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Richard N. Bergman

Researcher at Cedars-Sinai Medical Center

Publications -  489
Citations -  97005

Richard N. Bergman is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 130, co-authored 477 publications receiving 91718 citations. Previous affiliations of Richard N. Bergman include University of Southern California & University of California, Los Angeles.

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Activation of NPRs and UCP1-independent pathway following CB1R antagonist treatment is associated with adipose tissue beiging in fat-fed male dogs.

TL;DR: The data suggest that the upregulation of NPRs, β-1R and β-3R, lipolysis, and SERCA2b and RYR2 may be one of the mechanisms by which RIM promotes beiging and overall the improvement of metabolic homeostasis induced by RIM.

Genome-wide physical activity interactions in adiposity. A meta-analysis of 200,452 adults

Mariaelisa Graff, +280 more
TL;DR: This paper performed genome-wide interaction meta-analyses of BMI and BMI-adjusted waist circumference and waist-hip ratio from up to 200,452 adults of European (n = 180,423) or other ancestry.
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A Peripheral CB1R Antagonist Increases Lipolysis, Oxygen Consumption Rate, and Markers of Beiging in 3T3-L1 Adipocytes Similar to RIM, Suggesting that Central Effects Can Be Avoided.

TL;DR: It is shown, for the first time, that AM6545 significantly increases markers of adipose tissue beiging, mitochondrial biogenesis, and lipolysis in 3T3-L1 adipocytes, supporting the importance of focus on peripheral CB1R antagonism pharmacology for reducing the incidence of obesity and T2D.
Journal ArticleDOI

Lack of hepatic "interregulation" during inhibition of glycogenolysis in a canine model.

TL;DR: In conclusion, infusion of DAB inhibited glycogenolysis; however, the absolute contribution of gluconeogenesis to glucose production was not affected, suggesting that inhibition of glycogensolysis could be an effective antidiabetic treatment.