Leptin is a protein hormone predominantly made by adipocytes and its primary role is likely to regulate long-term energy balance.
Adipose tissue (also known as body fat, or simply fat) is a loose connective tissue composed mostly of adipocytes. In addition to adipocytes, adipose tissue contains the stromal vascular fraction(SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages. Adipose tissue is derived from preadipocytes. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body. Far from being hormonally inert, adipose tissue has, in recent years, been recognized as a major endocrine organ, as it produces hormones such as leptin, estrogen, resistin, and cytokines (especially TNFα). In obesity, adipose tissue is also implicated in the chronic release of pro-inflammatory markers known as adipokines, which are responsible for the development of metabolic syndrome, a constellation of diseases, including type 2 diabetes, cardiovascular disease and atherosclerosis. The two types of adipose tissue are white adipose tissue (WAT), which stores energy, and brown adipose tissue (BAT), which generates body heat. The formation of adipose tissue appears to be controlled in part by the adipose gene. Adipose tissue – more specifically brown adipose tissue – was first identified by the Swiss naturalist Conrad Gessner in 1551.
Adipocytes, also known as lipocytes and fat cells, are the cells that primarily compose adipose tissue, specialized in storing energy as fat. Adipocytes are derived from mesenchymal stem cells which give rise to adipocytes through adipogenesis. In cell culture, adipocyte progenitors can also form osteoblasts, myocytes and other cell types.
Ghrelin is a hormone produced by enteroendocrine cells of the gastrointestinal tract, especially the stomach, and is often called a "hunger hormone" because it increases the drive to eat. Blood levels of ghrelin are highest before meals when hungry, returning to lower levels after mealtimes. Ghrelin may help prepare for food intake by increasing gastric motility and stimulating the secretion of gastric acid.
The adipokines, or adipocytokines are cytokines secreted by adipose tissue. Some contribute to an obesity-related low-grade state of inflammation or to the development of metabolic syndrome, a constellation of diseases including, but not limited to, type 2 diabetes, cardiovascular disease and atherosclerosis. The first adipokine to be discovered was leptin in 1994. Since that time, hundreds of adipokines have been discovered.
Agouti-related protein (AgRP), also called agouti-related peptide, is a neuropeptide produced in the brain by the AgRP/NPY neuron. It is synthesized in neuropeptide Y (NPY)-containing cell bodies located in the ventromedial part of the arcuate nucleus in the hypothalamus. AgRP is co-expressed with NPY and acts to increase appetite and decrease metabolism and energy expenditure. It is one of the most potent and long-lasting of appetite stimulators. In humans, the agouti-related peptide is encoded by the AGRP gene.
The Instituto Gulbenkian de Ciência (IGC) is an international centre for biological and biomedical research and graduate training based in Oeiras, Portugal. Founded by the Calouste Gulbenkian Foundation (FCG) in 1961, and still supported by the Foundation, the IGC is organised in small independent research groups that work in an environment designed to encourage interactions with minimal hierarchical structure.
Jeffrey M. Friedman is a molecular geneticist at New York City's Rockefeller University and an Investigator of the Howard Hughes Medical Institute. His discovery of the hormone leptin and its role in regulating body weight has had a major role in the area of human obesity. Friedman is a physician scientist studying the genetic mechanisms that regulate body weight. His research on various aspects of obesity received national attention in late 1994, when it was announced that he and his colleagues had isolated the mouse ob gene and its human homologue. They subsequently found that injections of the encoded protein, leptin, decreases body weight of mice by reducing food intake and increasing energy expenditure. Current research is aimed at understanding the genetic basis of obesity in human and the mechanisms by which leptin transmits its weight-reducing signal.
White adipose tissue or white fat is one of the two types of adipose tissue found in mammals. The other kind is brown adipose tissue. White adipose tissue is composed of monolocular adipocytes.
