Decreased expression of adipogenic genes in obese subjects with type 2 diabetes

Dubois, Severine, Heilbronn, Leonie K., Smith, Steven R., Albu, Jeanine B., Kelley, David and Ravussin, Eric 2006, Decreased expression of adipogenic genes in obese subjects with type 2 diabetes, Obesity, vol. 14, no. 9, pp. 1543-1552.

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Title Decreased expression of adipogenic genes in obese subjects with type 2 diabetes
Author(s) Dubois, Severine
Heilbronn, Leonie K.
Smith, Steven R.
Albu, Jeanine B.
Kelley, David
Ravussin, Eric
Journal name Obesity
Volume number 14
Issue number 9
Start page 1543
End page 1552
Publisher North American Association for the Study of Obesity
Place of publication Silver Spring, Md.
Publication date 2006
ISSN 1930-739X
1930-7381
Keyword(s) insulin resistance
gene expression
adipogenesis
fat cell size
type 2 diabetes
Summary Objective: Our objective was to delineate the potential role of adipogenesis in insulin resistance and type 2 diabetes. Obesity is characterized by an increase in adipose tissue mass resulting from enlargement of existing fat cells (hypertrophy) and/or from increased number of adipocytes (hyperplasia). The inability of the adipose tissue to recruit new fat cells may cause ectopic fat deposition and insulin resistance.

Research Methods and Procedures: We examined the expression of candidate genes involved in adipocyte proliferation and/or differentiation [ CCAAT/enhancer-binding protein (C/EBP) alpha, C/EBPdelta, GATA domain-binding protein 3 (GATA3), C/EBPbeta, peroxisome proliferator-activated receptor (PPAR) gamma2, signal transducer and activator of transcription 5A (STAT5A), Wnt-10b, tumor necrosis factor alpha, sterol regulatory element-binding protein 1c (SREBP1c), 11 beta-hydroxysteroid dehydrogenase, PPARG angiopoietin-related protein (PGAR), insulin-like growth factor 1, PPARitalic gamma coactivator 1alpha, PPARitalic gamma coactivator 1beta, and PPARdelta] in subcutaneous adipose tissue from 42 obese individuals with type 2 diabetes and 25 non-diabetic subjects matched for age and obesity.

Results: Insulin sensitivity was measured by a 3-hour 80 mU/m2 per minute hyperinsulinemic glucose clamp (100 mg/dL). As expected, subjects with type 2 diabetes had lower glucose disposal (4.9 plusminus 1.9 vs. 7.5 plusminus 2.8 mg/min per kilogram fat-free mass; p < 0.001) and larger fat cells (0.90 plusminus 0.26 vs. 0.78 plusminus 0.17 mum; p = 0.04) as compared with obese control subjects. Three genes (SREBP1c, p < 0.01; STAT5A, p = 0.02; and PPARitalic gamma2, p = 0.02) had significantly lower expression in obese type 2 diabetics, whereas C/EBPbeta only tended to be lower (p = 0.07).

Discussion: This cross-sectional study supports the hypothesis that impaired expression of adipogenic genes may result in impaired adipogenesis, potentially leading to larger fat cells in subcutaneous adipose tissue and insulin resistance.
Language eng
Field of Research 060405 Gene Expression (incl Microarray and other genome-wide approaches)
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2006, NAASO
Persistent URL http://hdl.handle.net/10536/DRO/DU:30004148

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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