Hypothesis: prostaglandins mediate defective glucose recognition in diabetes mellitus.
The glucoreceptor hypothesis proposes that diabetics have a selective defect in both pancreatic and extra-pancreatic tissues in the recognition of, and hormonal responses to glucose. Many of these defective or even paradoxical responses to hyperglycemia and hypoglycemia can be mimicked by known actions of prostaglandins, particularly PGE, in normal subjects. Inhibition of PGE synthesis in diabetics partially reverses several abnormal responses. We propose that excessive production of, or sensitivity to, prostaglandins may play a role in some of the metabolic abnormalities associated with defective glucose recognition in diabetes mellitus.
D003920:Diabetes Mellitus / Q000503:physiopathology*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology; D007003:Hypoglycemia / Q000503:physiopathology; D007328:Insulin / Q000378:metabolism / Q000502:physiology; D000078790:Insulin Secretion; D011453:Prostaglandins / Q000502:physiology*; D011955:Receptors, Drug / Q000378:metabolism*
D007328:Insulin; D011453:Prostaglandins; D011955:Receptors, Drug; D005947:Glucose