Garbowska Marta, Łukaszuk Bartłomiej, Mikłosz Agnieszka, Wróblewski Igor, Kurek Krzysztof, Ostrowska Lucyna, Chabowski Adrian, Żendzian-Piotrowska Małgorzata, Zalewska Anna
Department of Hygiene, Epidemiology and Ergonomics, Medical University of Bialystok, Bialystok, Poland.
Department of Physiology, Medical University of Bialystok, Bialystok, Poland.
J Cell Physiol. 2017 Oct;232(10):2766-2775. doi: 10.1002/jcp.25939. Epub 2017 Apr 27.
Diabetes is considered a major public health problem affecting millions of individuals worldwide. Remarkably, scientific reports regarding salivary glands sphingolipid metabolism in diabetes are virtually non-existent. This is odd given the well-established link between the both in other tissues (e.g., skeletal muscles, liver) and the key role of these glands in oral health preservation. The aim of this paper is to examine sphingolipids metabolism in the salivary glands in (pre)diabetes (evoked by high fat diet feeding or streptozotocin). Wistar rats were allocated into three groups: control, HFD-, or STZ-diabetes. The content of major sphingolipid classes in the parotid (PSG) and submandibular (SMSG) glands was assessed via chromatography. Additionally, Western blot analyses were employed for the evaluation of key sphingolipid signaling pathway enzyme levels. No changes in ceramide content in the PSG were found, whereas an increase in ceramide concentration for SMSG of the STZ group was observed. This was accompanied by an elevation in SPT1 level. Probably also sphingomyelin hydrolysis was increased in the SMSG of the STZ-diabetic rats, since we observed a significant drop in the amount of SM. PSG and SMSG respond differently to (pre)diabetes, with clearer pattern presented by the later gland. An activation of sphingomyelin signaling pathway was observed in the course of STZ-diabetes, that is, metabolic condition with rapid onset/progression. Whereas, chronic HFD lead to an inhibition of sphingomyelin signaling pathway in the salivary glands (manifested in an inhibition of ceramide de novo synthesis and accumulation of S1P).
糖尿病被认为是一个影响全球数百万人的主要公共卫生问题。值得注意的是，关于糖尿病患者唾液腺鞘脂代谢的科学报告几乎不存在。鉴于两者在其他组织（如骨骼肌、肝脏）中已确立的联系以及这些腺体在口腔健康维护中的关键作用，这很奇怪。本文的目的是研究（糖尿病前期）糖尿病状态下唾液腺中的鞘脂代谢（由高脂饮食喂养或链脲佐菌素诱发）。将Wistar大鼠分为三组：对照组、高脂饮食组或链脲佐菌素诱导糖尿病组。通过色谱法评估腮腺（PSG）和颌下腺（SMSG）中主要鞘脂类别的含量。此外，采用蛋白质免疫印迹分析来评估关键鞘脂信号通路酶的水平。未发现PSG中神经酰胺含量有变化，而在链脲佐菌素组的SMSG中观察到神经酰胺浓度增加。这伴随着SPT1水平的升高。由于我们观察到SM含量显著下降，可能链脲佐菌素诱导糖尿病大鼠的SMSG中鞘磷脂水解也增加。PSG和SMSG对（糖尿病前期）糖尿病的反应不同，后一种腺体呈现出更清晰的模式。在链脲佐菌素诱导糖尿病过程中观察到鞘磷脂信号通路的激活，即一种发病/进展迅速的代谢状态。而慢性高脂饮食导致唾液腺中鞘磷脂信号通路受到抑制（表现为神经酰胺从头合成受到抑制和S1P积累）。
