Leptin

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Leptin is a hormone predominantly made by adipose cells and enterocytes in the small intestine that helps to regulate energy balance by inhibiting hunger. It acts on the hypothalamus region of the brain, playing a critical role in body weight homeostasis.

Leptin and ghrelin

Introduction[edit | edit source]

Leptin, from the Greek 'leptos' meaning thin, is a 16-kDa protein hormone. It was discovered in 1994 and is primarily produced in the adipocytes of white adipose tissue, as well as by the gastric chief cells in the stomach, and by the placenta. Leptin is integral to the body's energy regulation and is one of the most important adipose derived hormones.[1]

Function[edit | edit source]

Leptin functions as an "adipostat," a term for the physiological system that maintains fat mass homeostasis. It provides negative feedback in the body's energy regulation loops - as body fat mass increases, leptin release increases, acting on the hypothalamus to suppress appetite and burn fat stored in adipocytes. Similarly, as fat mass decreases, leptin levels drop, stimulating hunger and conserving energy to restore fat mass.[2]

Role in Obesity[edit | edit source]

Obesity is commonly associated with leptin resistance, where despite high levels of circulating leptin, the body behaves as if it is leptin-deficient. The exact mechanisms of leptin resistance are still under research, but chronic inflammation and cellular stress are considered significant contributors. Consequently, leptin therapy has had limited success in obesity treatment.[3]

Clinical Significance[edit | edit source]

Apart from its role in body weight and energy balance, leptin has a broad spectrum of other physiological roles, as it's involved in the regulation of the immune system, bone formation, and fertility. Moreover, its dysregulation has been linked with various pathologies like diabetes, hypertension, and cardiovascular diseases.[4]

See Also[edit | edit source]

References[edit | edit source]

  1. Zhang, Y., et al. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372(6505), 425-432.
  2. Friedman, J. M., & Halaas, J. L. (1998). Leptin and the regulation of body weight in mammals. Nature, 395(6704), 763-770.
  3. Myers, M. G., et al. (2012). Obesity and leptin resistance: distinguishing cause from effect. Trends in Endocrinology & Metabolism, 21(11), 643-651.
  4. Fruhbeck, G., et al. (2019). The ABCD of Obesity: An EASO Position Statement on a Diagnostic Term with Clinical and Scientific Implications. Obesity Facts, 12(2), 131-136.
Leptin Resources
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