OBJECTIVES: We tested whether African-American (AA) women are different from Caucasian women in regard to lipotoxicity, adipokines, and gene expression in adipose tissue and muscle. DESIGN: Insulin sensitivity (S(I)), plasma adipocytokine levels, intramyocellular lipid (IMCL), and the expression of candidate genes in adipose tissue and muscle were measured in AA and Caucasian women. SETTING: This study was performed in an ambulatory general clinical research center. SUBJECTS: Subjects were healthy, nondiabetic AA and Caucasian women. INTERVENTIONS: There were no interventions. MAIN OUTCOME MEASURES: Comparison of S(I), IMCL, plasma adiponectin, and the expression of candidate genes regulating adipogenesis, lipogenesis, and inflammation in adipose tissue and muscle. RESULTS: AA had lower plasma adiponectin and IMCL when compared with Caucasian women with similar S(I). In sc adipose tissue (SAT), the expression of genes involved in adipogenesis including peroxisomal proliferator-activated receptor-gamma (PPARgamma) and lipin-1beta were also reduced in SAT of AA subjects (19%, P = 0.06, and 25%, P = 0.05, respectively). Similarly, 1-acylglycerol-3-phosphate acyltransferase 2 (AGPAT 2), stearoyl-coenzyme A desaturase-1 (SCD1), and CD36 mRNA expression was significantly reduced in SAT by 19, 54, and 28% respectively (P < 0.01 for all) in AA compared with Caucasian women. Yet the expression of CD68 in SAT was similar in both ethnic groups. Gene expression studies in muscle revealed a 31% reduction in expression of AGPAT 2 and a 72% reduction in SCD1 genes in AA. CONCLUSION: AA women demonstrated lower expression of several PPARgamma-responsive genes in adipose tissue, lower plasma adiponectin, and decreased IMCL levels as compared with Caucasians, which suggests that African-Americans may be protected from lipotoxicity. Together these data suggest significant ethnic differences in the pathophysiology of insulin resistance.
OBJECTIVES: We tested whether African-American (AA) women are different from Caucasian women in regard to lipotoxicity, adipokines, and gene expression in adipose tissue and muscle. DESIGN:Insulin sensitivity (S(I)), plasma adipocytokine levels, intramyocellular lipid (IMCL), and the expression of candidate genes in adipose tissue and muscle were measured in AA and Caucasian women. SETTING: This study was performed in an ambulatory general clinical research center. SUBJECTS: Subjects were healthy, nondiabetic AA and Caucasian women. INTERVENTIONS: There were no interventions. MAIN OUTCOME MEASURES: Comparison of S(I), IMCL, plasma adiponectin, and the expression of candidate genes regulating adipogenesis, lipogenesis, and inflammation in adipose tissue and muscle. RESULTS: AA had lower plasma adiponectin and IMCL when compared with Caucasian women with similar S(I). In sc adipose tissue (SAT), the expression of genes involved in adipogenesis including peroxisomal proliferator-activated receptor-gamma (PPARgamma) and lipin-1beta were also reduced in SAT of AA subjects (19%, P = 0.06, and 25%, P = 0.05, respectively). Similarly, 1-acylglycerol-3-phosphate acyltransferase 2 (AGPAT 2), stearoyl-coenzyme A desaturase-1 (SCD1), and CD36 mRNA expression was significantly reduced in SAT by 19, 54, and 28% respectively (P < 0.01 for all) in AA compared with Caucasian women. Yet the expression of CD68 in SAT was similar in both ethnic groups. Gene expression studies in muscle revealed a 31% reduction in expression of AGPAT 2 and a 72% reduction in SCD1 genes in AA. CONCLUSION: AA women demonstrated lower expression of several PPARgamma-responsive genes in adipose tissue, lower plasma adiponectin, and decreased IMCL levels as compared with Caucasians, which suggests that African-Americans may be protected from lipotoxicity. Together these data suggest significant ethnic differences in the pathophysiology of insulin resistance.
Authors: Gina B Di Gregorio; Aiwei Yao-Borengasser; Neda Rasouli; Vijayalakshmi Varma; Tong Lu; Leslie M Miles; Gouri Ranganathan; Charlotte A Peterson; Robert E McGehee; Philip A Kern Journal: Diabetes Date: 2005-08 Impact factor: 9.461
Authors: M I Harris; K M Flegal; C C Cowie; M S Eberhardt; D E Goldstein; R R Little; H M Wiedmeyer; D D Byrd-Holt Journal: Diabetes Care Date: 1998-04 Impact factor: 19.112
Authors: Severine G Dubois; Leonie K Heilbronn; Steven R Smith; Jeanine B Albu; David E Kelley; Eric Ravussin Journal: Obesity (Silver Spring) Date: 2006-09 Impact factor: 5.002
Authors: Laura Pickersgill; Gary J Litherland; Andrew S Greenberg; Mark Walker; Stephen J Yeaman Journal: J Biol Chem Date: 2007-03-03 Impact factor: 5.157
Authors: S M Haffner; R D'Agostino; M F Saad; M Rewers; L Mykkänen; J Selby; G Howard; P J Savage; R F Hamman; L E Wagenknecht Journal: Diabetes Date: 1996-06 Impact factor: 9.461
Authors: Maria P Martinez Cantarin; Scott W Keith; Stephanie Deloach; Yonghong Huan; Bonita Falkner Journal: Am J Med Sci Date: 2011-09 Impact factor: 2.378
Authors: Kendra A Young; Amita Maturu; Carlos Lorenzo; Carl D Langefeld; Lynne E Wagenknecht; Yii-Der I Chen; Kent D Taylor; Jerome I Rotter; Jill M Norris; Neda Rasouli Journal: J Diabetes Complications Date: 2018-11-03 Impact factor: 2.852
Authors: Anand Vaidya; John P Forman; Patricia C Underwood; Paul N Hopkins; Gordon H Williams; Luminita H Pojoga; Jonathan S Williams Journal: Eur J Endocrinol Date: 2011-03-14 Impact factor: 6.664
Authors: Julia H Goedecke; Dheshnie Keswell; Carsten Weinreich; Jia Fan; Jon Hauksson; Hendriena Victor; Kristina Utzschneider; Naomi S Levitt; Estelle V Lambert; Steven E Kahn; Tommy Olsson Journal: Diabetologia Date: 2015-08-01 Impact factor: 10.122