Barnstable Brown Diabetes and Obesity Center
Barnstable Brown Diabetes and Obesity Center
Smith L.M.,Central Baptist College |
Yao-Borengasser A.,University of Arkansas for Medical Sciences |
Starks T.,University of Arkansas for Medical Sciences |
Tripputi M.,University of Colorado at Denver |
And 4 more authors.
Journal of Clinical Endocrinology and Metabolism | Year: 2010
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 (SI), 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 SI, 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 SI. In sc adipose tissue (SAT), the expression of genes involved in adipogenesis including peroxisomal proliferator-activated receptor-γ(PPARγ) and lipin-1β 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 PPARγ-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. Copyright © 2010 by The Endocrine Society.
PubMed | University of Kentucky, Barnstable Brown Diabetes and Obesity Center and Muǧla University
Type: Journal Article | Journal: The Journal of biological chemistry | Year: 2015
Lipid accumulation in liver and skeletal muscle contributes to co-morbidities associated with diabetes and obesity. We made a transgenic mouse in which the adiponectin (Adipoq) promoter drives expression of lipoprotein lipase (LPL) in adipocytes to potentially increase adipose tissue lipid storage. These mice (Adipoq-LPL) have improved glucose and insulin tolerance as well as increased energy expenditure when challenged with a high fat diet (HFD). To identify the mechanism(s) involved, we determined whether the Adipoq-LPL mice diverted dietary lipid to adipose tissue to reduce peripheral lipotoxicity, but we found no evidence for this. Instead, characterization of the adipose tissue of the male mice after HFD challenge revealed that the mRNA levels of peroxisome proliferator-activated receptor- (PPAR) and a number of PPAR-regulated genes were higher in the epididymal fat pads of Adipoq-LPL mice than control mice. This included adiponectin, whose mRNA levels were increased, leading to increased adiponectin serum levels in the Adipoq-LPL mice. In many respects, the adipose phenotype of these animals resembles thiazolidinedione treatment except for one important difference, the Adipoq-LPL mice did not gain more fat mass on HFD than control mice and did not have increased expression of genes in adipose such as glycerol kinase, which are induced by high affinity PPAR agonists. Rather, there was selective induction of PPAR-regulated genes such as adiponectin in the adipose of the Adipoq-LPL mice, suggesting that increasing adipose tissue LPL improves glucose metabolism in diet-induced obesity by improving the adipose tissue phenotype. Adipoq-LPL mice also have increased energy expenditure.
Walton R.G.,Barnstable Brown Diabetes and Obesity Center |
Zhu B.,Barnstable Brown Diabetes and Obesity Center |
Unal R.,Muǧla University |
Spencer M.,Barnstable Brown Diabetes and Obesity Center |
And 8 more authors.
Journal of Biological Chemistry | Year: 2015
Background: Lipoprotein lipase regulates fat uptake into adipose tissue. Results: A mouse model with increased adipose tissue lipoprotein lipase has improved glucose metabolism when challenged with a high fat diet. Conclusion: Increasing adipose tissue lipoprotein lipase improves adipose tissue function. Significance: Adipose tissue lipoprotein lipase protects against obesity-induced glucose and insulin intolerance. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc.