Prostaglandins and obesity.
In metabolic obesity energy in triglyceride stores is not readily accessible, and lipolysis to free fatty acid and glycerol seems to be somehow restrained. In the normal situation, there is a balance between a forward reaction via cyclic A.M.P. ending in lipolysis and a negative-feedback mechanism in which prostaglandins participate. In metabolic obesity there may be a biochemical error leading to overproduction of prostaglandins; as a result the forward reaction is overwhelmed and lipolysis does not take place. Since prostaglandin antagonists and inhibitors of prostaglandin synthesis are known, this hypothesis is not without therapeutic interest.
D000067956:Adenylyl Cyclase Inhibitors; D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D000324:Adrenocorticotropic Hormone / Q000502:physiology; D002395:Catecholamines / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005246:Feedback; D005990:Glycerol / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D009765:Obesity / Q000378:metabolism*; D010726:Phosphodiesterase Inhibitors; D011453:Prostaglandins / Q000096:biosynthesis* / Q000494:pharmacology / Q000502:physiology; D047428:Protein Kinase Inhibitors; D011941:Receptors, Adrenergic; D014280:Triglycerides / Q000378:metabolism
D000067956:Adenylyl Cyclase Inhibitors; D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D010726:Phosphodiesterase Inhibitors; D011453:Prostaglandins; D047428:Protein Kinase Inhibitors; D011941:Receptors, Adrenergic; D014280:Triglycerides; D000324:Adrenocorticotropic Hormone; D005990:Glycerol