Gáspár Róbert, Hajagos-Tóth Judit, Schaffer Annamária, Kothencz Anna, Siska-Szabó Lilla, Ducza Eszter, Csányi Adrienn, Tábi Tamás, Bagaméry Fruzsina, Szökő Éva, Kovács Orsolya, Barna Tamara, Samavati Reza, Mirdamadi Mohsen, Sztojkov-Ivanov Anita, Szűcs Kálmán Ferenc, Vari Sandor G
Department of Pharmacology and Pharmacotherapy, Albert Szent-Györgyi Medical School, University of Szeged, 6720 Szeged, Hungary.
Department of Pharmacodynamics and Biopharmacy, Faculty of Pharmacy, University of Szeged, 6720 Szeged, Hungary.
Life (Basel). 2022 May 26;12(6):794. doi: 10.3390/life12060794.
In obesity, the adipose tissue becomes a very significant endocrine organ producing different factors called adipokines, such as leptin, adiponectin and kisspeptin; however, no data are available about their actions on uterine contraction in obese pregnant rats. Our aim was to study the impact of obesity on pregnant uterine contraction in a rat model.
Obesity was induced by the consumption of a high fat high sucrose diet (HFHSD) for 9 weeks, including pregnancy. Glucose tolerance, sex hormone, cytokine and adipokine levels were measured. Uterine contractions and cervical resistance, as well as their responses to adipokines, were tested along with the expressions of their uterine receptors.
HFHSD increased body weight, and altered glucose tolerance and fat composition. The uterine leptin and kisspeptin pathway affect increased. The levels of proinflammatory cytokines were reduced, while the plasma level of progesterone was increased, resulting in weaker uterine contractions, and improving the uterine relaxing effects of adipokines. HFHSD reduced cervical resistance, but the core effect of adipokines is difficult to determine.
Obesity in pregnant rats reduces uterine contractility and cytokine-induced inflammatory processes, and therefore obese pregnant rat methods are partially applicable for modelling human processes.
在肥胖状态下,脂肪组织成为一个非常重要的内分泌器官,可产生多种被称为脂肪因子的物质,如瘦素、脂联素和 kisspeptin;然而,关于它们对肥胖妊娠大鼠子宫收缩的作用尚无相关数据。我们的目的是在大鼠模型中研究肥胖对妊娠子宫收缩的影响。
通过给予高脂高糖饮食(HFHSD)9周来诱导肥胖,包括妊娠期间。测量葡萄糖耐量、性激素、细胞因子和脂肪因子水平。检测子宫收缩和宫颈阻力,以及它们对脂肪因子的反应,并检测子宫受体的表达。
HFHSD增加了体重,改变了葡萄糖耐量和脂肪组成。子宫瘦素和 kisspeptin 途径的影响增强。促炎细胞因子水平降低,而血浆孕酮水平升高,导致子宫收缩减弱,并增强了脂肪因子对子宫的舒张作用。HFHSD降低了宫颈阻力,但脂肪因子的核心作用难以确定。
妊娠大鼠肥胖会降低子宫收缩力和细胞因子诱导的炎症过程,因此肥胖妊娠大鼠模型部分适用于模拟人类过程。