4.4 Article

Obesity and Insulin Resistance-Related Changes in the Expression of Lipogenic and Lipolytic Genes in Morbidly Obese Subjects

Journal

OBESITY SURGERY
Volume 20, Issue 11, Pages 1559-1567

Publisher

SPRINGER
DOI: 10.1007/s11695-010-0194-z

Keywords

Peroxisome proliferator-activated receptor-gamma; Phosphoenolpyruvate carboxykinase; Adipose triglyceride lipase; Adipose tissue; Insulin resistance; Obesity

Categories

Funding

  1. Instituto de Salud Carlos III [CP04/00133, CP04/0039, PS09/01060, PS09/00997]
  2. Programa Juan de la Cierva [JC1-2009-04086]
  3. Servicio Andaluz de Salud [PI 0255/2007, 0438/2006]

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Background The storage capacity of adipose tissue may be an important factor linking obesity, insulin resistance (IR), and associated morbidities. The aim of this study was to analyze the expression of lipogenic and lipolytic genes in adipose tissue and the influence of IR. Methods We studied the mRNA expression of peroxisome proliferator-activated receptor-gamma (PPAR gamma) and lipogenic and lipolytic enzymes in the visceral (VAT) and subcutaneous adipose tissue (SAT) from 23 morbidly obese patients (MO; 13 with low IR and ten with high IR) and from 15 healthy, lean controls. Results In the VAT and SAT from the MO, we found an increased expression of PPAR gamma (p=0.001 and p=0.022, respectively), acyl-coenzyme A (CoA)/cholesterol acyltransferase (p < 0.001 and p < 0.001), aquaporin 7 (p < 0.001 and p=0.003), and adipose triglyceride lipase (p < 0.001 and p < 0.001) and a reduced expression of acetyl-coenzyme A carboxylase (p=0.004 and p < 0.001), independently of the state of IR. The expression of phosphoenolpyruvate carboxykinase and acyl-CoA synthetase, however, was significantly lower in the MO with high IR (p < 0.05). Glycerol kinase (p=0.010), hormone-sensitive lipase (p<0.001), and perilipin (p=0.006) were only significantly increased in VAT. Acyl-CoA synthetase (p=0.012) and fatty acid binding protein-4 (p=0.003) were only significantly decreased in SAT. The expression of the genes studied was only greater in the SAT than the VAT in the controls. Conclusion Our results show an upregulation of genes facilitating triglyceride/fatty acid cycling and a reduction in the genes involved in de novo synthesis of fatty acids in morbid obesity. The expression of some of the genes studied seems to be related with the state of IR. VAT and SAT differ metabolically and also between controls and MO.

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