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Beta and alpha cell function in metabolically healthy but obese subjects: relationship with entero-insular axis.
Obesity (Silver Spring). 2013 Feb; 21(2):320-5.O

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.

Authors+Show Affiliations

Department of Clinical and Molecular Biomedicine, University of Catania, Catania, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

23404781

Citation

Calanna, Salvatore, et al. "Beta and Alpha Cell Function in Metabolically Healthy but Obese Subjects: Relationship With Entero-insular Axis." Obesity (Silver Spring, Md.), vol. 21, no. 2, 2013, pp. 320-5.
Calanna S, Piro S, Di Pino A, et al. Beta and alpha cell function in metabolically healthy but obese subjects: relationship with entero-insular axis. Obesity (Silver Spring). 2013;21(2):320-5.
Calanna, S., Piro, S., Di Pino, A., Maria Zagami, R., Urbano, F., Purrello, F., & Maria Rabuazzo, A. (2013). Beta and alpha cell function in metabolically healthy but obese subjects: relationship with entero-insular axis. Obesity (Silver Spring, Md.), 21(2), 320-5. https://doi.org/10.1002/oby.20017
Calanna S, et al. Beta and Alpha Cell Function in Metabolically Healthy but Obese Subjects: Relationship With Entero-insular Axis. Obesity (Silver Spring). 2013;21(2):320-5. PubMed PMID: 23404781.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beta and alpha cell function in metabolically healthy but obese subjects: relationship with entero-insular axis. AU - Calanna,Salvatore, AU - Piro,Salvatore, AU - Di Pino,Antonino, AU - Maria Zagami,Rose, AU - Urbano,Francesca, AU - Purrello,Francesco, AU - Maria Rabuazzo,Agata, PY - 2012/01/24/received PY - 2012/05/18/revised PY - 2012/06/18/accepted PY - 2013/2/14/entrez PY - 2013/2/14/pubmed PY - 2013/10/1/medline SP - 320 EP - 5 JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 21 IS - 2 N2 - 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. SN - 1930-739X UR - https://www.unboundmedicine.com/medline/citation/23404781/Beta_and_alpha_cell_function_in_metabolically_healthy_but_obese_subjects:_relationship_with_entero_insular_axis_ L2 - https://doi.org/10.1002/oby.20017 DB - PRIME DP - Unbound Medicine ER -