Research Information System
18th International Microscopy Congress, Prag, Czech Republic, 7 - 12 September 2014, pp.3087
In this study our aim was to investigate the effects of pyridoxine which has neurotrophic
effects and is known to be deficient in diabetes mellitus on pancreatic islet cells of
streptozotocin (STZ)- induced diabetic rats.
Adult female Wistar rats (n=24) each weighing 200-250 g. were used. The first group was the
control group. The second and third groups were injected single dose of streptozotocin (i.p, 50
mg/kg). Second group was not given any treatment. The third group received, 5 mg/kg/day
prydoxine for a period of one month. The pancreatic tissue sections were immunostained with
insulin, glucagon, somatostatin, pdx-1, PCNA and synaptophysin antibodies. Body weight and
blood glucose levels of the animals in all groups were measured. All values were analyzed with
statistical methods.
Blood glucose levels of STZ+Pyridoxine groups, were significantly decreased (p<0,001) when
compared with the untreated STZ group. The number of insulin, pdx1 and PCNA
immunopositive cells within the islet was detected to be higher in the STZ+ Pyridoxine group
than the STZ group (p<0.001). In the treated and untreated STZ diabetic groups number of
glucagon and somatostatin immunopositive cells significantly increased (p<0.001) compared
to the control group. The glucagon and somatostatin cells were centrally localized in the islets
of STZ group, whereas their localisation in the STZ+Pyridoxine group were similar to the
control group. Synaptophysin immuno reactivity was detected in all of the endocrine cells of
islets in all groups.
We concluded that pyridoxine induced beta cell proliferation.This effect might depend on the
neuronal like properties of pancreatic B cells.
1. Tamai H : Nippon Rinsho 57: 2362-2365 ,1999
2. Victor M , Adams RD :Am. J Clin Nutr 4: 346-355 ,1996
3. Nawale RB et al : Indian J. Biochem. Biophys. : 43 (337-44), 2006