Barbu Andreea, Hedlund Gabriella Persdotter, Lind Jenny, Carlsson Carina
Department of Medical Cell Biology, BMC, Husargatan 3, Box 571, Uppsala University, 751 23 Uppsala, Sweden.
Mol Cell Endocrinol. 2009 Feb 27;299(2):163-71. doi: 10.1016/j.mce.2008.11.019. Epub 2008 Nov 25.
In view of the central role of preadipocyte factor-1, adiponectin and leptin in white adipose tissue function, the aim of the present study was to analyze the mRNA expression of these proteins and of the inflammatory markers interleukin-6 and tumor necrosis factor-alpha in visceral and subcutaneous fat pads of rats with different metabolic disorders. We demonstrated highly divergent expression of preadipocyte factor-1, upregulated expression of adiponectin, interleukin-6 and TNF-alpha mRNA in adipose tissues of the diabetic Goto Kakizaki rat compared to the obese Zucker rat. This was correlated to an increased number of large adipocytes and serum levels of adiponectin. Furthermore, in all four strains studied (as above plus Wistar Furth and Zucker Lean), significant heterogeneity was evident in adipokine expression within specific adipose tissues previously defined as belonging to the visceral or subcutaneous fat depots. These results suggest that significantly increased levels of inflammation and redistribution of adipocyte size are mechanisms contributing to the development of type 2 diabetes in the GK rat.
鉴于前脂肪细胞因子-1、脂联素和瘦素在白色脂肪组织功能中的核心作用,本研究的目的是分析这些蛋白质以及炎症标志物白细胞介素-6和肿瘤坏死因子-α在患有不同代谢紊乱的大鼠内脏和皮下脂肪垫中的mRNA表达。我们证明,与肥胖的 Zucker 大鼠相比,糖尿病 Goto Kakizaki 大鼠脂肪组织中前脂肪细胞因子-1的表达高度不同,脂联素、白细胞介素-6和肿瘤坏死因子-α mRNA的表达上调。这与大脂肪细胞数量增加和脂联素血清水平相关。此外,在研究的所有四个品系(上述加上 Wistar Furth 和 Zucker Lean)中,在先前定义为属于内脏或皮下脂肪库的特定脂肪组织内,脂肪因子表达存在明显的异质性。这些结果表明,炎症水平显著升高和脂肪细胞大小重新分布是导致 GK 大鼠发生 2 型糖尿病的机制。