Department of Biology and Physiology of Organisms (LBPO), Nutrition-Metabolism/FSB/USTHB, Algiers, Algeria.
Division of Endocrinology, Department of Internal Medicine, Metabolism and Diabetes, University of Utah School of Medicine, Salt Lake City, Utah.
Int J Exp Pathol. 2018 Aug;99(4):172-179. doi: 10.1111/iep.12284.
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.
本研究旨在探讨链脲佐菌素(STZ)诱导的糖尿病沙土鼠(Gerbillus gerbillus)的 HPA 轴损伤。将 26 只雄性沙土鼠(体重约 27g)分为 3 组: vehicle control(n=10)、2 天糖尿病(n=09)和 30 天糖尿病(n=07)。后 2 组沙土鼠接受腹腔注射 STZ(150mg/kg 体重)。在糖尿病的第 2 天和第 30 天,糖尿病沙土鼠通过眼眶后穿刺术评估生化和激素参数。随后,动物被断头处死,取出肾上腺称重,并进行光镜和体视学检查。注射柠檬酸盐缓冲液的非糖尿病对照沙土鼠作为对照进行检查。在糖尿病的第 2 天,STZ 沙土鼠出现了与人类 1 型糖尿病特征性的症状。肾上腺重量显著增加,与皮质层增大、束状细胞肥大以及核质比显著降低有关。与非糖尿病对照相比,这些变化与较高的血浆 ACTH 和皮质醇浓度有关。在糖尿病后 30 天,ACTH 水平仍然升高,而皮质醇水平与糖尿病早期相比下降。组织学分析显示,存在一条结缔组织(胶原)带,将皮质和髓质分开,而在人类或实验室啮齿动物中不存在,这是整个疾病过程中观察到的一个显著变化。STZ 诱导的沙土鼠糖尿病导致 HPA 轴在糖尿病早期的过度激活,但在疾病的晚期并未持续存在,提示随着时间的推移,肾上腺皮质敏感性可能降低。