Leptin is secreted from adipose tissue, maintains energy balance in our body, and regulates appetite via the arcuate nucleus of the hypothalamus. It binds with its receptor (LEPR) to kick-start multiple reaction cascades like JAK2-STAT3-SOCS3, IRS1-PI3K, and PKB-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 towards 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. Keeping obesity in the spotlight, by finding out the point of convergence between insulin and leptin signaling pathways, this review interprets that obesity and chronic leptin resistance are responsible for insulin resistance.
Keywords: Obesity; Diabetes; Leptin; Leptin Resistance; Insulin Resistance
Abbreviations: LEPR: Leptin Receptor; JAK2-STAT3: Janus-activating kinase2-signal transducer and activator of transcription 3; SOCS3: Suppressor of Cytokines Signaling 3;
IRS: Insulin Receptor Subunit; PI3K: Phosphatidyl Inositol 3 Kinase; AMPK: AMP-activated protein kinase; CNS: Central Nervous System; PMOC: Pro-opiomelanocortin;
MCH: Melanin-Concentrating Hormone; NPY: Neuropeptide-Y; MC3R: Melanocortin-3
Receptor; MC4R: Melanocortin-4 Receptor; Sirt-1: Sirtuin 1; CSF: Cerebrospinal Fluid;
SHP-2: Src Homology 2-Containing Tyrosine Phosphatase; Grb2: Growth Factor Receptor Binding 2; CRP: C Reactive Protein
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