مجله غدد درون ریز و متابولیسم ایران
سال بیست و سوم شماره 2 (پیاپی 116، خرداد و تیر 1400)

The expression of adiponectin hormone and its receptors in the ovary suggests a regulatory role for this hormone in the female reproductive system. To identify the pathogenic mechanism of polycystic ovary syndrome (PCOS) and explain the effects of prenatal hyperandrogenization, the expression of the adiponectin gene (AdipoQ), and its receptors (R1 and R2) were assessed in the ovaries and granulosa cells (GCs) of PCOS rats.

Five pregnant Wistar rats in the experimental group received 5mg of free testosterone dissolved in 0.5ml of sesame oil and benzyl benzoate on the 20th day of pregnancy, and five mice in the control group received 0.5ml of solvent. AdipoQ, R1, and R2 expression were examined in female offspring ovaries at birth, 10 and 100 days (puberty), and in GCs of adult offspring. Relative gene expression was measured by TaqMan real-time polymerase chain reaction.

The expression of AdipoQ and its receptors in the ovaries of experimental mice at birth did not show a statistically significant difference from the control group. AdipoQ expression in the ovaries of the experimental group showed a decrease ten days after birth (P=0.001), after puberty (P=0.008), and in GCs (P=0.001) compared to the expression level at birth. There was a decreased expression of R1 and R2 at ten days of age compared to birth (P=0.046 and 0.001, respectively). AdipoQ and R2 expression were reduced in 10-day-old ovaries and GCs of adult offspring compared to the control group (P<0.05).

Prenatal hyperandrogenization could dysregulate the reproductive system by affecting AdipoQ, R1, and R2 ovarian expression after birth and puberty and play a role in the pathogenesis of PCOS.

Based on available evidence, exposure of the female fetus to androgens during the prenatal period, by affecting the expression of some genes, can cause polycystic ovary syndrome (PCOS) in adulthood. On the other hand, changes in luteinizing hormone (LH) levels and its receptor are associated with the risk of reproductive disorders, including PCOS. The present study aimed to evaluate the expression of the LH receptor gene in the ovaries of a rat model of PCOS induced by androgen exposure in the prenatal period.

In adult rats with PCOS and controls (eight animals in each group), different phases of the sexual cycle (estrous cycle) were determined using vaginal smears, and the anogenital distance (AGD) was measured using a vernier caliper. Ovarian granulosa cells were isolated, and RNA was extracted. The LH receptor gene expression levels in these cells were determined using the real-time polymerase chain reaction (PCR). Data were analyzed by GraphPad Prism software.

Irregular and longer sexual cycles, an increase in AGD (17.32 17 0.3 vs. 11.73 ± 0.26 mm (P=0.0001)), and a decrease in LH receptor gene expression (42. ± 0.12) 0 vs. 0.88 (0.13 (P=0.02)) were observed in the adult rat model of PCOS compared to controls.

A decrease in LH receptor gene expression in the ovarian granulosa cells may be one of the mechanisms involved in the pathophysiology of PCOS following prenatal exposure of the female fetus to androgens.

Foods with low glycemic index (GI) and high satiety index (SI) have been associated with decreased risk of chronic diseases and obesity. This study investigated the effect of date seed flour (DSF) on the GI, glycemic load (GL), and SI of white bread (WB).

Ten healthy subjects were examined on four different days within 3-6 days intervals to determine GI and GL. The blood sugar level was measured during fasting, and 15, 30, 45, 60, 90, and 120 min after receiving glucose, WB, and breads containing 20% and 40% DSF, and GI and GL were calculated. To determine SI, 20 healthy individuals consumed 240 kcal portions of test breads in separate instants at 3-6 day intervals. The satiety ratings were collected at fasting and every 15 min for over 120 min after food ingestion, and SI was calculated.

The GI of breads containing 20% (52.64) and 40% (49.11) DSF was significantly lower than that of WB (73.9) (p<0.004, p<0.005, respectively). Also, the GL of breads containing 20% (9.45) and 40% (7.32) DSF was lower than that of WB (p<0.001, p<0.001, respectively). The SI of breads containing 20% (200) and 40% (290.79) DSF was significantly greater than that of WB (p<0.001, p<0.001, respectively). Finally, the SI of bread containing 40% DSF (290.79) was greater than that of bread containing 20% DSF (200) (p<0.01).

