Decreased Expression of Adipogenic Genes in Obese Subjects with Type 2 Diabetes

• DOI: 10.1038/oby.2006.178
• Publication Date: 2008-04-23T14:27:09Z
• Authors: Severine G. Dubois; Leonie K. Heilbronn; Steven R. Smith; Jeanine B. Albu; David E. Kelley; Eric Ravussin
• Keywords: Adult; Male; 0301 basic medicine; 571; fat cell size; adipogenesis; 03 medical and health sciences; Humans; Obesity; Aged; 2. Zero hunger; Insulin resistance; Cell Differentiation; Middle Aged; 3. Good health; PPAR gamma; Cross-Sectional Studies; Adipose Tissue; Diabetes Mellitus, Type 2; Case-Control Studies; gene expression; CCAAT-Enhancer-Binding Proteins; Glucose Clamp Technique; Intercellular Signaling Peptides and Proteins; Female; type 2 diabetes; Insulin Resistance; Sterol Regulatory Element Binding Protein 1; Cell Division

Abstract Objective: Our objective was to delineate the potential role of adipogenesis in insulin resistance and type 2 diabetes. Obesity is characterized by an increase adipose tissue mass resulting from enlargement existing fat cells (hypertrophy) and/or increased number adipocytes (hyperplasia). The inability recruit new may cause ectopic deposition resistance. Research Methods Procedures: We examined expression candidate genes involved adipocyte proliferation differentiation [CCAAT/enhancer‐binding protein ( C/EBP ) α, δ, GATA domain‐binding 3 GATA3 ), β, peroxisome proliferator‐activated receptor PPAR γ , signal transducer activator transcription 5A STAT5A Wnt‐10b tumor necrosis factor sterol regulatory element‐binding 1c SREBP1c 11 beta‐hydroxysteroid dehydrogenase, PPARG angiopoietin‐related PGAR insulin‐like growth 1, PPARγ coactivator 1α, 1 δ] subcutaneous 42 obese individuals with diabetes 25 non‐diabetic subjects matched for age obesity. Results: Insulin sensitivity measured a 3‐hour 80 mU/m per minute hyperinsulinemic glucose clamp (100 mg/dL). As expected, had lower disposal (4.9 ± 1.9 vs. 7.5 2.8 mg/min kilogram fat‐free mass; p < 0.001) larger (0.90 0.26 0.78 0.17 μm; = 0.04) as compared control subjects. Three 0.01; 0.02; PPARγ2 0.02) significantly diabetics, whereas C/EBPβ only tended be 0.07). Discussion: This cross‐sectional study supports hypothesis that impaired adipogenic result adipogenesis, potentially leading