Human visfatin expression: Relationship to insulin sensitivity, intramyocellular lipids, and inflammation

Vijayalakshmi Varma; Aiwei Yao-Borengasser; Neda Rasouli; Angela M. Bodles; Bounleut Phanavanh; Mi Jeong Lee; Tasha Starks; Leslie M. Kern; Horace J. Spencer; Robert E. McGehee; Susan K. Fried; Philip A. Kern

doi:10.1210/jc.2006-1303

Human visfatin expression: Relationship to insulin sensitivity, intramyocellular lipids, and inflammation

Vijayalakshmi Varma, Aiwei Yao-Borengasser, Neda Rasouli, Angela M. Bodles, Bounleut Phanavanh, Mi Jeong Lee, Tasha Starks, Leslie M. Kern, Horace J. Spencer, Robert E. McGehee, Susan K. Fried, Philip A. Kern

Research output: Contribution to journal › Article › peer-review

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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 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 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.

Original language	English
Pages (from-to)	666-672
Number of pages	7
Journal	Journal of Clinical Endocrinology and Metabolism
Volume	92
Issue number	2
DOIs	https://doi.org/10.1210/jc.2006-1303
State	Published - Feb 2007

Bibliographical note

Funding Information:
Disclosure Statement: V.V., A.Y.-B., A.M.B., B.P., M.-J.L., T.S., L.M.K., H.J.S., R.E.M. and S.K.F. have nothing to disclose. P.A.K. has received lecture fees from Takeda Pharmaceuticals and Merck. N.R. has received investigator initiated grant support from Takeda Pharmaceuticals and Abbott.

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Biochemistry
Endocrinology
Clinical Biochemistry
Biochemistry, medical

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10.1210/jc.2006-1303

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Varma, V., Yao-Borengasser, A., Rasouli, N., Bodles, A. M., Phanavanh, B., Lee, M. J., Starks, T., Kern, L. M., Spencer, H. J., McGehee, R. E., Fried, S. K., & Kern, P. A. (2007). Human visfatin expression: Relationship to insulin sensitivity, intramyocellular lipids, and inflammation. Journal of Clinical Endocrinology and Metabolism, 92(2), 666-672. https://doi.org/10.1210/jc.2006-1303

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title = "Human visfatin expression: Relationship to insulin sensitivity, intramyocellular lipids, and inflammation",

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 (SI). Setting: The study was conducted at a University Hospital and General Clinical Research Center. Intervention: SI 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, SI, 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 SI 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 SI. Plasma VF and muscle VF mRNA did not correlate with BMI or SI 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 SI, and high levels of inflammatory markers. VAT VF and SAT VF are regulated oppositely with BMI.",

author = "Vijayalakshmi Varma and Aiwei Yao-Borengasser and Neda Rasouli and Bodles, {Angela M.} and Bounleut Phanavanh and Lee, {Mi Jeong} and Tasha Starks and Kern, {Leslie M.} and Spencer, {Horace J.} and McGehee, {Robert E.} and Fried, {Susan K.} and Kern, {Philip A.}",

note = "Funding Information: Disclosure Statement: V.V., A.Y.-B., A.M.B., B.P., M.-J.L., T.S., L.M.K., H.J.S., R.E.M. and S.K.F. have nothing to disclose. P.A.K. has received lecture fees from Takeda Pharmaceuticals and Merck. N.R. has received investigator initiated grant support from Takeda Pharmaceuticals and Abbott.",

year = "2007",

month = feb,

doi = "10.1210/jc.2006-1303",

language = "English",

volume = "92",

pages = "666--672",

number = "2",

}

Varma, V, Yao-Borengasser, A, Rasouli, N, Bodles, AM, Phanavanh, B, Lee, MJ, Starks, T, Kern, LM, Spencer, HJ, McGehee, RE, Fried, SK & Kern, PA 2007, 'Human visfatin expression: Relationship to insulin sensitivity, intramyocellular lipids, and inflammation', Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 2, pp. 666-672. https://doi.org/10.1210/jc.2006-1303

TY - JOUR

T1 - Human visfatin expression

T2 - Relationship to insulin sensitivity, intramyocellular lipids, and inflammation

AU - Varma, Vijayalakshmi

AU - Yao-Borengasser, Aiwei

AU - Rasouli, Neda

AU - Bodles, Angela M.

AU - Phanavanh, Bounleut

AU - Lee, Mi Jeong

AU - Starks, Tasha

AU - Kern, Leslie M.

AU - Spencer, Horace J.

AU - McGehee, Robert E.

AU - Fried, Susan K.

AU - Kern, Philip A.

N1 - Funding Information: Disclosure Statement: V.V., A.Y.-B., A.M.B., B.P., M.-J.L., T.S., L.M.K., H.J.S., R.E.M. and S.K.F. have nothing to disclose. P.A.K. has received lecture fees from Takeda Pharmaceuticals and Merck. N.R. has received investigator initiated grant support from Takeda Pharmaceuticals and Abbott.

PY - 2007/2

Y1 - 2007/2

N2 - 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 (SI). Setting: The study was conducted at a University Hospital and General Clinical Research Center. Intervention: SI 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, SI, 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 SI 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 SI. Plasma VF and muscle VF mRNA did not correlate with BMI or SI 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 SI, and high levels of inflammatory markers. VAT VF and SAT VF are regulated oppositely with BMI.

AB - 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 (SI). Setting: The study was conducted at a University Hospital and General Clinical Research Center. Intervention: SI 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, SI, 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 SI 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 SI. Plasma VF and muscle VF mRNA did not correlate with BMI or SI 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 SI, and high levels of inflammatory markers. VAT VF and SAT VF are regulated oppositely with BMI.

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Human visfatin expression: Relationship to insulin sensitivity, intramyocellular lipids, and inflammation

Abstract

Bibliographical note

ASJC Scopus subject areas

UN SDGs

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