4.2 Article

Role of peroxisome proliferator-activated receptor gamma Pro12Ala polymorphism in human adipose tissue: assessment of adipogenesis and adipocyte glucose and lipid turnover

Journal

ADIPOCYTE
Volume 7, Issue 4, Pages 285-296

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/21623945.2018.1503030

Keywords

human adipose tissue; metabolism and adipogenesis; PPAR gamma Pro12Ala

Funding

  1. Swedish Research Council [2015-02907]
  2. Goran Gustafsson Foundation
  3. Swedish Heart-Lung Foundation [20140422]
  4. Knut och Alice Wallenberg Foundation [2013.0126]
  5. Swedish Diabetes Foundation
  6. Swedish National Strategic Research Initiative EXODIAB (Excellence of Diabetes Research in Sweden)
  7. Swedish government
  8. Ernfors Foundation
  9. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK106236, P30DK116074] Funding Source: NIH RePORTER

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The protective mechanisms of peroxisome proliferator-activated receptor gamma (PPAR gamma) Pro12Ala polymorphism in type 2 diabetes (T2D) are unclear. We obtained subcutaneous adipose tissue (AT) before and 3 h after oral glucose (OGTT) in carriers and non-carriers of the Ala allele (12 Pro/Pro, 15 Pro/Ala, and 13 Ala/Ala). Adipogenesis, adipocyte glucose uptake and lipolysis as well as PPAR gamma target gene expression were investigated and compared between the genotype groups. During fasting and post-OGTT, neither basal nor insulin-stimulated adipocyte glucose uptake differed between genotypes. Compared to fasting, a decreased hormone-sensitive lipase gene expression in Pro/Pro (p < 0.05) was accompanied with a higher antilipolytic effect of insulin postOGTT (p < 0.01). The adipocyte size was similar across groups. Preadipocyte differentiation rates between Pro/Pro and Ala/Ala were unchanged. In conclusion, no major differences in AT differentiation, glucose uptake, lipolysis or expression of PPAR gamma target genes were observed between different PPAR gamma Pro12Ala genotypes. Albeit small, our study may suggest that other pathways in AT or effects exerted in other tissues might contribute to the Pro12Ala-mediated protection against T2D.

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