Impaired sensitivity to insulin (the so called insulin resistance, IR) occurs in a number of genetic and acquired conditions, including obesity, non-insulin dependent diabetes mellitus, polycystic ovary syndrome (PCOS) and metabolic syndrome (MS). In this review we discuss the correlation between IR, the adipose tissue hormones and appetite and body weight regulators. Leptin acts as a major adipostat: it suppresses food intake and activates catabolic pathways associated with increased energy production. It improves the peripheral insulin sensitivity and affects β-cell function. Adiponectin is the only adipocytokine discovered so far that has anti-atherogenic properties. There is a reverse correlation between the serum adiponectin levels and the degree of obesity, IR, impaired glucose tolerance, dyslipidemia and atherosclerosis. Ghrelin stimulates food intake; of all circulating orexigenic hormones ghrelin is the most thoroughly studied. Ghrelin levels are decreased in MS and PCOS patients as this hormone is negatively correlated with body mass. Resistin is a hormone secreted by adipose tissues; a growing body of evidence suggests that it might be implicated in the link between obesity and diabetes. It has been found that the hormone‘s levels are significantly higher in obese people than those in normal body mass people. The recently discovered adipose tissue hormones, vaspin, visfatin, omentin-1 and their effect on IR development, have been increasingly researched.

The essential biological action of vitamin D is regulation of calcium and phosphorus metabolism and preserving bone health. In recent years there have been reports about the extraskeletal actions of vitamin D and its role in the regulation of immune system. Vitamin D supplementation appears to reduce the incidence of cardiovascular diseases, cancer, and infections and be able to reduce all-cause mortality. Deficiency of vitamin D has been found to correlate with the increased incidence of autoimmune diseases, including type 1 diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis. Autoimmune thyroid diseases (AITD), including Graves’ disease, Hashimoto’s thyroiditis are relatively common autoimmune disorders affecting more than 5% of general population. It has been shown that vitamin D receptors (VDR) and 1-alpha hydroxylase are expressed in papillary thyroid cancer and normal thyroid tissue, suggesting local synthesis of 1,25(OH)2D in the thyroid. While VDR gene polymorphism has been found in much research to be associated with AITDs, very few studies have examined the impact of vitamin D deficiency on the incidence of AITDs in humans with conflicting results. This review focuses on the association between vitamin D and autoimmune thyroid diseases and summarizes the results of vitamin D supplementation studies in patients with AITD.

The study was aimed at elucidating the influence of a 3-month treatment with routine therapeutic regimens--oral hormonal contraceptives (OHC) with antiandrogenic activity (a standard combination of ethynil estradiol 35 microg plus cyproterone acetate 2 mg) in combination with insulin sensitizing agents--metformin (Group I) and rosiglitazone (Group II) on adipose tissue hormones and hypothalamic neuropeptide Y (NPY) in women with polycystic ovary syndrome. The study included 66 overweight insulin resistant women with PCOS according to the recent ESHRE-ASRM criteria randomized into 2 age-matched therapeutic groups. Significant decrease of leptin (P < 0.01; P = 0.001, resp.), resistin (P < 0.01; P < 0.01, resp.), tumour necrosis factor alpha (TNF alpha) (P = 0.001; P < 0.001, resp.), and NPY (P < 0.05; P < 0.001, resp.) was observed in both groups after treatment. These findings were in parallel with a significant decrease in the anthropometric parameters of body weight in the metformin group only. No significant changes in hormonal characteristics of the groups were found except for a significant decrease in androstenedione and DHEA-S (P < 0.05) in the metformin group and in 17-OH-progesterone (P < 0.05) in the rosiglitazone group. HDL-cholesterol rose and diastolic blood pressure fell significantly (P < 0.05) in the metformin group. Our data suggest beneficial effects of the treatment on potential cardiovascular risk in insulin resistant PCOS women.

