Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human

By A. Ichimura, A. Hirasawa, O. Poulain-Godefroy, A. Bonnefond, Takafumi Hara, L. Yengo, I. Kimura, A. Leloire, Ning Liu, Keiko Iida and 34 more. Nature, 2012

646 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/29e4580c1251eae461f3bde8a7458fd029c611ca

How researchers see this paper

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In Molecular Biology

1. J. Tschopp
2. Rongbin Zhou
3. Greta Guarda
4. Aubry Tardivel
5. Wei Jiang
6. Zhigang Tian
7. Yiqing Yan
8. B. Kahn

In Surgery

1. J. Tschopp
2. B. Kahn

Citations in the corpus

• Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. (2013, background): “…GPR40 and GPR120 to inhibit NLRP3 inflammasome activation and may explain the enhanced inflammation observed in adipose tissue of Gpr120 / mice (Ichimura et al., 2012). b-arrestin-2 (ARRB2) is a downstream scaffold protein of GPR120 (Oh et al., 2010), so to further investigate the molecular…”
• Discovery of a class of endogenous mammalian lipids with anti-diabetic and anti-inflammatory effects (2014, background): “The potential importance of identifying an endogenous GPR120 ligand is demonstrated by the fact that loss of function mutations in GPR120 in humans promote obesity and insulin resistance (Ichimura et al., 2012).”