Leptin and its metabolic interactions: an update

Diabetes Obes Metab. 2008 Nov;10(11):973-93. doi: 10.1111/j.1463-1326.2008.00852.x. Epub 2008 Feb 18.


Obesity results from an abnormal accumulation of fat in the white adipose tissue. Recent research utilizing genetic models of obesity in rodents has implicated a major role of leptin as a controller of obesity. Leptin is a 167-amino acid peptide hormone encoded by the obesity gene (ob), which is secreted by adipocytes and plays an important role in regulating food intake, energy expenditure and adiposity. Leptin receptors (OB-R) are expressed in the central nervous system mainly in afferent satiety centres of hypothalamus and in peripheral organs such as adipose tissues, skeletal muscles, pancreatic beta-cells and liver, thus indicating the autocrine and paracrine role of leptin in energy regulation. In human beings, a highly organized circadian pattern of leptin secretion is observed with peak levels in the midnight probably resulting from cumulative hyperinsulinemia of entire day. Leptin has a dual role in weight maintenance. Leptin reflects total body adipose tissue mass whereas in conditions of negative and positive energy balance, the dynamic changes in plasma leptin concentration function as a sensor of energy balance and influence the efferent energy regulation pathways. Many effects of leptin on metabolism are mediated by interaction with Insulin and also by synergistic action with cholecystokinin. Besides physiological roles, leptin may influence pathological conditions like obesity-associated atherosclerosis, oxidative stress and cancers. The purpose of the present review is to summarize the important aspects of the biology, actions, and regulation of leptin and to serve as an update of new information.

Publication types

  • Review

MeSH terms

  • Adipose Tissue, White / metabolism*
  • Animals
  • Circadian Rhythm
  • Energy Metabolism / physiology
  • Humans
  • Hypothalamus / metabolism
  • Insulin / metabolism
  • Leptin / metabolism*
  • Obesity / metabolism
  • Receptors, Leptin / metabolism
  • Signal Transduction / physiology*


  • Insulin
  • Leptin
  • Receptors, Leptin