Fitria Nurul Hidayah, Alfaina Wahyuni, Ana Majdawati
{"title":"Letrozole and HFD_HG on Insulin and GDP","authors":"Fitria Nurul Hidayah, Alfaina Wahyuni, Ana Majdawati","doi":"10.24018/ejbiomed.2023.2.4.77","DOIUrl":null,"url":null,"abstract":"The pathogenesis of Polycystic ovary syndrome (PCOS) involves several mechanisms, that include the disorders of carbohydrate and lipid metabolism, oxidative stress, and insulin resistance. That condition makes PCOS have a great impact on long-term health problems such as cardiovascular disease, atherosclerosis, and diabetes. What is the potential for increased diabetic in a PCOS model mouse? This study aims to determine the potential for diabetes cases in PCOS patients through observations in PCOS model mice. Research method: using Postest Only Control Group Design method. Samples included 24 female, 3 months aged rats Rattus norvegicus strain Wistar and weighing around 100–130 grams. After observing the estrous cycle, 16 rats were randomly selected to make a model PCOS with letrozol induction 1 mg/kg BW/day orally in combination with a high-fat high-fructose diet. The treatments were given for 18, 21, 24 and 27 days. Furthermore, after fasting for 12 hours, fasting sugar levels and insulin levels were measured using the ELISA method. The results were analyzed by One Way Anova test with a significance level of α = 0.05. Data analysis was conducted with the SPSS program version 24.0 for Windows. Results: There was no significant difference in fasting insulin levels between the control group and the PCOS group (p > 0.05), but fasting blood sugar levels increased significantly (p < 0.05). Conclusion: There was an increase in the diabetic potency of PCOS mice-induced by the combination of testosterone propionate and a high-fat, high-fructose diet even when insulin levels are not significantly increased.","PeriodicalId":72970,"journal":{"name":"European journal of biomedical research","volume":"14 8","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of biomedical research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.24018/ejbiomed.2023.2.4.77","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
The pathogenesis of Polycystic ovary syndrome (PCOS) involves several mechanisms, that include the disorders of carbohydrate and lipid metabolism, oxidative stress, and insulin resistance. That condition makes PCOS have a great impact on long-term health problems such as cardiovascular disease, atherosclerosis, and diabetes. What is the potential for increased diabetic in a PCOS model mouse? This study aims to determine the potential for diabetes cases in PCOS patients through observations in PCOS model mice. Research method: using Postest Only Control Group Design method. Samples included 24 female, 3 months aged rats Rattus norvegicus strain Wistar and weighing around 100–130 grams. After observing the estrous cycle, 16 rats were randomly selected to make a model PCOS with letrozol induction 1 mg/kg BW/day orally in combination with a high-fat high-fructose diet. The treatments were given for 18, 21, 24 and 27 days. Furthermore, after fasting for 12 hours, fasting sugar levels and insulin levels were measured using the ELISA method. The results were analyzed by One Way Anova test with a significance level of α = 0.05. Data analysis was conducted with the SPSS program version 24.0 for Windows. Results: There was no significant difference in fasting insulin levels between the control group and the PCOS group (p > 0.05), but fasting blood sugar levels increased significantly (p < 0.05). Conclusion: There was an increase in the diabetic potency of PCOS mice-induced by the combination of testosterone propionate and a high-fat, high-fructose diet even when insulin levels are not significantly increased.