Insulin effect on adipose tissue (AT) adiponectin expression is regulated by the insulin resistance status of the patients

• Published in: Clinical endocrinology (Oxford) 2008-09, Vol.69 (3), p.412-417
• Main Authors: Hernandez-Morante, J. J., Milagro, F. I., Lujan, J. A., Martinez, J. A., Zamora, S., Garaulet, M.
• Format: Article
• Language: English
• Subjects: Adiponectin - genetics; Adiponectin - metabolism; Adipose Tissue - drug effects; Adipose Tissue - metabolism; Adipose Tissue - pathology; Adult; Biological and medical sciences; Biopsy; Body Fat Distribution; Cell Culture Techniques; Cells, Cultured; Endocrinopathies; Female; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - drug effects; Humans; Insulin - pharmacology; Insulin Resistance - genetics; Insulin Resistance - physiology; Male; Medical sciences; Metabolic Syndrome - genetics; Metabolic Syndrome - metabolism; Metabolic Syndrome - pathology; Middle Aged; Obesity, Morbid - genetics; Obesity, Morbid - metabolism; Obesity, Morbid - pathology; Vertebrates: endocrinology
• ISSN: 0300-0664; 1365-2265
• DOI: 10.1111/j.1365-2265.2008.03185.x

Summary Objective  The objective of the present study was to determine a possible depot‐specific effect of insulin‐stimulation on adiponectin gene expression in adipose tissue (AT) explants from subcutaneous and visceral AT. A secondary aim was to analyse the associations of adiponectin plasma levels, as well as control and insulin‐stimulated gene expression levels with different features of the metabolic syndrome. Design  Visceral and subcutaneous AT biopsies were obtained from 20 subjects (10 men and 10 women) with morbid obesity. Metabolic syndrome and other clinical features were studied. Adiponectin expression from isolated adipocytes was measured both in control and after insulin‐stimulation conditions by quantitative PCR. Results  Subcutaneous adipocytes expressed significantly higher amounts of adiponectin mRNA than visceral tissue (P = 0·027). Insulin increased adiponectin expression specifically in the omental tissue (P = 0·011). In these patients, waist : hip ratio was directly correlated with adiponectin expression in the visceral depot (r = 0·660; P = 0·014), while fasting glucose levels were inversely associated with adiponectin mRNA in the subcutaneous tissue (r =–0·604; P = 0·022). Adiponectin expression after addition of insulin was positively correlated with some metabolic risk factors (cholesterol, LDL‐cholesterol, insulin, C‐peptide). Interestingly, local insulin induced an up‐regulation of adiponectin expression in the AT of those patients with higher metabolic syndrome disturbances. Conclusions  Our results clearly demonstrate that insulin exerts a stimulating effect on adiponectin gene expression in a depot‐specific manner. The AT response to insulin stimulus depends on the physiopathological situation, being higher in those individuals with impaired insulin‐sensitivity and lipid metabolism.