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Jan-Bernd Funcke

Researcher at University of Ulm

Publications -  32
Citations -  1133

Jan-Bernd Funcke is an academic researcher from University of Ulm. The author has contributed to research in topics: Adipose tissue & Adipocyte. The author has an hindex of 15, co-authored 28 publications receiving 666 citations. Previous affiliations of Jan-Bernd Funcke include University of Texas Southwestern Medical Center.

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Beyond adiponectin and leptin: adipose tissue-derived mediators of inter-organ communication

TL;DR: The diverse signaling mediators and mechanisms adipose tissue utilizes to relay information to other organs are reviewed and recently identified adipokines (proteins, lipids, and metabolites) are discussed and the contributions of noncoding RNAs and EVs to the ever-increasing complexities of adipose tissues inter-organ communication are outlined.
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Biologically Inactive Leptin and Early-Onset Extreme Obesity

TL;DR: Treating a 2-year-old boy with early-onset extreme obesity due to a novel homozygous transversion in LEP with recombinant human leptin (metreleptin) rapidly normalized eating behavior and resulted in weight loss.
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Extracellular vesicle-based interorgan transport of mitochondria from energetically stressed adipocytes.

TL;DR: In this paper, the authors found that adipocytes respond to mitochondrial stress by rapidly and robustly releasing small extracellular vesicles (sEVs), which contain respiration-competent, but oxidatively damaged mitochondrial particles, which enter circulation and are taken up by cardiomyocytes, where they trigger a burst of ROS.
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miR-146a-mediated suppression of the inflammatory response in human adipocytes

TL;DR: It is shown that miR-146a reduces the inflammatory response in human adipocytes, which might contribute to the regulation of inflammatory processes in WAT and possibly prevent an overwhelming inflammatory response.
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Monogenic forms of childhood obesity due to mutations in the leptin gene

TL;DR: This review describes the molecular and cellular characteristics of the eight distinct mutations found so far in humans caused by mutations in the leptin gene.