Two defects contribute to hypothalamic leptin resistance in mice with diet-induced obesity.
By K. El-Haschimi, D. Pierroz, S. Hileman, Christian Bjørbæk, J. Flier. Journal of Clinical Investigation, 2000
900 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Epidemiology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/7f3ca26acd95fd25a145078471492d250885fddb
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In Endocrine and Autonomic Systems
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Citations in the corpus
- The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review (2007, background): “demonstrated in studies with DIO mice that peripheral administered leptin was unable to activate hypothalamic Stat3 signalling, and the magnitude of Stat3 activation was substantially reduced after intracerebroventricular leptin (145).”
- Mechanisms of leptin action and leptin resistance. (2008, background): “Although the absolute lack or genetic alteration of LRb does not underlie most leptin resistance (95, 100), the preponderance of data confirm that alterations in cellular LRb signaling, especially in the ARC, play a crucial role in leptin resistance (98, 101, 102).”
- Leptin and Obesity: Role and Clinical Implication (2021, background): “A few hypothalamic areas (DMH, preoptic area (POA), paraventricular nucleus (PVN), VMH, ARC), but also some extra-hypothalamic regions as the nucleus tractus solitarius (NTS) participate in leptin-induced thermogenesis (125).”
- Consumption of a fat-rich diet activates a proinflammatory response and induces insulin resistance in the hypothalamus. (2005, methodology): “This diet composition has been previously used (9).”