Department of Animal Physiology and Biochemistry, Poznan University of Life Sciences, Poznan, Poland.
Int J Exp Pathol. 2014 Apr;95(2):86-94. doi: 10.1111/iep.12073.
Administration of streptozotocin (STZ) and nicotinamide (NA) to adult rats allows for the induction of mild diabetes. However, this experimental model has not been fully characterized. This study was undertaken to determine the metabolic and secretory activity of adipose tissue in rats with STZ-NA-induced diabetes. Experiments were performed using epididymal adipocytes isolated from control and mildly diabetic rats. Lipogenesis, glucose transport as well as glucose and alanine oxidation, lipolysis, anti-lipolysis, cAMP levels and adipokine secretion were compared in cells isolated from the control and diabetic rats. Lipogenesis, glucose transport and oxidation were diminished in the adipocytes of diabetic rats compared with the fat cells of control animals. However, alanine oxidation appeared to be similar in the cells of non-diabetic and diabetic animals. Lipolytic response to low epinephrine concentrations was slightly increased in the adipocytes of diabetic rats; however, at higher concentrations of the hormone, lipolysis was similar in both groups of cells. The epinephrine-induced rise in cAMP levels was higher in the adipocytes of STZ-NA-induced diabetic rats, even in the presence of insulin. Lipolysis stimulated by dibutyryl-cAMP did not significantly differ, whereas anti-lipolytic effects of insulin were mildly decreased in the cells of diabetic rats. Secretion of adiponectin and leptin was substantially diminished in the adipocytes of diabetic rats compared with the cells of control animals. Our studies demonstrated that the balance between lipogenesis and lipolysis in the adipose tissue of rats with mild diabetes induced by STZ and NA is slightly shifted towards reduced lipid accumulation. Simultaneously, adiponectin and leptin secretion is significantly impaired.
链脲佐菌素（STZ）和烟酰胺（NA）联合给药于成年大鼠可诱导轻度糖尿病。然而，这种实验模型尚未得到充分的表征。本研究旨在确定 STZ-NA 诱导的糖尿病大鼠脂肪组织的代谢和分泌活性。使用从对照和轻度糖尿病大鼠分离的附睾脂肪细胞进行实验。比较了从对照和糖尿病大鼠分离的细胞中的脂肪生成、葡萄糖转运以及葡萄糖和丙氨酸氧化、脂肪分解、抗脂肪分解、cAMP 水平和脂肪因子分泌。与对照动物的脂肪细胞相比，糖尿病大鼠的脂肪生成、葡萄糖转运和氧化减少。然而，丙氨酸氧化在非糖尿病和糖尿病动物的细胞中似乎相似。低肾上腺素浓度对糖尿病大鼠脂肪细胞的脂肪分解反应略有增加；然而，在激素的较高浓度下，两组细胞的脂肪分解相似。即使存在胰岛素，STZ-NA 诱导的糖尿病大鼠脂肪细胞中肾上腺素诱导的 cAMP 水平升高更高。二丁酰基-cAMP 刺激的脂肪分解没有显著差异，而胰岛素的抗脂肪分解作用在糖尿病大鼠的细胞中略有降低。与对照动物的细胞相比，糖尿病大鼠脂肪细胞中的脂联素和瘦素分泌显著减少。我们的研究表明，STZ 和 NA 诱导的轻度糖尿病大鼠脂肪组织中脂肪生成和脂肪分解之间的平衡略有向脂质积累减少的方向倾斜。同时，脂联素和瘦素的分泌显著受损。
