A Review on Role of Different Adipokines in Gestational Diabetes

Authors

  • Sovana Kotal
  • Paromita Mukherjee
  • Devali Chakraborty
  • Souvik Tewari

DOI:

https://doi.org/10.17762/jaz.v44iS6.2794

Keywords:

Cortisol, Ghrelin, Insulin resistance, Leptin, metabolic diseases, Nicotinamide Adenine Diphosphate.

Abstract

Adipokines are cell-signaling molecules produced by the adipose tissue that play functional roles in energy or metabolic status of the body, inflammation, obesity, gestational diabetes etc. Adipokines come in several forms, including adiponectin, leptin, chemeein, resistin, and nicotinamide phosphoribosyl transferase. The hormone adiponectin is primarily recognised for its anti- inflammatory and insulin-sensitizing properties. Through its anti-inflammatory, anti-fibrotic, and antioxidant properties, the adipocyte-secreted hormone adiponectin regulates lipid metabolism, insulin sensitivity, blood sugar levels, and adipocyte function. The hormone leptin, which is released from adipose tissue (body fat), aids the body in long-term maintenance of a healthy weight. In order to prevent the body from producing the hunger response when it doesn't need energy. White adipocytes release resistin, a hormone high in cysteine. Insulin resistance is influenced by resistin. Adipocytes secrete a protein called chemerin, which has endocrine functions in metabolism and immunity as well as autocrine/paracrine effects on adipose formation and function. Due to significantly greater oestrogen levels, there is an increase in insulin sensitivity in the first and second trimesters. Increased insulin resistance and decreased sensitivity are caused by a number of antagonistic hormones, particularly placental lactogen, leptin, progesterone, prolactin, and cortisol in the late second and early third trimester. In addition to outlining their mechanisms of action in the development of gestational diabetes, this review paper attempts to summarise the functions of adipokines in the induction of insulin resistance during pregnancy.

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Published

2023-12-14

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