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Jonathon N. Winnay

Researcher at Harvard University

Publications -  40
Citations -  7939

Jonathon N. Winnay is an academic researcher from Harvard University. The author has contributed to research in topics: Insulin receptor & Insulin resistance. The author has an hindex of 30, co-authored 40 publications receiving 7197 citations. Previous affiliations of Jonathon N. Winnay include Joslin Diabetes Center & Brigham and Women's Hospital.

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A Muscle-Specific Insulin Receptor Knockout Exhibits Features of the Metabolic Syndrome of NIDDM without Altering Glucose Tolerance

TL;DR: Insulin resistance in muscle contributes to the altered fat metabolism associated with type 2 diabetes, but tissues other than muscle appear to be more involved in insulin-regulated glucose disposal than previously recognized.
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Tissue-Specific Knockout of the Insulin Receptor in Pancreatic β Cells Creates an Insulin Secretory Defect Similar to that in Type 2 Diabetes

TL;DR: An important functional role for the insulin receptor in glucose sensing by the pancreatic beta cell is indicated and it is suggested that defects in insulin signaling at the level of the beta cell may contribute to the observed alterations in insulin secretion in type 2 diabetes.
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Adipose-derived circulating miRNAs regulate gene expression in other tissues

TL;DR: Transplantation of both white and brown adipose tissue—brown especially—into ADicerKO mice restores the level of numerous circulating miRNAs that are associated with an improvement in glucose tolerance and a reduction in hepatic Fgf21 mRNA and circulating FGF21.
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New role of bone morphogenetic protein 7 in brown adipogenesis and energy expenditure

TL;DR: It is demonstrated that whereas some members of the family of bone morphogenetic proteins (BMPs) support white adipocyte differentiation, BMP7 singularly promotes differentiation of brown preadipocytes even in the absence of the normally required hormonal induction cocktail.
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Development of a novel polygenic model of NIDDM in mice heterozygous for IR and IRS-1 null alleles.

TL;DR: This NIDDM mouse model in which diabetes arises in an age-dependent manner from the interaction between two genetically determined, subclinical defects in the insulin signaling cascade demonstrates the role of epistatic interactions in the pathogenesis of common diseases with non-Mendelian genetics.