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Discovery of mutations in leptin and the leptin receptor in humans Early studies carried out in obese humans showed that leptin mRNA concentrations in adipose tissue and serum leptin concentrations correlated positively and very closely with the
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important and widely studied players in the control of energy balance is the hormone leptin ( Friedman & Halaas 1998 , Elmquist et al . 2005 ). Leptin was discovered by Zhang et al . (1994) . Defects in leptin production underlie the massive obesity
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& Halaas 1998 ). While some of the features of this new hormonal system were predicted at the time, others were not. Science seldom proceeds in a straight line, and the field spawned by the identification of leptin and other genes that cause obesity is no
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(1973) . Efforts to identify the ob and db gene products then began in earnest ( Leibel et al . 1993 ). Coleman's ‘satiety factor’ of course proved to be leptin ( Zhang et al . 1994 ). Leptin repletion of congenitally leptin-deficient rodents and
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Section of Adult and Pediatric Endocrinology, Division of Endocrinology, Section of Endocrinology, Diabetes and Metabolism, The University of Chicago, 5841 South Maryland Avenue, MC 1027, Chicago, Illinois 60637, USA
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Introduction In 1974, Frisch proposed that the ability to reproduce requires a certain threshold of body fat to serve as the minimal store of energy necessary for ovulation, menstruation, and intended pregnancy ( Frisch & McArthur 1974 ). Leptin
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Introduction Leptin and the leptin receptor (LR) are essential components in the complex genetic wiring diagram underlying energy homeostasis and body weight. The hormone is now known to participate in a wide range of biological functions including
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Department of Pharmacology and Therapeutics, Department of Veterans Affairs, College of Medicine, University of Florida, PO Box 100267, Gainesville, Florida 32610, USA
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Department of Pharmacology and Therapeutics, Department of Veterans Affairs, College of Medicine, University of Florida, PO Box 100267, Gainesville, Florida 32610, USA
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Introduction The adipocyte-derived hormone, leptin, regulates appetite and energy expenditure through its action in the hypothalamus and other brain sites ( Li 2011 ). Our previous studies involving central leptin gene delivery (leptin
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critical periods is an essential component of normal physiology. In this review, we will address the leptin-mediated effects and associated mechanisms that pertain to the accumulation of adipose mass at critical times during the reproductive events of a
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a context in which any additional inflammatory stimulus results in an exaggerated inflammatory response ( Vachharajani 2008 ). The adipose tissue-derived hormone leptin has a well-characterised role in energy homoeostasis, but has also been suggested
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Gremse-IT GmbH, Aachen, Germany
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(db/db) alleles led to the milestone discovery of the leptin system. The hormone leptin ( ob gene) is released by adipose tissue in proportion to fat stores. Leptin signals the status of peripheral adipose stores to the brain, where it is received by
