Turmeric extract alleviates endocrine-metabolic disturbances in letrozole-induced PCOS by increasing adiponectin circulation: A comparison with Metformin

Abstract

One of the most common causes of female infertility is polycystic ovarian syndrome, which affects 6–21% of the population. Regrettably, the currently available treatments are mostly symptomatic and ineffective. As a result, safer options are needed now more than ever. In a letrozole PCOS albino mouse model, the current study compares the therapeutic advantages of Turmeric extract (Curcuma longa) to metformin. Adiponectin is a circulating protein generated by adipocytes that has been linked to metabolic diseases (MDs) in an inverse relationship. The effects of Turmeric Extract (Curcuma Longa) in contrast to Metformin, as well as the involvement of adiponectin in endocrine-metabolic abnormalities in experimentally induced PCOS mice model, were studied in this study. Letrozole (6 mg/kg) was administered orally (p.o) for 21 days to induce PCOS, followed by a dose of Turmeric Extract (Curcuma longa) (175 mg/kg and p.o) and Metformin (150 mg/kg) for 30 days, both with normal saline water (0.9%) as the carrier. The findings revealed that LET-treated mice displayed PCOS-like characteristics, such as higher LH levels, increased body weight growth, and ovarian morphology with numerous cysts, increase in fasting blood glucose, lipid profile, plasma lipid peroxidation (MDA) and IL-6, as well as a decrease in serum Progesterone, Estrogen, FSH, SOD and GSH levels in the ovary. These changes were linked to lower levels of circulating adiponectin and were reversed when treated Turmeric extract. By altering circulating androgen-adiponectin balance, the data implies that Turmeric extract alleviates endocrine-metabolic abnormalities and inflammation-related comorbidities associated with LET-induced PCOS.

Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor

“…Serum androgen levels were elevated in PCOS-affected mice, which was the most consistent hormonal trait. Increased testosterone and LH and reduced estrogen, FSH, and progesterone have also been noted in PCOS-afflicted mice [ 39 , 40 ]. In this investigation, in contrast to levels in PCOS-afflicted mice, CGA decreased serum testosterone, LH, and LH/FSH concentrations.…”

Gallic acid reverses ovarian disturbances in mice with letrozole-induced PCOS via modulating Adipo R1 expression

“…Due to its multidimer forms, adiponectin plays a variety of roles [12] . Nevertheless, its diminished secretion and the accompanying low levels of circulating adiponectin have been linked to metabolic issues including PCOS [13] , [14] . Furthermore, it has been found that visceral adiposity and adipocyte mass, two significant risk factors for metabolic and related disorders, have inverse relationship with the circulating adiponectin [15] , [9] , suggesting increasing visceral adiposity decreases its concentration.…”

“…PCOS has been studied experimentally in rats using a variety of methods, including the injection of DHEA, excess prepubertal androgen, and estradiol valerate [13] . These models all produce PCOS, but none of them are completely convincing or precisely match the symptoms of real PCOS.…”

Therapeutic effects of aqueous extract of bioactive active component of Ageratum conyzoides on the ovarian-uterine and hypophysis-gonadal axis in rat with polycystic ovary syndrome: Histomorphometric evaluation and biochemical assessment

“…Hyperandrogenism is characterized by a hormonal imbalance, chronic menstrual dysfunction (oligo- or anovulation), impaired fertility, hirsutism (excessive body hair growth), acne, obesity, diabetes mellitus, metabolic disturbances (dyslipidemia, hyperinsulinemia, insulin resistance, and type 2 diabetes), increased incidence of endometrial hyperplasia and cancer, and policy [ 3 ]. Polycystic ovary syndrome affects around 6–20% of women of reproductive age, and its incidence is on the rise and is the leading cause of female infertility [ 4 , 5 ]. Polycystic ovary syndrome can disrupt ovulation and can lead to infertility; as a result, it is not surprising that infertility affects 70–80% of women with PCOS [ 6 ].…”

“…Progesterone protects the uterus against estrogen-induced uterine development and proliferation [ 12 ]. The primary cause of glucose metabolic disease is insulin resistance (IR), which is also thought to be a key factor in the development of PCOS, which is strongly linked to concurrent metabolic difficulties [ 3 ].Low insulin sensitivity, often known as IR, is a syndrome that causes compensatory hyperinsulinemia and plays a significant role in the etiology of type 2 diabetes [ 4 ]. Increased levels of testosterone and luteinizing hormone are released as a result of hyperinsulinemia, which disrupts the uptake and utilization of glucose and results in prolonged anovulation [ 9 ].Allopathic medications such as clomiphene citrate, metformin, letrozole, tamoxifen, and troglitazone are now the most well-known treatments for PCOS [ 13 ].…”