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder connected with insulin resistance (IR), low-grade inflammation, dyslipidemia, and altered adipokine secretion. We evaluated serum levels of leptin, adiponectin, visfatin, resistin, IL-6, and TNF-α in 150 women with PCOS, stratified by IR status (IR, n = 76; non-IR, n = 74), and examined their associations with anthropometric, metabolic, hormonal, inflammatory, and atherogenic parameters. Anthropometric data included body weight, height, BMI, waist circumference, and waist-to-height ratio (WHtR), while IR was assessed using HOMA-IR and the Matsuda index. Serum adipokines were measured using ELISA, and lipid parameters and atherogenic indices—including non-HDL cholesterol, AIP, leptin/adiponectin, and adiponectin/resistin ratios—were calculated. Women with IR had higher levels of leptin, visfatin, resistin, and TNF-α, and lower levels of adiponectin. Leptin correlated positively with weight, WHtR, HOMA-IR, and atherogenic indices. Adiponectin showed the strongest and most consistent associations with anthropometric indices, HOMA-IR, and the Matsuda index. Resistin was linked to IR indices and IL-6, and visfatin correlated negatively with HDL-C and insulin sensitivity. In a multivariate general linear model, WHtR, but not HOMA-IR, remained independently associated with higher leptin levels and with atherogenic indices. These findings suggest that in PCOS, central adiposity rather than IR explains a substantial part of the adverse adipokine and inflammatory profile, thereby contributing to elevated cardiometabolic risk and highlighting the need for targeted treatment strategies.

Adipose tissue secretes a variety of adipokines involved in the regulation of energy metabolism and insulin resistance. Metabolic syndrome corresponds to a clinical condition in which white adipose tissue is characterized by an increased production and secretion of inflammatory molecules which may have local effects on adipose tissue physiology but also systemic effects on other organs. The aim of this study was to assess the expression of leptin, NGF and adiponectin in women with metabolic syndrome compared to healthy controls. Plasma leptin, NGF and adiponectin levels were measured by the ELISA method. Leptin and NGF immunohistochemical expression was analyzed in subcutaneous adipose tissue. The results indicated that in women with metabolic syndrome waist circumference, body mass index, HOMA index, glucose, total cholesterol and triglyceride levels were significantly increased in parallel with over-expressed plasma levels of leptin and NGF and decreased adiponectin. The immunohistochemical expression of leptin and NGF was very strong. In conclusion, this is the first study demonstrating a complex of immunochemical and immunohistochemical expression of the key adipokines including leptin, NGF and adiponectin in women with metabolic syndrome. Locally-produced pro-inflammatory adipokines probably contribute to the ethiopathogenic mechanisms of metabolic syndrome.

Introduction: Adipose tissue is immunologically and hormonally active, and these effects are mediated largely by adipocytokines. Thyroid hormones regulate metabolism and organ function, and Hashimoto’s thyroiditis (HT) is the most common autoimmune disease affecting thyroid function. Aim: To evaluate the levels of the adipocytokines leptin and adiponectin in patients with autoimmune HT, and to perform a comparative intragroup analysis in patients with different stages of gland functional activity, and in a control group. Materials and methods: Ninety-five patients with HT and 21 healthy controls were enrolled in the study. Venous blood was taken without anticoagulants after at least 12 hours of fasting, and serum samples were frozen at −70°C until analysis. Serum levels of leptin and adiponectin were determined by an enzyme-linked immunosorbent assay (ELISA). Results: Serum levels of leptin in HT patients were higher than those in the control group (4.5±5.2 ng/mL vs. 1.9±1.3 ng/mL). The hypothyroid patient’s group showed significantly higher levels of leptin than those of the healthy controls (5.1±5.2 ng/mL vs. 1.9±1.3 ng/mL), (p=0.031). Leptin levels correlated positively with body mass index (r=0.533, p<0.001), triglycerides (r=0.223, p=0.033), and immunoreactive insulin (r=0.488, p<0.001) levels. Serum adiponectin concentrations were higher in euthyroid HT patients than in the other groups, but the difference was not statistically significant (p=0.68). We found a positive correlation between adiponectin and HDL cholesterol levels (r=0.442, p<0.001), and negative with body mass index (r=−0.217, p=0.03), and immunoreactive insulin (r=−0.341, p=0.002). Conclusions: The results of this study suggest that leptin has a stronger effect than adiponectin in Hashimoto’s thyroiditis, which can be used to develop new therapeutic agents that modify its effect in the organism.