α-Linolenic acid increases the G0/G1 switch gene 2 mRNA expression in peripheral blood mononuclear cells from obese patients: a pilot study

Naiqian Zhao,Li Wang,Na Guo

doi:10.1186/s12944-016-0207-6

Abstract

BackgroundRecent evidence has demonstrated that the G0/G1 switch gene 2 (G0S2) is an important negative regulator of the rate-limiting lipolytic enzyme adipose triglyceride lipase-mediated lipolysis. It has been revealed that α-linolenic acid (ALA), a plant-based essential omega-3 polyunsaturated fatty acids, reduces adipose tissue lipolysis. However, it is not known whether G0S2 is implicated in ALA-induced inhibition of lipolysis. The purpose of this pilot study is to investigate the effect of ALA on G0S2 gene expression in peripheral blood mononuclear cells (PBMC) of obese patients and the potential influence of G0S2 gene expression in ALA-induced inhibition of lipolysis.MethodsA total of 26 obese patients were randomly assigned to be treated with or without ALA treatment (~4.0 g daily) for 12 weeks: the ALA-treated group (n = 14) or the untreated control group (n = 12). Plasma triglyceride (TG), free fatty acids (FFA), glycerol, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), as well as the mRNA expression levels of proliferator-activated receptor gamma (PPAR-γ), G0S2, and G protein-coupled receptor 120 (GPR120) in PBMC were repeatedly examined from fasting obese patients before and after ALA treatment.ResultsALA significantly decreased plasma TG, FFA, glycerol, IL-6, and TNF-α levels and increased the mRNA expression levels of PPAR-γ, G0S2, and GPR120 in PBMC, compared with the untreated control group. In obese patients from the ALA-treated group, decreased plasma FFA (a biomarker for lipolysis) level was significantly correlated with increased PPAR-γ (a functional omega-3 fatty acids receptor) and G0S2 (a direct target gene of PPAR-γ) mRNA expression in PBMC, while decreased plasma FFA level was not correlated with increased GPR120 (another functional omega-3 fatty acids receptor) mRNA expression in PBMC.ConclusionThis study shows that ALA increases G0S2 gene expression in PBMC in parallel with the decrease of plasma FFA level in obese patients. Increased G0S2 gene expression might contribute to the beneficial anti-lipolytic effect of ALA in obese patients.

Highlights

Recent evidence has demonstrated that the G0/G1 switch gene 2 (G0S2) is an important negative regulator of the rate-limiting lipolytic enzyme adipose triglyceride lipase-mediated lipolysis
The two groups were well matched for age, body weight, body mass index (BMI), total cholesterol (TC), triglyceride (TG), free fatty acids (FFA), glycerol, IL-6, and tumor necrosis factor-α (TNF-α)
After acids include α-linolenic acid (ALA) treatment for 12 weeks, BMI and plasma concentrations of TG, FFA, glycerol, IL-6, and TNF-α were significantly lower in obese patients from the ALAtreated and control groups compared with before ALA treatment

Summary

Introduction

Recent evidence has demonstrated that the G0/G1 switch gene 2 (G0S2) is an important negative regulator of the rate-limiting lipolytic enzyme adipose triglyceride lipase-mediated lipolysis. It has been revealed that α-linolenic acid (ALA), a plant-based essential omega-3 polyunsaturated fatty acids, reduces adipose tissue lipolysis It is not known whether G0S2 is implicated in ALA-induced inhibition of lipolysis. Ω-3 Fatty acids have been shown to improve NAFLD, reduce blood triglyceride levels and incidences of cardiovascular diseases [7,8,9,10] These beneficial effects of ω-3 fatty acids may be due to reduced adipose tissue lipolysis. Animal studies have shown that dietary supplementation of EPA and DHA inhibits basal lipolysis and reduces postprandial plasma FFA and glycerol levels in rats fed highfat diets [11], and that dietary Salba seed rich in ALA improves the impaired anti-lipolytic action of insulin in rats fed high-sucrose diets [12]. A human study has demonstrated that dietary fish oil rich in EPA and DHA significantly reduces plasma concentrations of triglyceride and FFA [13]

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Conclusion