4.6 Article

Adiponectin secretion and response to pioglitazone is depot dependent in cultured human adipose tissue

Journal

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.90359.2008

Keywords

adipose tissue physiology; type 2 diabetes mellitus; body fat distribution; thiazolidinediones; leptin

Funding

  1. National Institute of Diabetes and Digestive and Kidney Disease [KO8-DK-061987, RO1-DK-258291]
  2. American Diabetes Association
  3. Medical Research Service, Department of Veterans Affairs
  4. San Diego Healthcare System [M01-RR-00827]
  5. General Clinical Research Branch, Division of Research Resources, NIH

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The subcutaneous (S) and visceral (V) adipose tissue (AT) depots are increasingly recognized as distinct. To test the hypothesis that depot differences exist for adiponectin, fresh and cultured human VAT and SAT from obese type 2 diabetic (T2D) and obese nondiabetic (ND) subjects was examined to determine whether differences in adiponectin content and secretion occurred as a function of depot studied, diabetic status, and response to thiazolidinedione treatment. VAT and SAT were obtained by biopsy and AT explants cultured in defined media for 7 days. Protein expression was assessed by Western blot. Adiponectin content of conditioned medium was determined by radioimmunoassay. Diabetic status had no effect on adiponectin secretion over days 0-2 of culture. In ND SAT, secretion fell over days 2-4 but was sustained at greater levels vs. T2D SAT. In both ND and T2D VAT, adiponectin secretion was low, similar to T2D SAT. Over the 7-day culture period, cellular adiponectin increased in ND SAT and VAT; it remained unchanged in T2D SAT and VAT. Pioglitazone increased adiponectin secretion and content in all SAT. Pioglitazone failed to increase adiponectin secretion from either ND or T2D VAT and increased cellular content only in ND VAT. AT depot differences exist in the secretion of adiponectin and responsiveness to thiazolidinedione treatment. These data suggest that SAT, not VAT, appears to be the major contributor to increased circulating adipopnectin levels in response to pioglitazone treatment.

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