direct relationship occurs between hyper-B-Ep-hyper-IRI in obesity. A further insight into the role of hyper-B-Ep in obesity is, thus, necessary, assuming as hypothesis that the increase in B-Ep may be a cause and not a corollary of the polymorphic aspects of obesity.

PubMed Disclaimer

Publication types