Morphogenesis of pancreas under the conditions of glutamate-induced obesity: mechanisms of correction effect of melanin

Abstract

The aim of work was to study the morphogenesis of pancreas in rats with glutamate-induced obesity and to evaluate the effects of melanin under these conditions. We included 45 newborn Wistarmale rats, divided into 3 groups of 15 animals each.1 group – newborns rats of intact group were administered with saline subcutaneously (s.c.) in the volume of 8 µl/g at 2–10th postnatal days. 2group – newborns rats of MSG-group received a solution of MSG (4,0 mg/g of body weight) s.c. at 2–10th postnatal days. 3 group – rats received aqueous solution of melanin in dose 1 mg/kg at volume 2,5 ml/kg per os (p.o.). Melanin was obtained from yeast-like fungi Nadsoniellanigra X1 strain from Ukrainian Antarctic station. Melanin administration was started at the age of 4 weeks just after wean and continued for 3 months intermittently alternating two- week course of introduction with two-week course of break. Within 4 months after birth, rats had a normal diet. Pancreas tissue was fixed in 10 % formalin, dehydrated and imbedded in paraffin wax. Paraffin sections of 5μm were cut and stained with hematoxylin and eosin. As low-grade inflammation is one of the leading mechanisms of pancreas lesion in obesity, the proinflammatory activation of pancreas cells was analyzed by immunohistochemical assessment of CD68 cells, NF-kB and TNF-α expression. The injection of glutamate sodium causes the development of obesity with an increase in the amount of visceral fat, an increase in the number of proinflammatory macrophages in it and an increase in the expression of NF-kB and TNFα. In the pancreas, there is a hyperplasia of the insular apparatus, associated with macrophage infiltration and an increase in the expression of COX-2. The introduction of melanin prevented the morphogenesis of the pancreas in animals from glutamate-induced obesity, leveling the activation of proinflammatory signaling paths.