Disclosure: The authors declared non conflict of interest.
Beta and alpha cell function in metabolically healthy but obese subjects: Relationship with entero-insular axis†
Article first published online: 26 MAR 2013
Copyright © 2012 The Obesity Society
Volume 21, Issue 2, pages 320–325, February 2013
How to Cite
Calanna, S., Piro, S., Di Pino, A., Maria Zagami, R., Urbano, F., Purrello, F. and Maria Rabuazzo, A. (2013), Beta and alpha cell function in metabolically healthy but obese subjects: Relationship with entero-insular axis. Obesity, 21: 320–325. doi: 10.1002/oby.20017
- Issue published online: 26 MAR 2013
- Article first published online: 26 MAR 2013
- Accepted manuscript online: 28 AUG 2012 10:57AM EST
- Manuscript Accepted: 18 JUN 2012
- Manuscript Revised: 18 MAY 2012
- Manuscript Received: 24 JAN 2012
Obesity is widely acknowledged as a critical risk factor for metabolic complications. Among obese subjects, there is a phenotype of metabolically healthy but obese (MHO) individuals that shows a favorable cardiometabolic risk profile. We aimed to evaluate the potential mechanisms underlying the metabolic profile of this subset, including alpha and beta cell function and entero-insular axis.
Design and Methods:
One hundred twenty-nine obese and 24 nonobese subjects were studied. Obese participants were defined as MHO or at-risk obese, according to the homeostasis model of assessment-insulin resistance (HOMA-IR) index (MHO: lower tertile of HOMA-IR, n = 43; at-risk: upper tertile of HOMA-IR index, n = 41). Insulin, glucagon, and incretin responses after a 120′ oral glucose tolerance test (75-g OGTT) were investigated.
During OGTT, MHO individuals showed in comparison with at-risk subjects: lower fasting and afterloads plasma levels of glucose, insulin, and C-peptide; higher disposition index; lower fasting (P = 0.004) and at 30′ (P = 0.01) plasma glucose-dependent insulinotropic polypeptide (GIP) levels; lower area under the curve (AUC) (0-30) for GIP (P = 0.008); higher glucagon-like peptide-1 (GLP-1) plasma levels at 90′ (P = 0.02) and 120′ (P = 0.02); lower glucagon plasma levels at baseline (P = 0.04) and at 30′ (P = 0.03); and appropriate glucagon suppression after the oral glucose load.
MHO subjects show, as well as normal-weight individuals, a lower diabetogenic profile by virtue of higher disposition index and unaffected entero-insular axis. At-risk obese individuals present increased GIP levels that might play a role in determining increased glucagon secretion and inappropriate glucagon responses after glucose load, thus contributing to impaired glucose homeostasis.