Plasma immuno-reactive insulin (IRI) and peripherel glucose utilization in bilharzial patients with impaired renal functions
El-Badry, A.; Hassaballah, A.M.; El-Ayadi, A.; Barsoum, R.S.; Shaheen, M.H.; El-Ghoneimy, E.H.; Abdel-Rahman, Y.; El-Bagoury, I.
Journal of the Egyptian Medical Association 58(7-8): 361-369
1975
ISSN/ISBN: 0013-2411 PMID: 1236509 Document Number: 93278
Ten patients with chronic pyelonephritis associated with bilharziasis and 14 normal controls were given oral and intravenous glucose tolerance tests. Abnormalities in oral tests were found in 9 in the form of delayed peak, high peak, or delayed descent. The intravenous test was normal, and the K-value was insignificantly increased. Fasting insulin was raised and the response to glucose stimulation was increased. These findings were interpreted to indicate an impaired tissue sensitivity to insulin that is corrected by compensatory hyperinsulinaemia. Decreased insulin dissimilation by the diseased tubules does not seem to contribute to this hyperinsulinaemia. Abnormalities in oral glucose tolerance may be attributed to diminished absorption, inefficient pancreatic stimulation or defective mechanisms of pancreatic response to an excessive load. Thus there was no basic difference between the results in bilharziasis associated with pyelonephritis and those reported by other authors, exploring carbohydrate metabolism in other renal diseases. An abnormality of oral glucose tolerance was demonstrated in 9 of 10 patients with pyelonephritis associated with urinary schistosomiasis. This took the form of a delayed peak, high peak or delayed descent of the glucose tolerance curve. The intravenous glucose tolerance curve was normal, however, and the K-value was insignificantly elevated. The fasting insulin level was raised and the response to intravenous glucose stimulation was augmented. These findings indicate an impaired tissue sensitivity to insulin that is corrected by compensatory hyperinsulinaemia. Abnormalities in oral glucose tolerance may be attributed to diminished absorption, inefficient pancreatic stimulation or defective mechanisms of pancreatic response to an excessive load.