Abnormal zinc metabolism in diabetes mellitus type II

This study included 20 adult patients with type II diabetes mellitus and 10 normal controls. We estimated serum glucose and zinc [Fasting and at 60, 120, 180 minutes after oral ingestion of gelatin capsule containing 25 mg zinc sulfate], serum creatinine, creatinine clearance, urine volume/ 24 hours and its contents of zinc, glucose and protein. We found that all patients had diminished serum zinc concentrations, and all demonstrated hyperzincuria as compared to the control group. Urinary loss was greater when proteinuria was present. Studies of gastrointestinal zinc absorption suggested zinc mal-absorption in patients with type II diabetes mellitus. Glucose metabolism was improved by zinc supplementation. It is concluded that zinc deficiency in our diabetics may be due to malabsorption of zinc, hyperzincuria, or both. We also concluded that glucose metabolism was improved by addition of zinc

Pentoxifylline [RBC deformability modulator] and glucose homeostasis

Oral glucose tolerance test with the estimation of S. glucose S. insulin, and S. C-peptide was carried out in 10 non-insulin dependent patients and 8 healthy control patient before and after the administration of oral dose of 400 mg pentoxifylline twice daily for 2 weeks. The diabetic patients were controlled by glibenclamide. Statistical analysis of the results revealed that pentoxifylline caused increase in the serum glucose which persisted inspite of the simultaneous increased levels of serum insulin and c-peptide all through the curve both in the control and diabetics. There could be two possible explanations for these results either pentoxifylline causes release of other diabetogenic hormones which neutralizes the insulin effect, or pentoxifylline blocks or decreases the post-receptor action of insulin by increasing the level of CAMP intracellularly and hence glucose utilization at cellular level