The pro-/anti-inflammatory effects of different fatty acids on visceral adipocytes are partially mediated by GPR120

Eur J Nutr. 2017 Jun;56(4):1743-1752. doi: 10.1007/s00394-016-1222-0. Epub 2016 Jun 14.

Abstract

Purpose: 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.

Methods: 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.

Results: In adipocytes from non-obese subjects, palmitic and linoleic acids increased TNF-α 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-α 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-α, 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.

Conclusions: FAs are capable of directly acting on visceral adipocytes to modulate differently TNF-α, 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.

Keywords: Fatty acids; GPR120; Inflammation; Obesity; Visceral adipocytes.

MeSH terms

  • Adipocytes / drug effects*
  • Adipokines / genetics
  • Adipokines / metabolism
  • Adult
  • Anti-Inflammatory Agents / pharmacology*
  • Body Mass Index
  • Body Weight
  • Cholesterol / blood
  • Chronic Disease
  • Fatty Acids / pharmacology*
  • Female
  • Gene Silencing
  • Humans
  • Inflammation / drug therapy*
  • Insulin / blood
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Male
  • Middle Aged
  • Receptors, G-Protein-Coupled / metabolism*
  • Triglycerides / blood
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Adipokines
  • Anti-Inflammatory Agents
  • FFAR4 protein, human
  • Fatty Acids
  • IL10 protein, human
  • IL6 protein, human
  • Insulin
  • Interleukin-6
  • Receptors, G-Protein-Coupled
  • Triglycerides
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Cholesterol