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

Authors

Vijayalakshmi Varma, University of Arkansas for Medical Sciences
Aiwei Yao-Borengasser, University of Arkansas for Medical Sciences
Neda Rasouli, University of Colorado
Angela M. Bodles, University of Arkansas for Medical Sciences
Bounleut Phanavanh, University of Arkansas for Medical Sciences
Mi-Jeong Lee, University of Maryland
Tasha Starks, University of Arkansas for Medical Sciences
Leslie M. Kern, University of Arkansas for Medical Sciences
Horace J. Spencer III, University of Arkansas for Medical Sciences
Robert E. McGehee Jr., University of Arkansas for Medical Sciences
Susan K. Fried, University of Maryland
Philip A. Kern, University of Kentucky

Abstract

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 SI, and the association of SAT VF mRNA with S_I was independent of BMI. IMCL and markers of inflammation (adipose CD68 and plasma TNFα) 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.

Document Type

Article

Publication Date

2-2007

Digital Object Identifier (DOI)

10.1210/jc.2006-1303

Repository Citation

Varma, Vijayalakshmi; Yao-Borengasser, Aiwei; Rasouli, Neda; Bodles, Angela M.; Phanavanh, Bounleut; Lee, Mi-Jeong; Starks, Tasha; Kern, Leslie M.; Spencer, Horace J. III; McGehee, Robert E. Jr.; Fried, Susan K.; and Kern, Philip A., "Human Visfatin Expression: Relationship to Insulin Sensitivity, Intramyocellular Lipids, and Inflammation" (2007). Clinical and Translational Science Faculty Publications. 37.
https://uknowledge.uky.edu/ccts_facpub/37