Polycystic ovary syndrome (PCOS), described as the presence of polycystic ovaries, ovulatory dysfunction, and hyperandrogenism, is one of the most common hormonal disorders in premenopausal women and leads to a decrease in quality of life. The worldwide prevalence of PCOS accounts for 1.6-4 percent among reproductive age, but the estimate increases to approximately 18-20 percent due to the complexity of diagnostic criteria and phenotypes.
Though the Rotterdam consensus has described the PCOS criteria well and has been widely used for diagnosis, the heterogeneous phenotype still cannot be fixed. Clinical signs are not limited to anovulation, polycystic ovarian, and the increasing level of testosterone, but also the increase in insulin resistance and body weight, as well as an alteration of gut microbiota composition. The etiology of PCOS is still unknown. However, Rosenfield and Ehrmann describe that there are many predisposing factors to PCOS, such as genetic and environmental factors. Dietary intake is one of the important environmental factors that cause PCOS. A case-controlled study by Barrea et al. showed that a high-fiber and monounsaturated fat diet can be a supportive therapy to improve insulin resistance and hyperandrogenism in pathogenesis. Additionally, diet is a key factor that can modify the composition and stability of the enteric microbiota, which could eventually contribute to the development of PCOS [12]. This evidence indicates that the diet can indirectly or directly induce PCOS by triggering gut microbiota dysbiosis.
An observational study suggested that sucrose beverages have been positively correlated with the prevalence of PCOS among Brazilians. This finding also showed that a high-sucrose diet induces increased blood glucose, reduces insulin sensitivity, and promotes fat tissue accumulation in vivo. Despite a clear correlation between high-sucrose intake and PCOS, less is known about the effect of a combination of high-sucrose and high-cholic acid (HSCA) dietary intake. Cholic acid, a primary water-insoluble bile acid, is thought to have a link with PCOS. Studies have shown that cholic acid is elevated in PCOS women and there is a positive correlation between hyperandrogenism and conjugated primary bile acid levels. Furthermore, cholic acid levels in the gut may have an association with the composition of the fecal microbiota in individuals with PCOS. The Enterobacteriaceae family is found to be elevated in patients with PCOS and may play an important role in the pathophysiology. Therefore, the objective of the present in vivo study was to evaluate the impact of the HSCA diet on Enterobacteriaceae, insulin sensitivity, testosterone level, and histological parameters in female Rattus novergicus ovaries.
Female Wistar rats were classified into HSCA and normal diet groups for four weeks, each group consists of twenty rats. The rats’ weights were measured both pre-examination and post-examination. Blood samples and fecal samples were collected to measure the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and testosterone levels using ELISA and Enterobacteriaceae isolates grown on MacConkey Agar. The collected ovarian tissues were stained with H&E. HSCA rats demonstrated a reduction in Enterobacteriaceae colonies (median 4.75 × 105 vs. 2.47 × 104/CFU, p < 0.001) and an elevated HOMA-IR (mean 2.94 ± 1.30 vs. 4.92 ± 0.51, p < 0.001), as well as an increase in testosterone level (median 0.65 vs. 3.00 ng/mL, p < 0.001), despite no statistical differences in the change in body weight (mean −2.31 ± 14.42 vs. −3.45 ± 9.32, p = 0.769). In H&E staining, HSCA rats had a reduction in preovulatory follicle count (median 0.50 vs. 0.00, p = 0.005). The HSCA diet caused insulin resistance and high testosterone levels, which contribute to the development of PCOS, and affected folliculogenesis by altering follicular maturation, but had no effect on ovulation.
Author: Widjiati
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