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Obesity (Silver Spring). 2013 Feb;21(2):320-5. doi: 10.1002/oby.20017.

Beta and alpha cell function in metabolically healthy but obese subjects: relationship with entero-insular axis.

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1
Department of Clinical and Molecular Biomedicine, University of Catania, Catania, Italy.

Abstract

OBJECTIVE:

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.

RESULTS:

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.

CONCLUSIONS:

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.

PMID:
23404781
DOI:
10.1002/oby.20017
[Indexed for MEDLINE]
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