Abstract #1002545: Prediction of Gut Microbial Community Structure and Function in Polycystic Ovary Syndrome with High Low-density Lipoprotein Cholesterol

2021 ◽  
Vol 27 (6) ◽  
pp. S135
Author(s):  
Xuping zhu ◽  
Yanyu Li ◽  
yanmin Jiang ◽  
Jisheng Zhang ◽  
Ru Duan ◽  
...  
Author(s):  
Xuping Zhu ◽  
Yanyu Li ◽  
Yanmin Jiang ◽  
Jisheng Zhang ◽  
Ru Duan ◽  
...  

Gut microbiota has been proved to be involved in the occurrence and development of many diseases, such as type 2 diabetes, obesity, coronary heart disease, etcetera. It provides a new idea for the pathogenesis of polycystic ovary syndrome (PCOS). Our study showed that the gut microbial community of PCOS with high low-density lipoprotein cholesterol (LDLC) has a noticeable imbalance. Gut microbiota of PCOS patients was significantly changed compared with CON, and these changes were closely related to LDLC. Gut microbiota may affect the metabolic level of PCOS patients through multiple metabolic pathways, and lipid metabolism disorder may further aggravate the imbalance of gut microbiota. Actinomycetaceae, Enterobacteriaceae and Streptococcaceae had high accuracy in the diagnosis of PCOS and the differentiation of subgroups, suggesting that they may play an important role in the diagnosis and treatment of PCOS in the future. Also, the model we built showed good specificity and sensitivity for distinguishing PCOS from CON (including L_CON and L_PCOS, H_CON and H_PCOS). In conclusion, this is the first report on the gut microbiota of PCOS with high LDLC, suggesting that in the drug development or treatment of PCOS patients, the difference of gut microbiota in PCOS patients with different LDLC levels should be fully considered.


2008 ◽  
Vol 93 (5) ◽  
pp. 1820-1826 ◽  
Author(s):  
Sergio E. Recabarren ◽  
Rosita Smith ◽  
Rafael Rios ◽  
Manuel Maliqueo ◽  
Bárbara Echiburú ◽  
...  

Abstract Context: Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder with strong familial aggregation. It has been demonstrated that parents and brothers of PCOS women exhibit insulin resistance and related metabolic defects. However, metabolic phenotypes in sons of PCOS women have not been described. Objective: Our objective was to assess the metabolic profiles in sons of women with PCOS during different stages of life: early infancy, childhood, and adulthood. Design: Eighty sons of women with PCOS (PCOSS) and 56 sons of control women without hyperandrogenism (CS), matched for age, were studied. In early infancy, glucose and insulin were determined in the basal sample. In children and adults, a 2-h oral glucose tolerance test was performed with measurements of glucose and insulin. Adiponectin, leptin, C-reactive protein, SHBG, and serum lipids were determined in the basal sample during the three periods. Results: During early infancy, PCOSS showed higher weight (P = 0.038) and weight sd score (P = 0.031) than CS. During childhood, weight (P = 0.003), body mass index (BMI) (P < 0.001), BMI sd score (P < 0.001), waist circumference (P = 0.001), total cholesterol (P = 0.007), and low-density lipoprotein cholesterol (P = 0.022) were higher in PCOSS compared with CS, but after adjusting for BMI, these differences were nonsignificant. During adulthood, PCOSS exhibited higher weight (P = 0.022), BMI (P = 0.046), and waist circumference (P = 0.028) than CS. Fasting insulin (P = 0.030), homeostasis model assessment for insulin resistance (P = 0.034), total cholesterol (P = 0.043), low-density lipoprotein cholesterol (P = 0.034), and 2-h insulin (P = 0.006) were also significantly higher and insulin sensitivity index composite significantly lower in PCOSS than in CS (P = 0.003). After adjusting for BMI, only 2-h insulin and insulin sensitivity index composite remained significantly different. Conclusions: This study indicates that sons of PCOS women exhibit higher body weight from early infancy. In addition, insulin resistance became evident as the subjects got older, which may place them at risk for the development of type 2 diabetes and cardiovascular disease.


Sign in / Sign up

Export Citation Format

Share Document