Intelectin-1 and Endocrinological Parameters in Women with Polycystic Ovary Syndrome: Effect of Insulin Resistance

Abstract

Objectives:We aimed to evaluate the effect of insulin resistance (IR) on serum In telectin1 and endocrinological hormones levels in obese and nonobese women with and without polycystic ovary syndrome (PCOS) in Basrah, Iraq. Methods: From 124 women volunteers, 60 patients with primary and 64 patients with secondary, while 56 normal ovulatory women were taken as controls. Their fasting in sulin hormone, intelectin1, antiMullerian hormone, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), estradiol (E2) and testosterones (T) were determined by ELISA methods. BMI, glucose and quantitative insulin sensitivity check index as well as IR was determined by the homeostasis model assessment. Results: A significant changes (P<0.05) were seen in the level of homeostasis model assessmentIR, E2 and T. Levels of antiMullerian hormone, LH, LH/FSH ratio and pro lactin were significantly (P<0.01) increased and level of intelectin1 and E2/T ratio were significantly (P<0.01) decreased, while quantitative insulin sensitivity check index level was not significantly different (P>0.05) between the patients (1 o PCOS and 2 o PCOS) and control groups. On the other hand, our data reported that FSH level was significantly (P<0.05) lower in obese and higher in nonobese patients with PCOS as compared to control group. Conclusion: Levels of intelectin1 and endocrinological hormones have significantly associated with body mass index, IR and physical activity in patients and normal groups and the strategies that can modulate levels of these parameters would improve metabolic disarrangements in women with PCOS.

Insulin resistance and specific biomarkers in blood and urine of type 2 diabetic patients with or without nephropathy in Basrah, Iraq

“…In our current study, the serum level of Mg showed a high significant decreasing in T2DM patients with and without DN when compared with healthy subjects. Mg is essential for many enzymes that play a key role in glucose metabolism (Al-Fartosy et al, 2020b). The hypomagnesaemia in T2DM patients with and without DN in our study may be due to poor dietary intake, elevated urinary loss because of hyperglycemia, impaired absorption of Mg, imperfect Mg reabsorption from kidney tubules, osmotic diuresis and loss of plasma protein bound to Mg. Mg diminution is said to decrease the insulin sensitivity, thereby, raising the risk of secondary complications.…”

“…This condition makes the pancreas produces high doses of insulin to endeavour getting the glucose out of blood into cells. So, this leads to decrease in the ability of insulin to adjust and signal changes in the levels of glucose in the blood and perhaps grows IR (Al-Fartosy et al, 2020b). Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was used as a substitute measure of IR in our study.…”

Clinical markers and some trace elements in patients with type-2 diabetic nephropathy : Impact of insulin resistance

“…It plays a key role in glucose metabolism. The hypomagnesaemia in T2DM patients with and without DN in our study may be due to poor dietary intake, elevated urinary loss because of hyperglycemia, impaired absorption of Mg, imperfect Mg reabsorption from kidney tubules, osmotic diuresis and loss of plasma protein bound to Magnesium (21). Magnesium diminution is said to decrease the insulin sensitivity, thereby, raising the risk of secondary complications.…”

“…This condition makes the pancreas produces high doses of insulin to endeavour getting the glucose out of blood into cells. So, this leads to decrease in the ability of insulin to adjust and signal changes in the levels of glucose in the blood and perhaps grows IR (21). HOMA-IR was used as a substitute measure of IR in our study.…”

“…Thereby, perhaps taking a causal function in the forward and pathogenesis of T2DM. Moreover, elevated oxidative stress and glycosylation play a main pathogenic role in diabetic endothelial cell dysfunc-tion in T2DM patients with and without DN (21).…”