Abstract
BackgroundInsulin is the drug of choice in the management of diabetes mellitus (DM). About 76 % of diabetic patients suffer from gastrointestinal (GI) disorders. Therapy of DM with insulin primarily involves lowering of elevated blood glucose levels. Hence, on any organ in addition to insulin's effect, hypoglycaemic effect also prevails. A systematic study exploring the effect of insulin on small intestinal transit in normal laboratory animals is lacking. Hence, in the present study, the possible effect of insulin with or without associated hypoglycaemia on small intestinal transit in normal mice was examined.ResultsInsulin in all the doses tested (2 μ, 2 m and 2 U/kg) elicited a significant acceleration of SIT. The lower doses of insulin (2 μ and 2 m U/kg) produced significant acceleration of SIT and were associated with normal blood glucose levels. However, the highest dose of insulin (2 U/kg) produced an acceleration of SIT that was associated with significant fall in blood glucose levels. Further, the 2 m and 2 U doses of insulin significantly elevated serum insulin and C-peptide levels.ConclusionInsulin at the lowest dose produced an acceleratory effect on SIT that was independent of blood glucose and serum insulin levels in normal mice.
Highlights
Insulin is the drug of choice in the management of diabetes mellitus (DM)
The higher dose (2 U/kg) produced an acceleration of small intestinal transit (SIT) that was associated with a profound fall in blood glucose levels (P < 0.01)
With the higher doses of insulin (2 m and 2 U/kg), the serum insulin levels were significantly elevated (P < 0.01) (Fig 3). These findings indicate that exogenously administered insulin is solely responsible for significant acceleration of SIT, but with the higher doses of insulin elevated endogenous insulin levels produced cannot be ruled out in acceleration of SIT
Summary
About 76 % of diabetic patients suffer from gastrointestinal (GI) disorders. Therapy of DM with insulin primarily involves lowering of elevated blood glucose levels. A systematic study exploring the effect of insulin on small intestinal transit in normal laboratory animals is lacking. In the present study, the possible effect of insulin with or without associated hypoglycaemia on small intestinal transit in normal mice was examined. The diagnosis as well as the progression/remission of DM are usually based on evaluation of biochemical parameters viz., blood glucose, serum insulin and C-peptide levels [2]. Complications involving the enteric neuropathy causes considerable morbidity in patients with long standing insulin-dependent diabetes with poor glucose control and peripheral neuropathy [5,6]. The small intestine (page number not for citation purposes)
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