Key result
Alpha-linolenic acid supplementation for 12 weeks significantly increased G0S2 mRNA expression in peripheral blood mononuclear cells and decreased plasma free fatty acid levels in obese patients.
Why the study?
Does alpha-linolenic acid improve G0S2 gene expression and reduce lipolysis in obese patients?
RCT (n=26)
Open-label
Simple randomization
No
Does alpha-linolenic acid improve G0S2 gene expression and reduce lipolysis in obese patients?
Absolute Event Rate: 2.25% vs 1.17%
p-value: p=<0.0001
Alpha-linolenic acid supplementation increases G0S2 gene expression in PBMC and reduces plasma free fatty acids, suggesting an anti-lipolytic effect in obese patients.
ALA may upregulate G0S2 to curb lipolysis in obese patients; hypothesis-generating pilot data require confirmation in larger trials.
BACKGROUND: 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. 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. METHODS: A 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. RESULTS: ALA 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. CONCLUSION: This 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.
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Zhao et al. (2016) conducted an RCT in Obesity (n=26). alpha-Linolenic acid vs. Untreated control group was evaluated on G0S2 mRNA expression in PBMC (p=<0.0001). Alpha-linolenic acid supplementation for 12 weeks significantly increased G0S2 mRNA expression in peripheral blood mononuclear cells and decreased plasma free fatty acid levels in obese patients.
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