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REVIEW ARTICLE
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Obesity and chronic leptin resistance foster insulin resistance: An analytical overview


1 Department of Physiology, University of Gour Banga, Malda; Experimental Medicine and Stem Cell Research Laboratory, Department of Physiology, West Bengal State University, Kolkata, West Bengal, India
2 Department of Physiology, University of Gour Banga, Malda, West Bengal, India
3 Experimental Medicine and Stem Cell Research Laboratory, Department of Physiology, West Bengal State University, Kolkata, West Bengal, India
4 Department of Biotechnology, University of North Bengal, Darjeeling, West Bengal, India

Correspondence Address:
Biplab Giri,
Department of Physiology, University of Gour Banga, Malda - 732 103, West Bengal
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bjhs.bjhs_29_20

Leptin is secreted from adipose tissue, maintains energy balance in our body, and regulates appetite via arcuate nucleus of the hypothalamus. It binds with its receptor (LepR) to kick-start multiple reaction cascades such as Janus kinase 2/signal transducer and activator of transcription 3, suppressor of cytokine signaling-3, insulin receptor substrate 1, phosphatidyl inositol 3-kinase, and protein kinase B-Akt. Insulin increases the uptake of fatty acids and enhances cellular glucose uptake and utilization. Insulin's metabolic effects are mediated by a number of tissue-specific pathways, some of which crosstalk leptin-mediated signaling. Studies showed that leptin resistance is instigated due to the excess release of leptin from adipocytes. It causes a lack of sensitivity toward leptin, for which the body fails to attain satiety and results in more food intake which in turn induces more obesity and aggravates further leptin resistance. Emphasizing on obesity, this review directs toward a possibility of chronic leptin resistance being responsible for insulin resistance. The above statement has been elicited by delineating the point of convergence between insulin and leptin signaling pathways.


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