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Michael R. Schön

Researcher at Leipzig University

Publications -  81
Citations -  7731

Michael R. Schön is an academic researcher from Leipzig University. The author has contributed to research in topics: Adipose tissue & Insulin resistance. The author has an hindex of 35, co-authored 81 publications receiving 6978 citations. Previous affiliations of Michael R. Schön include University of Freiburg & Humboldt University of Berlin.

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Plasma visfatin concentrations and fat depot-specific mRNA expression in humans

TL;DR: Visceral and subcutaneous adipose tissue display important metabolic differences that underlie the association of visceral obesity with obesity-related cardiovascular and metabolic alterations, but correlation with measures of obesity but not with visceral fat mass or waist-to-hip ratio is found.
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Insulin-sensitive obesity

TL;DR: In this paper, the association between obesity and impaired insulin sensitivity has been recognized, although a subgroup of obese individuals seems to be protected from insulin resistance, while the rest of the population appears to be obese.
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Dysregulation of the Peripheral and Adipose Tissue Endocannabinoid System in Human Abdominal Obesity

TL;DR: The findings suggest that abdominal fat accumulation is a critical correlate of the dysregulation of the peripheral endocannabinoid system in human obesity and may represent a primary target for the treatment of abdominal obesity and associated metabolic changes.
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A novel ChREBP isoform in adipose tissue regulates systemic glucose metabolism

TL;DR: It is reported that adipose tissue GLUT4 regulates the expression of carbohydrate-responsive-element-binding protein (ChREBP; also known as MLXIPL), a transcriptional regulator of lipogenic and glycolytic genes, and adipose ChREBP is a major determinant of adipOSE tissue fatty acid synthesis and systemic insulin sensitivity.
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Serum retinol-binding protein is more highly expressed in visceral than in subcutaneous adipose tissue and is a marker of intra-abdominal fat mass.

TL;DR: It is reported that, in 196 subjects, RBP4 is preferentially expressed in visceral (Vis) versus subcutaneous (SC) fat, and Vis fat may be a major source ofRBP4 in insulin-resistant states.