Obesity and Leptin Resistance: Distinguishing Cause from Effect
By M. Myers, Rudolph L. Leibel, R. Seeley, M. Schwartz. Trends in endocrinology and metabolism, 2010
867 citations recorded by the source corpus.
Because leptin reduces food intake and body weight, the coexistence of elevated leptin levels with obesity is widely interpreted as evidence of “leptin resistance.” Indeed, obesity promotes multiple cellular processes that attenuate leptin signaling (referred to here as “cellular leptin resistance”), and which amplify the extent of weight gain induced by genetic and environmental factors. As commonly employed, however, the term “leptin resistance” embraces a range of phenomena that are distinct with respect both to underlying mechanisms and pathophysiological implications. Moreover, the induction of cellular leptin resistance by obesity complicates efforts to distinguish the mechanisms that predispose to weight gain from those that result from it. We suggest a framework for approaching these issues and important avenues for future investigation.
Subfields: Endocrine and Autonomic Systems, Epidemiology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/8f34d7d55d4d8203135e385747a8c8e3bf60b1ed
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In Epidemiology
Citations in the corpus
- The role of estrogens in control of energy balance and glucose homeostasis. (2013, background): “These effects are mediated via the long form of the leptin receptor (leprb) (63, 90, 91).”
- Treatment of Obesity with Celastrol (2015, positive): “Nutritional and hormonal inputs from the periphery to the central nervous system (CNS) are interpreted by a complex neuronal circuitry that maintains energy balance in the organism (Dietrich and Horvath, 2013; Myers et al., 2010).”
- Paradoxical effects of obesity on T cell function during tumor progression and PD-1 checkpoint blockade (2018, neutral): “Leptin can increase T cell activation 33,34 and obesity can cause leptin resistance 35,36 .”