Ghorbani A, Varedi M, Hadjzadeh M-Al-R, Omrani G H
Department of Physiology, Faculty of Medicine, Shiraz University of Medical Science, Shiraz, Iran.
Exp Clin Endocrinol Diabetes. 2010 Jul;118(7):442-8. doi: 10.1055/s-0030-1247566. Epub 2010 Mar 2.
Type-1 diabetes (T1D) is a metabolic disorder associated with massive reduction in mass of adipose tissue. Measuring cell diameter, an index of fat metabolism, we determined depot-specific alterations in weight of adipose tissue, fat cell diameter and size heterogeneity and distribution at 5 depots in streptozotocin (STZ)-induced diabetic rats. T1D was induced by a single injection of STZ. Seven days after the injection, fat depots were isolated, weighted, washed and maintained in tissue culture medium. Using a microscope equipped with calibrated micrometer, cell diameter as well as size distribution pattern and heterogeneity of adipocytes were determined in fresh tissue slices of subcutaneous (SC), proximal epididymal (PE), distal epididymal (DE), perirenal (PR) and retroperitoneal (RP) fat depots. The T1D induced marked reductions in fat mass and mean of fat cell diameter at all depots. The most affected depot was the SC. With the exception of PE, adipocytes at all depots showed significant increases in size heterogeneity. The effect of the diabetes on mean fat cell diameter and size heterogeneity was minimal at PE depot. Depots with similar cell size distribution pattern exhibited similar fat mass reduction. However, the DE depot with a unique cell size distribution pattern showed a fat mass reduction similar to that of PE and PR depots. These data indicate that T1D induces a massive fat mass reduction in a reasonably depot-specific manner and that the fat depots close to survival organs are less vulnerable to fat mobilization. Moreover, peculiar disagreement between cell size distribution and heterogeneity as well as the level of fat mass reduction at DE and PE depots suggests that not only cell size and heterogeneity but also local factors may play roles in depot-specific fat mobilization.
1型糖尿病(T1D)是一种与脂肪组织大量减少相关的代谢紊乱疾病。通过测量作为脂肪代谢指标的细胞直径,我们确定了链脲佐菌素(STZ)诱导的糖尿病大鼠5个脂肪储存部位的脂肪组织重量、脂肪细胞直径、大小异质性及分布的特定部位变化。通过单次注射STZ诱导T1D。注射7天后,分离脂肪储存部位,称重、冲洗并置于组织培养基中。使用配备校准测微计的显微镜,在皮下(SC)、附睾近端(PE)、附睾远端(DE)、肾周(PR)和腹膜后(RP)脂肪储存部位的新鲜组织切片中测定细胞直径以及脂肪细胞的大小分布模式和异质性。T1D导致所有脂肪储存部位的脂肪量和脂肪细胞平均直径显著降低。受影响最大的储存部位是SC。除PE外,所有储存部位的脂肪细胞大小异质性均显著增加。糖尿病对PE储存部位的平均脂肪细胞直径和大小异质性影响最小。具有相似细胞大小分布模式的储存部位脂肪量减少相似。然而,具有独特细胞大小分布模式的DE储存部位脂肪量减少与PE和PR储存部位相似。这些数据表明,T1D以合理的特定部位方式诱导大量脂肪量减少,且靠近生存器官的脂肪储存部位对脂肪动员的敏感性较低。此外,DE和PE储存部位细胞大小分布与异质性以及脂肪量减少水平之间存在特殊差异,这表明不仅细胞大小和异质性,而且局部因素可能在特定部位的脂肪动员中起作用。