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Downregulation of lipogenesis and fatty acid oxidation in the subcutaneous adipose tissue of morbidly obese women
Author(s) -
Auguet Teresa,
GuiuJurado Esther,
Berlanga Alba,
Terra Ximena,
Martinez Salomé,
Porras José Antonio,
Ceausu Andra,
Sabench Fátima,
Hernandez Mercé,
Aguilar Carmen,
Sirvent Joan Josep,
Castillo Daniel Del,
Richart Cristóbal
Publication year - 2014
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20809
Subject(s) - lipogenesis , adipose tissue , morbidly obese , downregulation and upregulation , subcutaneous adipose tissue , subcutaneous fat , medicine , endocrinology , beta oxidation , obesity , fatty acid , chemistry , weight loss , biochemistry , metabolism , gene
Objective The aim of this study was to analyse the expression of crucial genes in fatty acid metabolism in visceral (VAT) and subcutaneous (SAT) adipose tissue samples from morbidly obese women. Methods The VAT and SAT expression of key genes in 145 morbidly obese women (MO, BMI > 40 Kg/m 2 ) and 18 normal weight control women by RT‐PCR and Western Blot was analyzed. Results In SAT, the expression levels of the genes related to lipogenesis and fatty acid oxidation were significantly lower in MO than in controls. In VAT, most of the lipogenic genes studied had similar expression levels in MO and control cohort. Regarding inflammation, IL6 was significantly higher in MO in both tissues whereas TNFα mRNA expression was significantly higher only in VAT. Conclusions Our results indicate that in morbidly obese patients, lipogenesis and fatty acid oxidation are downregulated in SAT, whereas in VAT these pathways are almost unchanged. By contrast, inflammation is induced in both adipose tissues. It is hypothesized that, in this type of extreme obesity, SAT works to limit any further development of fat mass, decreasing the expression of lipogenic and FA oxidative genes whereas VAT depot might have lost this capability.