| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Clinica Medica (R.B., M.Z., C.F., P.V., A.P., M.F., B.C., L.C., G.G.), Department of Clinical, Morphological and Technological Sciences, University of Trieste, 34127 Trieste, Italy; and Department of Nuclear Medicine (M.M., F.D.), Azienda Ospedaliera Ospedali Riuniti, 34127 Trieste, Italy
Address all correspondence and requests for reprints to: Rocco Barazzoni, M.D., Ph.D., Clinica Medica, University of Trieste, Ospedale Cattinara, Strada di Fiume 447, 34127 Trieste, Italy. E-mail: barazzon{at}units.it.
Context: Metabolic syndrome shows clustered metabolic abnormalities with major roles for insulin resistance and obesity. Ghrelin is a gastric hormone whose total plasma concentration (T-Ghr) is associated positively with insulin sensitivity and is reduced in obesity. Ghrelin circulates in acylated (A-Ghr) and desacylated (D-Ghr) forms, but their potential differential associations with insulin resistance and whether they are differentially altered in obesity remain undefined.
Objective: Our objective was to determine potential differential associations of ghrelin forms with insulin resistance [homeostasis model assessment of insulin resistance (HOMA-IR)] and the impact of obesity on their plasma concentrations in metabolic syndrome.
Design: This is a cross-sectional study.
Setting: The study was performed in a metabolic outpatient unit.
Patients: Patients with metabolic syndrome (National Cholesterol Education Program-Adult Treatment Panel III; n = 45, 23 males/22 females) were included in the study.
Main Outcomes: The main study outcomes were metabolic syndrome criteria, HOMA-IR, and ghrelin forms.
Results: Plasma insulin and HOMA-IR were associated negatively with T-Ghr and D-Ghr but positively with A-Ghr and acylated to desacylated ghrelin (A/D-Ghr) ratio (n = 45; P < 0.05). Compared with nonobese [body mass index (BMI) < 27.5 kg/m2; n = 12, six males/six females], obese metabolic syndrome patients (BMI > 27.5 kg/m2; n = 33) had lower T-Ghr and D-Ghr but comparable A-Ghr and higher A/D-Ghr ratio (P < 0.05). BMI and waist circumference (WC) were positively related with HOMA-IR (n = 45; P < 0.05). However, opposite associations between A/D-Ghr ratio and HOMA-IR remained significant after adjustment for sex and BMI (or WC). Additional obese individuals without metabolic syndrome (n = 10: age-, sex-, BMI-, and WC-matched to obese metabolic syndrome patients) had lower T-Ghr but higher A-Ghr (P < 0.05) compared with age-, sex-matched healthy nonobese counterparts (n = 15). T-Ghr and A-Ghr were comparable in obese with or without metabolic syndrome.
Conclusion: Obesity could alter circulating ghrelin profile, and relative A-Ghr excess could contribute to obesity-associated insulin resistance in metabolic syndrome.
This article has been cited by other articles:
![]() |
U. Mager, M. Kolehmainen, V. D F de Mello, U. Schwab, D. E Laaksonen, R. Rauramaa, H. Gylling, M. Atalay, L. Pulkkinen, and M. Uusitupa Expression of ghrelin gene in peripheral blood mononuclear cells and plasma ghrelin concentrations in patients with metabolic syndrome. Eur. J. Endocrinol., April 1, 2008; 158(4): 499 - 510. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |