Laboratory of Experimental Research on Gynecology and Obstetrics, Postgraduate Course on Tocogynecology, Botucatu Medical School, Sao Paulo State University (UNESP), Botucatu, Sao Paulo State, Brazil.
Laboratory of Experimental Research on Gynecology and Obstetrics, Postgraduate Course on Tocogynecology, Botucatu Medical School, Sao Paulo State University (UNESP), Botucatu, Sao Paulo State, Brazil; Laboratory of System Physiology and Reproductive Toxicology, Institute of Biological and Health Sciences, Federal University of Mato Grosso (UFMT), Barra do Garças, Mato Grosso State, Brazil.
Life Sci. 2022 Dec 1;310:121108. doi: 10.1016/j.lfs.2022.121108. Epub 2022 Oct 20.
To evaluate the morphological changes in the pancreatic islet cells of adult female pups born to diabetic rats and fed a high-fat diet.
Female Sprague-Dawley rats were distributed into four experimental groups (n = 10 animals/group): 1) female pups from non-diabetic dams and fed a standard diet (OC/SD), 2) female pups from non-diabetic dams and fed a high-fat (OC/HFD), 3) female pups from diabetic dams and fed a standard diet (OD/SD) and 4) female pups from diabetic dams and fed a high-fat diet (OD/HFD). In adulthood, the rats were submitted to the oral glucose tolerance test and later euthanized to collect the pancreas for the analysis of pancreatic islets.
The OC/HFD and OD/SD groups showed an increased percentage of cells immunostained for insulin and a decreased percentage and intensity of staining for somatostatin. The OD/HFD group showed an increased percentage of cells immunostained for insulin and glucagon and a higher staining intensity for glucagon. There was a progressive increase in blood glucose in the OC/HFD, OD/SD, and OD/HFD groups.
The association between maternal diabetes and/or the administration of high-fat diet-induced changes in the pancreatic hormonal triad of female pups in adulthood. In turn, these changes in the pancreatic islets are not capable of causing decreased blood glucose in the offspring, contributing to the development of glucose intolerance in adulthood.
评估糖尿病大鼠所生雌性幼鼠胰岛细胞的形态变化，并给予高脂肪饮食。
将雌性 Sprague-Dawley 大鼠分为四组实验（每组 n=10 只动物）：1）来自非糖尿病母鼠且喂食标准饮食的雌性幼鼠（OC/SD），2）来自非糖尿病母鼠且喂食高脂肪饮食的雌性幼鼠（OC/HFD），3）来自糖尿病母鼠且喂食标准饮食的雌性幼鼠（OD/SD），4）来自糖尿病母鼠且喂食高脂肪饮食的雌性幼鼠（OD/HFD）。成年后，大鼠接受口服葡萄糖耐量试验，然后处死收集胰腺进行胰岛分析。
OC/HFD 和 OD/SD 组胰岛素免疫染色的细胞百分比增加，生长抑素染色的细胞百分比和强度降低。OD/HFD 组胰岛素和胰高血糖素免疫染色的细胞百分比增加，胰高血糖素染色强度增加。OC/HFD、OD/SD 和 OD/HFD 组的血糖水平逐渐升高。
母体糖尿病和/或高脂肪饮食的联合作用导致成年雌性幼鼠胰岛激素三联体发生变化。反过来，胰岛的这些变化不能导致后代血糖降低，导致成年后葡萄糖耐量受损。
