title: Endocrine regulation of energy metabolism: review of pathobiochemical and clinical chemical aspects of leptin, ghrelin, adiponectin, and resistin.
abstract: BACKGROUND
  Recent studies point to the adipose tissue as a highly active endocrine organ secreting a range of hormones. Leptin, ghrelin, adiponectin, and resistin are considered to take part in the regulation of energy metabolism.
  
  
  METHODS
  This review summarizes recent knowledge on leptin and its receptor and on ghrelin, adiponectin, and resistin, and emphasizes their roles in pathobiochemistry and clinical chemistry.
  
  
  BACKGROUND
  Leptin, adiponectin, and resistin are produced by the adipose tissue. The protein leptin, a satiety hormone, regulates appetite and energy balance of the body. Adiponectin could suppress the development of atherosclerosis and liver fibrosis and might play a role as an antiinflammatory hormone. Increased resistin concentrations might cause insulin resistance and thus could link obesity with type II diabetes. Ghrelin is produced in the stomach. In addition to its role in long-term regulation of energy metabolism, it is involved in the short-term regulation of feeding. These hormones have important roles in energy homeostasis, glucose and lipid metabolism, reproduction, cardiovascular function, and immunity. They directly influence other organ systems, including the brain, liver, and skeletal muscle, and are significantly regulated by nutritional status. This newly discovered secretory function has extended the biological relevance of adipose tissue, which is no longer considered as only an energy storage site.
  
  
  CONCLUSIONS
  The functional roles, structures, synthesis, analytical aspects, and clinical significance of leptin, ghrelin, adiponectin, and resistin are summarized.
authors.affiliation: Institute of Clinical Chemistry and Pathobiochemistry, Rhenish-Westphalian Technical University, University Hospital Aachen, Pauwelsstrasse 30, D-52074, Germany. umeier@ukaachen.de
authors.forename: Ursula
authors.initials: U
authors.lastname: Meier
authors.forename: Axel M
authors.initials: AM
authors.lastname: Gressner
mesh_terms: D052242:Adiponectin; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism / Q000502:physiology*; D005753:Gastric Mucosa / Q000378:metabolism; D054439:Ghrelin; D006729:Hormones, Ectopic / Q000097:blood / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin / Q000097:blood / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000378:metabolism; D036361:Peptide Hormones / Q000097:blood / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D011506:Proteins / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000097:blood / Q000737:chemistry / Q000378:metabolism; D054411:Receptors, Leptin; D052243:Resistin
chemical_list: D052242:Adiponectin; D054439:Ghrelin; D006729:Hormones, Ectopic; D036341:Intercellular Signaling Peptides and Proteins; C515448:LEPR protein, human; D020738:Leptin; D036361:Peptide Hormones; D011506:Proteins; C499624:RETN protein, human; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D052243:Resistin