Abstract:
Recent studies have implicated pre-beta and beta lipoproteins (VLDL and LDL) in the etiopathogenesis of complications of diabetes mellitus (DM). In contrast, alpha lipoprotein (HDL) is protective of the beta cells of the pancreas. This study examined the distribution of HDL in the islets of Langerhans of murine models of type 1 diabetic rats (streptozotocin (STZ)-induced DM in Wistar rats) and type 2 models of DM rats (Goto-Kakizaki (GK), non-diabetic Zucker lean (ZL), and Zucker diabetic and fatty (ZDF)). The extent by which HDL co-localizes with insulin or glucagon in the islets of the pancreas was also investigated. Pancreatic tissues of Wistar non-diabetic, diabetic Wistar, GK, ZL, and ZDF rats were processed for immunohistochemistry. Pancreatic samples of GK rats fed with either a low-fat or a high-fat diet were prepared for transmission immune-electron microscopy (TIEM) to establish the cytoplasmic localization of HDL in islet cells. HDL was detected in the core and periphery of pancreatic islets of Wistar non-diabetic and diabetic, GK, ZL, and ZDF rats. The average total of islet cells immune positive for HDL was markedly (<0.05) reduced in GK and ZDF rats in comparison to Wistar controls. The number of islet cells containing HDL was also remarkably (p < 0.05) reduced in Wistar diabetic rats and GK models fed on high-fat food. The co-localization study using immunofluorescence and TIEM techniques showed that HDL is detected alongside insulin within the secretory granules of β-cells. HDL did not co-localize with glucagon. This observation implies that HDL may contribute to the metabolism of insulin.
摘要:
最近的研究表明,前β和β脂蛋白(VLDL和LDL)与糖尿病(DM)并发症的病因有关。相比之下,α脂蛋白(HDL)对胰腺的β细胞具有保护作用。这项研究检查了1型糖尿病大鼠模型(链脲佐菌素(STZ)诱导的Wistar大鼠DM)和2型DM大鼠模型(Goto-Kakizaki(GK),非糖尿病ZuckerLean(ZL),和Zucker糖尿病和脂肪(ZDF))。还研究了HDL与胰岛素或胰高血糖素在胰岛中共同定位的程度。Wistar非糖尿病胰腺组织,糖尿病Wistar,GK,ZL,对ZDF大鼠进行免疫组织化学处理。制备低脂或高脂饮食喂养的GK大鼠的胰腺样品,用于透射免疫电子显微镜(TIEM),以建立HDL在胰岛细胞中的细胞质定位。在Wistar非糖尿病和糖尿病患者的胰岛核心和外周检测到HDL,GK,ZL,和ZDF大鼠。与Wistar对照相比,GK和ZDF大鼠中HDL免疫阳性的胰岛细胞的平均总数显著降低(<0.05)。在Wistar糖尿病大鼠和饲喂高脂肪食物的GK模型中,含有HDL的胰岛细胞数量也显着减少(p<0.05)。使用免疫荧光和TIEM技术的共定位研究表明,在β细胞的分泌颗粒中与胰岛素一起检测到HDL。HDL不与胰高血糖素共定位。这一观察表明HDL可能有助于胰岛素的代谢。