Disorders of gastrointestinal motility have been associated with Diabetes mellitus. Hyperglycaemia particularly
has been reported to inhibit gastrointestinal transit time while glibenclamide, a sulphonylurea and insulin, both increased
transit time.
Musa sapientum
has also been reported as an antidiabetic agent but there is dearth of information on the effect
of this plant on gastrointestinal motility. This study was therefore carried out to investigate the effect of methanolic extract
of
Musa sapientum leaves (MEMSL) on Gastrointestinal Transit time (GITT) in male albino rats with and without
hyperglycaemia and to elucidate possible mechanism by which this extract functions. Fifty five albino rats were divided
into 11 groups of five animals each. All animals were fasted for 24hrs before the begining of the experiment. Group 1
served as control; while the remaining groups (2 – 11) were treated with 250mg/kg; 500mg/kg MEMSL; diabetic control;
diabetic treated with 250mg/kg; 500mg/kg MEMSL; diabetic treated with glibenclamide (5mg/kg); normal rats treated
with Nifedipine (50mg/kg); normal rats treated with calcium chloride (CaCl
2) only (10mg/kg); groups 10 and 11 were both
pretreated with CaCl
2 and subsequently treated with 250mg/kg and 500mg/kg MEMSL respectively. All plant extracts
used for treatments were dissolved in normal saline and administered orally using orogastric tube. Charcoal meal was used
as marker in the estimation of GITT. The study showed significant decrease in GITT in the normal rats treated with
250mg/kg and 500mg/kg of extract. However, in the diabetic rats treated with 500mg/kg MEMSL, there was significant
increase in GITT and this is comparable with the gut response to glibenclamide (5mg/kg).
Musa sapientum extract
produced significant decrease in transit time in the calcium chloride pre-treated normal rats and this is comparable to the
effect observed in Nifedipine treated group. The significant reduction in GITT produced by MEMSL in the normal rats
reflects a strong possibility of MEMSL acting as calcium channel antagonist through the voltage gated calcium channel
which may be due to the presence of alkaloids, saponins, cardenolides. There is the possibility of the extract acting as an
inhibitor of potassium channel at higher concentration as observed in glibenclamide treated groups.
