Effect of alloxan on ultrastructural and hormonal changes of the endocrine pancreas with hormonal profiles of adrenal gland and their influence on carbohydrate metabolism in soft-shelled turtles,Lissemys punctata punctataBonnoterre

Abstract

Alloxan action on B-and non-B-cells of the endocrine pancreas, adrenal gland and their influence on carbohydrate metabolism are not clearly understood in chelonians. Earlier findings were inconsistent and inexhaustive. These issues were investigated from cytological, ultrastructural, immunocytochemical (B cells) and hormonal (insulin) standpoints in soft-shelled turtles. Alloxan treatment (200 mg/kg body wt on alternate day for 6 days) significantly increased population of necrotic B-cells (87%) with decrease of healthy B-cell population, cell size and nuclear size, and increase of cell/nucleus (C/N) ratio. Ultrastructurally, B-cells were necrotic with extremely pycnotic nucleus, disorganized hypervacuolated cell cytoplasm, and indistinct, clustered secretory granules. The intensity of reaction of insulin-immunoreactive (insulin-IR) B cells and serum insulin level were drastically decreased. Alloxan also caused ultrastructural changes of A-cells, with hyperchromatic nucleus, clustered secretory granules and abundance of vacuoles in the cytoplasm. Population and size of A -cells were significantly declined without significant changes in necrotic cell population, nuclear size and C/N ratio. Alloxan partially increased necrotic D-cell population with decreased cell size and nuclear size, and increased population of healthy D-cells. Ultrastructurally, large vesicular structures and secretory granules, surrounded by peripheral halo were abundant. Small granule size was reduced with increase of its population and decrease of large granule population. Alloxan increased population of healthy PP-cells with increased cell and nuclear size. Granule size and population were altered in A-, D-and PP-cells after alloxan treatment. Adrenal corticosterone level was decreased with increased levels of epinephrine and norepinephrine. Liver glycogen level was declined with elevated level of serum glucose, but muscle glycogen level was increased with a fall in serum lactate level. Alloxan causes diabetes by inducing B-cell necrosis and also affects non -B cells of the endocrine pancreas. Alloxan also disturbs adrenal hormone production and affects carbohydrate metabolism in turtles.

Diabetogenic effects of streptozotocin on endocrine pancreatic islets, adrenal and carbohydrate profiles in turtles,Lissemys punctata punctata(Bonnoterre) (Reptilia: Chelonia)

“…In our earlier works we have shown that streptozotocin, like alloxan, also has a diabetogenic effect in soft-shelled turtles. Furthermore, streptozotocin, at least in the same dose and duration, is more potent than alloxan in causing diabetogenic effect in Lissemys turtles, because B-cell necrosis followed by depletion of serum insulin level and hyperglycemia were higher in streptozotocin than alloxan recipients in turtles (Sarkar 2008;Sarkar et al 2012). Moreover, recovery of the diabetogenic effect of SZ from necrosis of B-cells was faster in streptozotocin than alloxan recipients, because the regeneration of new B-cells with consequent rise in insulin level and hypoglycemia occurred in shorter time (14 days) in streptozotocin recipients than alloxan in turtles.…”