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Jason M. Montez

Researcher at Rockefeller University

Publications -  10
Citations -  3583

Jason M. Montez is an academic researcher from Rockefeller University. The author has contributed to research in topics: Leptin & Leptin receptor. The author has an hindex of 7, co-authored 7 publications receiving 3493 citations.

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Abnormal splicing of the leptin receptor in diabetic mice

TL;DR: A leptin receptor was recently cloned from choroid plexus and shown to map to the same 6-cM interval on mouse chromosome 4 as db8, suggesting that the weight-reducing effects of leptin may be mediated by signal transduction through a leptin receptor in the hypothalamus.
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Selective deletion of leptin receptor in neurons leads to obesity

TL;DR: The data suggest that the brain is a direct target for the weight-reducing and neuroendocrine effects of leptin and that the liver abnormalities of db/db mice are secondary to defective leptin signaling in the brain.
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Transgenic Mice Expressing Green Fluorescent Protein under the Control of the Melanocortin-4 Receptor Promoter

TL;DR: A transgenic mouse line expressing green fluorescent protein (GFP) under the control of the MC4-R promoter is generated, using a modified bacterial artificial chromosome, and it is confirmed that the CNS distribution of GFP-producing cells is identical to that of MC 4-R mRNA in wild-type mice and that nearly all GFP -producing cells coexpress MC4 -R mRNA.
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Regulation of T cell-mediated hepatic inflammation by adiponectin and leptin.

TL;DR: Although leptin increases susceptibility to hepatotoxicity by regulating cytokine production and T cell activation, adiponectin protects hepatocytes from TNF alpha-induced death, whereas leptin had no protective effect.
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Acute leptin deficiency, leptin resistance, and the physiologic response to leptin withdrawal.

TL;DR: The role of acute hypoleptinemia in regulating energy balance, the immune system, and reproductive function is established, and it is suggested that high-dosage leptin treatment can induce a state of acquired leptin resistance.