Increased risk of primary ovarian insufficiency by high-fructose diet consumption: a 90-day study in female rats

Mirzaei, Roya; Bidgoli, Sepideh Arbabi; Khosrokhavar, Roya; Shoeibi, Shahram; Ashtiani, Hamidreza Ahmadi

doi:10.1007/s11356-022-22258-8

Cited by 1 publication

(1 citation statement)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In developed countries, and developing countries as well, people highly rely on Western pattern diets, which include proteins (derived from fatty domesticated and processed meats), saturated fats, refined grains, sugar, alcohol, salt, and corn-derived fructose syrup with lower consumption of fruits and vegetables [ 4 ]. Moreover, fructose is utilized commercially as a sweetening alternative (fructose corn syrup) for glucose or sucrose in desserts, sauces, and carbonated beverages [ 5 ]. These unhealthy fast foods, convenience foods, energy-dense snacks, and soft drinks have resulted in serious overweight, obesity problems, diabetes, and various reproductive problems, such as PCOS, infertility, etc.…”

Section: Introductionmentioning

confidence: 99%

High Fat-High Fructose Diet Elicits Hypogonadotropism Culminating in Autophagy-Mediated Defective Differentiation of Ovarian Follicles

Rejani

Navin²,

Mumthaz³

et al. 2022

Cells

View full text Add to dashboard Cite

Pituitary gonadotropins directly govern ovarian functions, which are in turn regulated by the ovarian steroid hormones. The precise interplay of gonadotropins and steroid hormones is critical for follicle growth and differentiation. Furthermore, autophagy regulates ovarian follicle differentiation. However, how the high-fat-high fructose (HFD-HF) diet regulates gonadotropins and facilitates autophagy-mediated follicular differentiation in the ovary is obscure. We fed prepubertal rats (PND 25) an HFD-HF diet until PND 90. The results showed diminished adenohypophyseal GnRHR, PR, and aromatase expression, whereas AR, ERα, PRLR, and inhibin were augmented, resulting in gonadotropins decline. Interestingly, autophagy biomarkers, Beclin-1, ATG5, ATG12, LC3-II, and LAMP1 were reduced but SQSTM1/p62 was augmented in the ovaries of HFD-HF-fed rats, causing autolysosome to aggregation. The diet altered T, E2, P4, PRL, and their receptors status in the ovary, disturbed estrous cyclicity, and delayed vaginal opening. Ovarian histomorphology exhibited numerous cystic and atretic follicles, along with disturbed follicular maturation and ovulation. Moreover, the reduction of FSHR; steroidogenic proteins; receptor proteins AR, Erβ, PR; and signaling proteins Wnt2 and β-catenin was also noticed in the ovary, whereas PRLR, inhibin, and pGSK3β were augmented. In conclusion, exposure to a prepubertal HFD-HF diet leads to hypogonadotropism and the autophagy-mediated defective differentiation of ovarian follicles, abating fertility in adult rats.

show abstract

Section: Introductionmentioning

confidence: 99%