Background and aims: Obesity is widely acknowledged as a crucial risk factor for metabolic complications. Among obese subjects, there is a phenotype of metabolically healthy but obese (MHO) individuals that shows a favorable cardio- metabolic 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. Materials and methods: We studied 129 obese and 24 non-obese subjects. Obese participants were defined as MHO or at risk obese, according to the HOMA-IR index (MHO: lower tertile of HOMA-IR, n=43; at risk: upper tertile of HOMA-IR index, n=41). We investigated insulin, glucagon and incretin responses after a 120’ oral glucose tolerance test (75g- OGTT). Results: During OGTT, MHO individuals showed in comparison with at risk subjects: lower glucose, insulin and C-peptide fasting plasma levels and responses during the OGTT; higher disposition index; lower fasting (p=0.004) and at 30’(p=0.01) plasma glucose-dependent insulinotropic polypeptide (GIP) levels; lower 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); appropriate glucagon suppression after the oral glucose load. Conclusion: Metabolically healthy but obese 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.

Lower GIP and glucagon responses in metabolically healthy but obese (MHO) subjects in comparison with at risk obese individuals

PIRO, SALVATORE;Di Pino A;PURRELLO, Francesco;RABUAZZO, Agata Maria
2012-01-01

Abstract

Background and aims: Obesity is widely acknowledged as a crucial risk factor for metabolic complications. Among obese subjects, there is a phenotype of metabolically healthy but obese (MHO) individuals that shows a favorable cardio- metabolic 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. Materials and methods: We studied 129 obese and 24 non-obese subjects. Obese participants were defined as MHO or at risk obese, according to the HOMA-IR index (MHO: lower tertile of HOMA-IR, n=43; at risk: upper tertile of HOMA-IR index, n=41). We investigated insulin, glucagon and incretin responses after a 120’ oral glucose tolerance test (75g- OGTT). Results: During OGTT, MHO individuals showed in comparison with at risk subjects: lower glucose, insulin and C-peptide fasting plasma levels and responses during the OGTT; higher disposition index; lower fasting (p=0.004) and at 30’(p=0.01) plasma glucose-dependent insulinotropic polypeptide (GIP) levels; lower 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); appropriate glucagon suppression after the oral glucose load. Conclusion: Metabolically healthy but obese 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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/100792
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