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Barbara B. Kahn

Researcher at Beth Israel Deaconess Medical Center

Publications -  286
Citations -  57364

Barbara B. Kahn is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 103, co-authored 281 publications receiving 53325 citations. Previous affiliations of Barbara B. Kahn include Texas Tech University Health Sciences Center & Massachusetts Institute of Technology.

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Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase

TL;DR: It is shown that phosphorylation and activation of the 5′-AMP-activated protein kinase (AMPK) are stimulated with globular and full-length Ad in skeletal muscle and only with full- lengths Ad in the liver, indicating that stimulation of glucose utilization and fatty-acid oxidation by Ad occurs through activation of AMPK.
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Obesity and insulin resistance

TL;DR: Recent progress in understanding of the adipo-insulin axis is reviewed, areas of controversy or uncertainty are highlighted, and approaches to clarifying the unresolved issues are suggested.
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AMP-activated protein kinase: Ancient energy gauge provides clues to modern understanding of metabolism

TL;DR: Through signaling, metabolic, and gene expression effects, AMPK enhances insulin sensitivity and fosters a metabolic milieu that may reduce the risk for obesity and type 2 diabetes.
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Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase.

TL;DR: It is shown that leptin selectively stimulates phosphorylation and activation of the α2 catalytic subunit of AMPK (α2 AMPK) in skeletal muscle, thus establishing a previously unknown signalling pathway for leptin, and identifying AMPK as a principal mediator of the effects of leptin on fatty-acid metabolism in muscle.
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Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes

TL;DR: It is shown that expression of retinol binding protein-4 (RBP4) is elevated in adipose tissue of adipose-Glut4-/- mice and RBP4 is an adipocyte-derived ‘signal’ that may contribute to the pathogenesis of type 2 diabetes.