Journal
CELL METABOLISM
Volume 30, Issue 4, Pages 706-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2019.08.005
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Funding
- US National Institutes of Health [R03-HD059066, R01-HD059056, R01-DK55758, R01-DK099110, RC2-DK118620, P01DK088761, RO1-DK118725, R01-DK100699, R01 DK119169]
- Robert A. Welch Foundation [AU-0042-20030616]
- Fonds de Recherche Sante Quebec (FRQS)
- NIH [K99 DK120894, K99-DK114898]
- Canadian Institutes of Health Research (CIHR)
- Center for Translational Neuroscience [NIH NIGMS P20-GM103425]
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The physiological role of leptin is thought to be a driving force to reduce food intake and increase energy expenditure. However, leptin therapies in the clinic have failed to effectively treat obesity, predominantly due to a phenomenon referred to as leptin resistance. The mechanisms linking obesity and the associated leptin resistance remain largely unclear. With various mouse models and a leptin neutralizing antibody, we demonstrated that hyperleptinemia is a driving force for metabolic disorders. A partial reduction of plasma leptin levels in the context of obesity restores hypothalamic leptin sensitivity and effectively reduces weight gain and enhances insulin sensitivity. These results highlight that a partial reduction in plasma leptin levels leads to improved leptin sensitivity, while pointing to a new avenue for therapeutic interventions in the treatment of obesity and its associated comorbidities.
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