Obesity and chronic leptin resistance foster insulin resistance: An analytical overview
| Autor: | Biplab Giri, Shilpi Ghosh, Mayukh Bose, Sananda Dey, Nensina Murmu |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Janus kinase 2 biology Chemistry Insulin medicine.medical_treatment Leptin media_common.quotation_subject Glucose uptake digestive oral and skin physiology Adipose tissue Appetite General Medicine medicine.disease IRS1 Insulin resistance Endocrinology Internal medicine medicine biology.protein hormones hormone substitutes and hormone antagonists media_common |
| Zdroj: | BLDE University Journal of Health Sciences. 6:7 |
| ISSN: | 2468-838X |
| DOI: | 10.4103/bjhs.bjhs_29_20 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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