The adipocyte as an endocrine cell.
Communication between adipose and other tissues has been hypothesized since at least the 1940s to be bidirectional. Despite this expectation, early progress was largely limited to adipose tissue's role in metabolism and storage of fatty acids, its development, and its response to endocrine and neural cues. However, efforts of the last decade have identified several molecules that are secreted from adipocytes, apparently for the purpose of signaling to other tissues. Cloning of the mouse obesity gene in 1994 is perhaps the most famous impetus for recognition that adipocytes are active in the regulation of multiple body functions. The product of this gene, leptin, has since been found to inhibit feeding, enhance energy expenditure, and stimulate gonadotropes. Evidence for the roles of other adipocyte-derived signals is being generated. Resistin is a protein that can cause whole-body insulin resistance. Its expression is correlated with body fatness and is inhibited by thiazolidinediones, perhaps mediating the association of type 2 diabetes with obesity, and the effectiveness of these drugs. Resistin and a related molecule, RELM alpha, can also inhibit differentiation of preadipocytes. Adiponectin/Acrp30 secretion from adipocytes is diminished in obese states. This protein can enhance use of fatty acids in lean tissues, inhibit glucose production by liver, and consequently decrease both blood glucose and BW. Adiponectin may also be responsible for the effectiveness of thiazolidinediones, given that these drugs promote adiponectin secretion. Secretion of complement proteins has been observed in adipocytes, and these interact to generate a signal called acylation-stimulating protein, which can promote triacylglycerol synthesis. These signals seem to be largely unique to adipocytes. Other signals are derived from adipose tissue, and it is unlikely that all the adipocyte's endocrine signals have been identified. Certainly, there is much to learn about how these signals function; however, it is clear that these biomedical research discoveries comprise a useful model for our study of growth and development in livestock.
Miner
J L
JL
Department of Animal Science, University of Nebraska, Lincoln 68583-0908, USA. jminer1@unl.edu
D017667:Adipocytes / Q000378:metabolism / Q000502:physiology*; D052242:Adiponectin; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism / Q000502:physiology; D015926:Complement C3a / Q000031:analogs & derivatives*; D011416:Complement Factor D / Q000378:metabolism / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D006729:Hormones, Ectopic / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin / Q000378:metabolism* / Q000502:physiology; D011506:Proteins / Q000378:metabolism* / Q000502:physiology; D052243:Resistin; D015398:Signal Transduction
D052242:Adiponectin; D001798:Blood Proteins; D006729:Hormones, Ectopic; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D020738:Leptin; D011506:Proteins; C499624:RETN protein, human; D052243:Resistin; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; C493488:CFD protein, human; D011416:Complement Factor D; C493491:complement factor D, mouse