The Relationship among Glycemic, Small Intestinal Transit and Insulinemic States in Normal Mice

Gastrointestinal (GI) complications during diabetes mellitus (DM) are common. Attempts to ascribe changes in the glycemic state to the altered GI (gastrointestinal) motility in experimental models yielded varied results. In the present study the possible cause-effect relationship between the changes in the glycemic, insulinemic states and small intestinal transit (SIT) in normal mice was examined. Hypoglycemia induced by either short or long periods of food deprivation. Short periods was attempted in five groups of animals by depriving food for 0, 6, 12, 18 and 24 h duration. Blood glucose (BG) levels were recorded 10 min before the commencement of various periods and just few min before sacrificing the animals for SIT measurement. Charcoal meal was administered intragastrically after termination of periods for SIT measurement. Long periods of food deprivation was attempted in four groups for 30, 36, 42 or 48 h. Acute hyperglycemia was attempted in four groups by i.v or i.p administration of dextrose (0.4, 1 and 4 g/kg). Charcoal meal was administered 10 min after dextrose administration. Thirteen groups were treated similarly without SIT measurement but one ml of blood was collected for determination of serum insulin levels. A fall in BG levels and attenuation of SIT was associated in 5 groups. The difference in association was minimum in 12 and 6 h groups and maximum in 30 and 48 h groups. Whereas an association between fall in insulin levels and attenuation of SIT was observed in 4 groups. The difference between their association was minimum in 48h group and maximum in 30 h group. An acceleration of SIT was associated with fall in BG levels in the groups of 24 and 42 h. The difference in relationship was minimum in 42 h and maximum in 24 h group. A similar relationship was existed between acceleration of SIT and fall in insulin levels in 24 and 42 h groups. However in 6 h group a mild elevation of insulin level was associated with attenuation of SIT. No association between BG, insulin levels and SIT was observed in 36group. At a lower dose of dextrose administration (0.4 and 1 g/kg) no association of BG with SIT. But, when the dose was increased by 4 kg/kg an inverse relationship has been observed with SIT. Similarly with the lower doses of dextrose no association between insulinemic state and SIT observed. But, when the dose of dextrose increased to 4 g/kg an inverse relationship between serum insulin levels and SIT was observed. It can be concluded from this study that a fall in BG levels or serum insulin levels favours attenuation of SIT from 6-30 h of food deprivation. Normal to moderate glycemic or insulinemic states have no influence on SIT.