Hyperactivation of the hypothalamo-pituitary-adrenocortical axis in streptozotocin-diabetic gerbils (Gerbillus gerbillus).

This study was designed to investigate the HPA-axis impairment in the streptozotocin (STZ)-diabetic gerbils (Gerbillus gerbillus). Twenty-six male gerbils (body weight ~27 g) were divided into 3 groups: vehicle control (n = 10), 2 days of diabetes (n = 09) and 30 days of diabetes (n = 07). The latter 2 groups received an intraperitoneal injection of STZ (150 mg/kg of body weight). At 2 and 30 days of diabetes, streptozotocin-diabetic gerbils underwent a retro-orbital puncture for assessment of biochemical and hormonal parameters. Subsequently the animals were decapitated and the adrenal glands were removed, weighed and processed for light microscopy and stereology. Nondiabetic control gerbils that had been injected with citrate buffer were examined as a comparison. At 2 days of diabetes, STZ gerbils exhibited symptoms that are characteristic of human diabetes type 1. The adrenal gland showed significant increase in weight, associated with a larger cortex layer, hypertrophy of the fasciculate cells and a significant decrease in the nucleocytoplasmic index. These changes were associated with higher plasma ACTH and cortisol concentrations compared to nondiabetic controls. At 30 days postdiabetes, ACTH levels remained elevated, whereas cortisol levels decreased compared to the early stage of diabetes. Histological analysis revealed the existence of a band of connective tissue (collagen) that separates the cortical and medullary zones and is not present in humans or laboratory rodents, which represents a striking change seen throughout the disease. STZ-induced diabetes mellitus in Gerbillus gerbillus resulted in hyperactivation of the HPA axis in the early stages of diabetes mellitus which did not persist into the final stages of the disease, suggesting a possible reduction in adrenocortical sensitivity over time.

High-carbohydrate diet-induced metabolic disorders in Gerbillus tarabuli (a new model of non-alcoholic fatty-liver disease). Protective effects of 20-hydroxyecdysone.

The aim of our study was to reveal the effects of long-term consumption of a high-carbohydrate diet (HCD) on metabolic dysfunctions and histopathological liver alterations in Gerbillus tarabuli, as well as to assess the preventive effects of 20-hydroxyecdysone (20E) in the same animals. Contrary to control diet, HCD induces several metabolic disorders including increased adiposity, dyslipidemia, ectopic fat deposition in the liver, associated with higher levels of plasma AST and ALT. These gerbils showed enhanced oxidative stress with liver damages characteristic of steatohepatitis development. By contrast, adding 20E to HCD resulted in a dose-dependent reduction of all changes induced by HCD. In addition, the hepatoprotective effect of 20E was demonstrated by decreased plasma concentrations of AST, ALT and of hepatic malondialdehyde. Our results suggest that G. tarabuli represents a good model to study diet-induced metabolic disorders and hepatic dysfunctions. Moreover, they demonstrate the efficacy of 20E treatment to counteract the damaging effects of HCD.

Adrenal cortex disorders in a new model of obesity, Gerbillus gerbillus, exposed to a high carbohydrate diet.

Obesity is associated with several endocrine disorders, including hypersensitivity of the hypothalamic-pituitary-adrenal axis. The aim of this study was to investigate the effects of a high carbohydrate diet on structural and ultrastructural features of steroidogenic tissue, as well to evaluate adrenocorticotropic hormone (ACTH), cortisol, and insulin levels in the blood and steroidogenic acute regulatory protein (StAR) expression in the adrenals of gerbils. In electron microscopy, the most pronounced effect of the hypercaloric diet was observed in the zona fasciculata. Plasma levels of ACTH, cortisol, and insulin also showed significant increases. However, no significant change was noted in StAR protein levels. There is evidence that high carbohydrate intake brings about remarkable morphological and functional modifications. This could ultimately lead to mitochondrial alteration and accumulation of lipid droplets, which may lead to inflammation and degeneration of adrenal cells.