Journal
EUROPEAN JOURNAL OF NUTRITION
Volume 56, Issue 4, Pages 1743-1752Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00394-016-1222-0
Keywords
Fatty acids; GPR120; Visceral adipocytes; Inflammation; Obesity
Categories
Funding
- Talent Hub program of the Consejeria de Economia, Innovacion, Ciencia y Empresa de la Junta de Andalucia [TAHUB-042]
- Instituto de Salud Carlos III [PS09/01060]
- Consejeria de Economia, Innovacion, Ciencia y Empresa de la Junta de Andalucia [CTS-8081]
- FEDER funds
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This study examines whether G-protein coupled receptor 120 (GPR120) is involved in the pro-/anti-inflammatory effects of different types of fatty acids (FAs) in human visceral adipocytes, and whether these effects may be altered in obesity, a state with a chronic inflammation. Pro-/anti-inflammatory effects of palmitic, oleic, linoleic and docosahexaenoic acids on human visceral adipocytes were tested in mature adipocytes from non-obese and morbidly obese (MO) subjects. Also, the effects of these FAs were tested when the GPR120 gene was silenced. In adipocytes from non-obese subjects, palmitic and linoleic acids increased TNF-alpha and IL-6 mRNA expression (p < 0.05), and decreased IL-10 and adiponectin expression (p < 0.05). However, oleic and docosahexaenoic acids (DHA) produced the opposite effect (p < 0.05). In adipocytes from MO subjects, all FAs used increased TNF-alpha and IL-6 expression (p < 0.05). Palmitic and linoleic acids decreased IL-10 and adiponectin expression (p < 0.05), but oleic acid and DHA did not have significant effects. Only oleic acid increased adiponectin expression (p < 0.05). The effects of FAs on TNF-alpha, IL-6, IL-10 and adiponectin expression in non-obese and MO subjects were significantly annulled when the GPR120 gene was silenced in visceral adipocytes differentiated from human mesenchymal stem cells. FAs are capable of directly acting on visceral adipocytes to modulate differently TNF-alpha, IL-6, IL-10 and adiponectin expression, with a different and greater effect in MO subjects. These effects are largely annulled when GPR120 expression was silenced, which suggests that they could be mediated by GPR120.
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