Severely Impaired Adipsin Expression in Genetic and Acquired Obesity

• Published in: Science (American Association for the Advancement of Science) Vol. 237; no. 4813; pp. 405 - 408
• Main Authors: Flier, Jeffrey S., Cook, Kathleen Sue, Usher, Patricia, Spiegelman, Bruce M.
• Format: Journal Article
• Language: English
• Published: Washington, DC The American Association for the Advancement of Science 24.07.1987; American Association for the Advancement of Science
• Subjects: Actins; Adipocytes; Adipose Tissue - enzymology; Adipose tissues; Animal models; Animals; Antigen-Antibody Complex; Biological and medical sciences; Complement Factor D; Endopeptidases - genetics; Endopeptidases - metabolism; Enzymes; Genetic aspects; Genetics; Immune Sera; Insulin; Lipid metabolism; Medical sciences; Messenger RNA; Metabolic diseases; Mice; Mice, Obese; Obesity; Obesity - enzymology; Obesity - genetics; Rats; Reference Values; RNA, Messenger - genetics; Serine Endopeptidases; Thermogenesis; Transcription, Genetic; Animal model; Obesity; Rat; Diabetes mellitus; Proteinase; Rodentia; Sodium Glutamate; Metabolic diseases; Glucose tolerance test; Experimental animal; Gene expression; Proteins; Vertebrata; Experimental disease; Mammalia; Mouse; Adipsin; Streptozotocin; Cafeteria diet
• ISSN: 0036-8075; 1095-9203
• DOI: 10.1126/science.3299706

Adipsin, a serine protease homolog, is synthesized and secreted by adipose cells and is found in the bloodstream. The expression of adipsin messenger RNA (mRNA) and protein was analyzed in rodents during metabolic perturbations and in several experimental models of obesity. Adipsin mRNA abundance is increased in adipose tissue during fasting in normal rats and in diabetes due to streptozotocin-induced insulin deficiency. Adipsin mRNA abundance decreased during the continuous infusion of glucose, which induces a hyperglycemic, hyperinsulinemic state that is accompanied by an increased adipose mass; it is suppressed (>100-fold) in two strains of genetically obese mice (db/db and ob/ob), compared to their congenic counterparts, and is also reduced when obesity is induced chemically by injection of monosodium glutamate into newborn mice. Circulating adipsin protein is decreased in these animal models of obesity, as determined by immunoblotting with antisera to adipsin. Little change in adipsin expression is observed in a model of obesity obtained by pure overfeeding of normal rats (cafeteria model). These data suggest a possible role for adipsin in the above-mentioned disordered metabolic states, and raise the possibility that adipsin expression may be used to distinguish obesities that arise from certain genetic or metabolic defects from those that result from pure overfeeding.