Leptin receptor, also known as LEP-R or OB-R, is a type I cytokine receptor, a protein that in humans is encoded by the LEPR gene. LEP-R functions as a receptor for the fat cell-specific hormone leptin. LEP-R has also been designated as CD295. Its location is the cell membrane, and it has extracellular, trans-membrane and intracellular sections.
The central melanocortin system is defined anatomically as a collection of central nervous system circuits which include:
Chemerin, also known as retinoic acid receptor responder protein 2 (RARRES2), tazarotene-induced gene 2 protein (TIG2), or RAR-responsive protein TIG2 is a protein that in humans is encoded by the RARRES2 gene.
RPGRIP1L is a human gene.
Douglas L. Coleman was a scientist and professor emeritus at the Jackson Laboratory, in Bar Harbor, Maine. His work predicted that there exists a hormone that can cause mice to feel full, and that a mutation in the gene encoding this hormone can lead to obesity. The gene and corresponding hormone were discovered about 20 years later by Jeffrey M. Friedman, Rudolph Leibel, and their research teams at Rockefeller University, which Friedman named leptin.
Lipotoxicity is a metabolic syndrome that results from the accumulation of lipid intermediates in non-adipose tissue, leading to cellular dysfunction and death. The tissues normally affected include the kidneys, liver, heart and skeletal muscle. Lipotoxicity is believed to have a role in heart failure, obesity, and diabetes, and is estimated to affect approximately 25% of the adult American population.
Michael Warren Schwartz is Robert H. Williams Endowed Chair, Professor of Medicine in the Division of Metabolism, Endocrinology and Nutrition at the University of Washington and Director of the UW Medicine Diabetes and Obesity Center of Excellence. He is the Director of the NIH-funded Nutrition Obesity Research Center (NORC) at the University of Washington. His research investigates brain mechanisms governing energy balance and glucose metabolism and how obesity and diabetes result from impairment of these brain systems. He has published more than 200 articles and book chapters related to these topics and his research has been continuously funded by the NIH since joining the faculty of UW 18 years ago. Dr. Schwartz is a member of the Association of American Physicians, the Western Association of Physicians, and the American Society for Clinical Investigation, is the recipient of the 2007 Williams-Rachmiel Levine Award for Outstanding Mentorship from the Western Society for Clinical Investigation, the 2006 Naomi Berrie Award for Outstanding Achievement in Diabetes Research from Columbia University, and was the 2012 Solomon A. Berson Lecturer for the American Physiological Society, among other awards. He is a member of the editorial boards of the Journal of Clinical Investigation, American Journal of Physiology, Endocrine Reviews, Molecular Metabolism and Frontiers in Neuroendocrinology.
Rudolph Leibel is the Christopher J. Murphy Professor of Diabetes Research, Professor of Pediatrics and Medicine at Columbia University Medical Center, and Director of the Division of Molecular Genetics in the Department of Pediatrics. He is also co-director of the Naomi Berrie Diabetes Center and executive director of the Russell and Angelica Berrie Program in Cellular Therapy, Co-director of the New York Obesity Research Center and the Columbia University Diabetes and Endocrinology Research Center.
Asprosin is a protein hormone produced by mammals in tissues that stimulates the liver to release glucose into the blood stream. Asprosin is encoded by the gene FBN1 as part of the protein profibrillin and is released from the C-terminus of the latter by specific proteolysis. In the liver, asprosin activates rapid glucose release via a cyclic adenosine monophosphate (cAMP)-dependent pathway.
Ismaa Sadaf Farooqi is a Wellcome Trust Senior Research fellow in Clinical Science, professor of Metabolism and Medicine at the University of Cambridge and a consultant physician at Addenbrooke's Hospital in Cambridge, UK.
Pathophysiology of obesity is the study of disordered physiological processes that cause, result from, or are otherwise associated with obesity. A number of possible pathophysiological mechanisms have been identified which may contribute in the development and maintenance of obesity.
