(14C)Oxalate synthesis from (U-14C)xylitol: in vivo and in vitro studies.
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Animals↗
Biomedical subjects
A M Rofe
Publications and source records attributed to A M Rofe.
Formation of oxalate in pyridoxine or thiamin deficient rats during intravenous xylitol infusions.
Glucose, fructose, sorbitol and xylitol were assessed as precursors of oxalate in normal rats and rats deficient in thiamin or vitamin B-6. Urinary excretions of oxalate, glyoxylate and glycine were increased significantly in vitamin B-6 deficient rats infused with xylitol when compared with all other groups. Using [U-14C]xylitol, oxalate was shown to be derived directly from this polyalcohol in vitamin B-6 deficient rats. These results suggest that vitamin B-6 deficiency may be a factor contributing to oxalate crystal deposition seen in some patients infused with xylitol.
Animals↗
[14C]oxalate synthesis from [U-14C]glyoxylate and [1-14C]glycollate in isolated rat hepatocytes.
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Oxalate excretion during carbohydrate infusions.
Oxalate metabolism was assessed in normal rats and rats deficient in vitamins B-1 and B-6 during intravenous infusions of solutions containing glucose, fructose, sorbitol or xylitol. Urinary excretions of oxalate, glyoxylate and glycine were considerably increased in vitamin B-6 deficient rats infused with xylitol. Significant amounts of 14C-oxalate were excreted only in vitamin B-6 deficient rats infused with U 14C-xylitol. Correction of vitamin B-6 deficiency resulted in a return to normal of urinary oxalate excretion and percentage of U 14C-xylitol excreted as 14C-oxalate. The results suggest that xylitol metabolism produces an increased activity in pathways leading to oxalate formation in vitamin B-6 deficient rats.
Animals↗
Altered insulin response to glucose in weight-losing cancer patients.
Cancer cachexia and the underlying metabolic disturbances are due in part to either altered insulin release and action. Glucose intolerance in cancer patients is frequently observed but the nature of the insulin response is not usually described. The aim of this study was to investigate the insulin response in fasted, weigh-losing cancer patients following an oral glucose load (75 g). All cancer patients (n = 35) showed glucose intolerance. Three types of response were identified; those with an increased insulin: glucose ratio (I:G) at 60 min, (average 12.3, n = 13), those with a normal I:G (average 7.2 n = 7) and those with a decrease I:G (average 4.2, n = 15). Fasting plasma glucose concentrations were normal in all groups prior to the glucose tolerance test. However, patients with the lowest I:G also had the lowest fasting plasma insulin concentrations, the lowest plasma albumin concentrations and the highest plasma triglyceride concentrations. Those patients with an abnormal insulin response (either high or low I:G) had significantly greater weight loss (16% for low I:G group, 13% for the high I:G) compared to the normal responders (8%). Plasma fatty acid concentrations were increased in all cancer patients and decreased appropriately after glucose administration, indicating that lipolysis remained sensitive to the action of insulin. It is concluded that weight loss in cancer is associated with glucose intolerance and an abnormal insulin response, and that this response is indicative of either insulin resistance (high I:G) or decreased pancreatic function (low I:G). These findings suggest a role for insulin replacement therapy in the latter group of patients.
Blood Glucose↗