Replacing part of white wheat flour with DSF significantly reduces the GI and GL and increases the SI of WB.

This study aimed to identify a specific dietary pattern related to insulin resistance and hyperinsulinemia in Tehranian adults.

This cross-sectional study was performed on 1063 men and women ≥25 years of age participating in the third phase of the Tehran Lipid and Glucose Study. The dietary pattern was derived by reduced ranking regression (RRR), using 34 food items as predictors and serum insulin concentration and homeostatic model assessment for insulin resistance (HOMA-IR) as response variables. The relationship between a dietary pattern and odds of hyperinsulinemia and insulin resistance (IR) was investigated, and the odds ratio (OR) and 95% confidence interval (CI) were reported.

The mean, standard deviation of age, and BMI of the participants was 43.0±12.2 years and 27.4±4.8 kg/m2. The derived patterns included higher consumption of processed meat, fish, drinkable yogurt, lemon juice, pickles, leafy vegetables, and lower consumption of starchy vegetables, garlic and onions, dried fruits, nuts, red meat, high-fat dairy, and coffee. After adjustment for potential confounding variables, a higher adherence to this pattern was associated with increased odds of hyperinsulinemia (OR=1.69, 95%CI=1.17-1.23, Ptrend=0.005) and IR (OR=2.97, 95%CI=1.66-5.32, Ptrend <0.001).

In this study, an RRR-derived dietary pattern related to serum insulin and HOMA-IR was associated with a higher odds of hyperinsulinemia and IR.

The research results have shown that a healthy lifestyle can prevent the development of metabolic syndrome. This study aimed to investigate the association of nuts, as one of the components of a healthy diet, with components of metabolic syndrome (MetS) and assess the modifying effect of physical activity (PA) on this association.

In this prospective study, the consumption of nuts by 1452 individuals participating in the Tehran Lipid and Glucose Study (TLGS) was examined using a validated food frequency questionnaire. The Cox regression model was used to determine the association between nuts and the risk of components of MetS. Also, the modifying effect of PA was assessed on this association using Cox regression.

Mean (SE) age and BMI at baseline were 36.5±13.3 and 25.6±4.5, respectively. The median intake of nuts was 18.8 g/per week. After adjustments for confounders, a significant inverse association was found between nuts and the risk of hyperglycemia, hypertension, hyperglycemia, and abdominal obesity. Among participants with moderate and high PA levels, nuts (higher or lower than the median) reduced the risk of component of MetS. This association was not observed in participants with low PA levels.

PA modifies the relationship between nuts intake and the risk of some components of MetS. However, no association was found between nuts intake and incidence of components of MetS at low PA levels.

Restoration of blood flow to the ischemic heart muscle causes infarction and myocyte death. Quercetin can be effective in treating heart disease due to its antioxidant effect, but its use is limited due to its low solubility in water. Quercetin restriction can be removed by embedding it in carrier nanoparticles. The present study was designed to determine the effect of quercetin encapsulated nanoparticles(QEN) with intermittent exercise on the expression of JNK and ERK genes.

Thirty rats were randomly divided into five groups (healthy, myocardial infarction, myocardial infarction and supplement, myocardial infarction and exercise, myocardial infarction and exercise and supplement). Myocardial infarction was performed with isoprenaline in 24 rats by subcutaneous injection. In the supplement groups, supplemental gavage was performed after each training session. Cardiac tissue isolation was performed 48 hours after the last training session. Real-Time PCR measured the relative expression of JNK and ERK genes. Data analysis was performed by one-way analysis of variance at a significant level of 0.05.

The expression of JNK and ERK genes was significantly reduced in the exercise and supplementation group compared to the myocardial infarction group.

Taking QEN with periodic aerobic exercise can reduce the expression of JNK and ERK genes, which reducing the expression of JNK and ERK genes, it can reduce the activation of the JNK and ERK complex and thus reduce cell death through apoptosis and therefore have a protective effect on cardiac myocytes following ischemic injury.