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The Role of Leptin in the Regulation of Energy Balance and Adiposity
Author(s) -
Van Dijk Gertjan
Publication year - 2001
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.2001.00707.x
Subject(s) - leptin , endocrinology , medicine , thermogenesis , neuropeptide y receptor , hypothalamus , hormone , melanocortins , adipose tissue , melanocortin , biology , brown adipose tissue , neuropeptide , obesity , receptor
Since its discovery, leptin (a 167‐amino acid product of the OB gene) has quickly moved to the forefront as an important hormone for regulation of energy balance. It closes a feedback loop from adipose tissue to hypothalamic neuropeptide‐containing neural circuitry involved in regulation of food intake and neuroendocrine/autonomic outflow. While increased central leptin signalling reduces adiposity via a reduction in food intake, it also has remarkable metabolic effects that promote leanness, independent of food intake. These include: (i) increased energy expenditure, (ii) in‐place degradation of fat, and (iii) increased thermogenesis. Hypothalamic neurones that synthesize corticotropin releasing hormone and melanocortins (i.e. α‐melanocyte‐stimulating hormone and agouti‐related protein) are likely effector pathways that mediate the anorexigenic and metabolic effects of leptin. Activation of sympathetic outflow (via neuropeptidergic effector pathways of central leptin) to a number of tissues that store fat might be an important mechanism through which these peripheral metabolic effects are elicited. It is proposed that these peripheral metabolic effects contribute to the satiating properties of leptin.