牙周炎孕鼠影响成年子代脂肪细胞对胰岛素敏感性的研究

目的　探讨牙周炎孕鼠与子代出生低体重的关系以及是否会引起成年子代脂肪细胞产生胰岛素抵抗。 方法　将12只雌性成年Wistar大鼠分成实验性牙周炎组（PD）和对照组（CN）,每组各6只。牙周炎组造模7 d后,两组大鼠均与健康雄鼠交配。待孕鼠产后,将雄性子代分为牙周炎子代组（PDO）和对照子代组（CNO）,每组18只,分别测新生鼠出生体重和每周体重直至11周。11周后,将所有两组鼠麻醉,分组采血、处死,测血糖、血胰岛素、脂联素、TNF-α、脂肪细胞蛋白激酶B（Akt）丝氨酸磷酸化水平及葡萄糖转运蛋白4（Glut4）的表达水平。 结果　两组新生鼠的出生体重、每周体重和血糖浓度没有统计学差异（P>0.05）,PDO组的血胰岛素、脂联素和TNF-α均高于CNO组（P<0.05）,胰岛素诱导两组蛋白激酶B丝氨酸磷酸化（p-Akt）水平增加（P<0.05）,且胰岛素刺激后PDO组p-Akt水平更低（P<0.05）,PDO组Glut4在质膜的表达水平低于CNO组（P<0.05）。 结论　虽然牙周炎孕鼠的子代出生并无低体重,但是可以引起成年子代脂肪细胞产生胰岛素抵抗。

Periodontal disease in pregnancy rats induced insulin resistance in adipose cell of adult offspring

Objective To explore the relationship between maternal periodontal disease and PLBW and whether the offspring of rats with periodontal disease develop insulin resistance in adulthood.　Methods 12 female Wistar rats were divided into Periodontal disease (PD) and control (CN) groups, with 6 rats in each group. The rats in two groups were mated at the seventh day after induction of Periodontal disease. After delivery, male offspring were divided into Periodontal disease offspring (PDO) and control offspring (CNO), with 18 rats each group. Weight of the newborns was measured from birth to eleventh week. 11 weeks later, all offspring rats were euthanized and the glycemia, insulinemia, adiponectin content, level of TNF-α, Akt serine phosphorylation levels and Glut4 content in the adipose tissue were measured. 　Results　Weight of birth, weekly body weight and glucose content had no difference between CNO and PDO groups (P>0.05). However, the concentrations of insulin, adiponectin and TNF-α were increased in PDO group compared to CNO group. Akt serine phosphorylation levels increased in both groups after insulin stimulation (P<0.05), but PDO group increased less than CNO group(P<0.05). Expression level of Glut4 in the adipose tissue decreased in PDO group compared to CNO group(P<0.05).　Conclusion　There is no relationship between maternal periodontal disease and PLBW, but periodontal disease during pregnancy can induce insulin resistance in adipose cell of adult offspring.