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Human Visfatin Expression: Relationship to Insulin Sensitivity, Intramyocellular Lipids, and Inflammation

The Central Arkansas Veterans Healthcare System (V.V., A.Y.-B., N.R., A.M.B., B.P., T.S., L.M.K., P.A.K.), and the Department of Medicine, Division of Endocrinology, and the Department of Biostatistics (H.J.S.), and the Department of Pediatrics (R.E.M.), University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and Department of Medicine (M.-J.L., S.K.F.), University of Maryland, and Geriatric Research Education and Clinical Center, and Veterans Affairs Medical Center (S.K.F.), Baltimore, Maryland 21201

Address all correspondence and requests for reprints to: Philip A. Kern, M.D., Associate Chief of Staff, Research, Central Arkansas Veterans Healthcare System, 598/151 LR, 4300 West 7th Street, Little Rock, Arkansas 72205. E-mail: KernPhilipA{at}uams.edu.

Context: Visfatin (VF) is a recently described adipokine preferentially secreted by visceral adipose tissue (VAT) with insulin mimetic properties.

Objective: The aim of this study was to examine the association of VF with insulin sensitivity, intramyocellular lipids (IMCL), and inflammation in humans.

Design and Patients: VF mRNA was examined in paired samples of VAT and abdominal sc adipose tissue (SAT) obtained from subjects undergoing surgery. Plasma VF and VF mRNA was also examined in SAT and muscle tissue, obtained by biopsy from well-characterized subjects with normal or impaired glucose tolerance, with a wide range in body mass index (BMI) and insulin sensitivity (S_I).

Setting: The study was conducted at a University Hospital and General Clinical Research Center.

Intervention: S_I was measured, and fat and muscle biopsies were performed. In impaired glucose tolerance subjects, these procedures were performed before and after treatment with pioglitazone or metformin.

Main Outcome Measures: We measured the relationship between VF and obesity, S_I, adipose tissue inflammation, IMCL, and response to insulin sensitizers.

Results: No significant difference in VF mRNA was seen between SAT and VAT depots. VAT VF mRNA associated positively with BMI, whereas SAT VF mRNA decreased with BMI. SAT VF correlated positively with S_I, and the association of SAT VF mRNA with S_I was independent of BMI. IMCL and markers of inflammation (adipose CD68 and plasma TNF) were negatively associated with SAT VF. Impaired glucose tolerance subjects treated with pioglitazone showed no change in SAT VF mRNA despite a significant increase in S_I. Plasma VF and muscle VF mRNA did not correlate with BMI or S_I or IMCL, and there was no change in muscle VF with either pioglitazone or metformin treatments.

Conclusion: SAT VF is highly expressed in lean, more insulinsensitive subjects and is attenuated in subjects with high IMCL, low S_I, and high levels of inflammatory markers. VAT VF and SAT VF are regulated oppositely with BMI.

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