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Bin Feng

Researcher at Sichuan Agricultural University

Publications -  211
Citations -  3248

Bin Feng is an academic researcher from Sichuan Agricultural University. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 22, co-authored 147 publications receiving 1933 citations. Previous affiliations of Bin Feng include Brown University & Huazhong Agricultural University.

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Reduced Expression of MYC Increases Longevity and Enhances Healthspan

TL;DR: It is found that Myc haploinsufficient (Myc(+/-) mice exhibit increased lifespan and appear to be more active, with a higher metabolic rate and healthier lipid metabolism, and a gene expression signature enriched for metabolic and immune processes.
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FFA-Induced Adipocyte Inflammation and Insulin Resistance: Involvement of ER Stress and IKKβ Pathways

TL;DR: Free‐fatty acids can activate endoplasmic reticulum (ER) stress pathway by examination of ER stress sensor activation and marker gene expression and results indicate that ER stress pathway is a key mediator for FFA‐induced inflammation and insulin resistance in adipocytes with PERK and IKKβ as the critical signaling components.
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Clodronate Liposomes Improve Metabolic Profile and Reduce Visceral Adipose Macrophage Content in Diet-Induced Obese Mice

TL;DR: Intraperitoneal injection of clodronate liposomes reduces visceral adipose tissue macrophages, improves systemic glucose homeostasis and insulin sensitivity in DIO mice, which can be partially attributable to increased adiponectin levels.
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MAPK phosphatase-3 promotes hepatic gluconeogenesis through dephosphorylation of forkhead box O1 in mice.

TL;DR: It is shown that expression of MKP-3 is markedly increased in the liver of diet-induced obese mice, and inhibition of MKK phosphatase-3 activity may provide new therapies for type 2 diabetes mellitus, suggesting that inhibition of the protein in vivo is an important regulator of hepatic gluconeogenesis in vivo.
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Hepatic ERK activity plays a role in energy metabolism.

TL;DR: Increased hepatic ERK activity in DIO mice may contribute to increased liver glycogen content and decreased energy expenditure in obesity, and knocking down ERK expression in the liver of diet induced obese (DIO) mice improves systemic insulin and glucose tolerance.