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Open access

Thomas Reinehr, Alberto Sánchez-Guijo, Nina Lass, and Stefan A Wudy

), while obese men demonstrated decreased testosterone levels ( 4 ). Interestingly, obese women with increased androgens and obese men with low testosterone concentrations are more prone to metabolic disturbances such as insulin resistance, type 2 diabetes

Open access

Raymond J Rodgers, Jodie C Avery, Vivienne M Moore, Michael J Davies, Ricardo Azziz, Elisabet Stener-Victorin, Lisa J Moran, Sarah A Robertson, Nigel K Stepto, Robert J Norman, and Helena J Teede

, central adiposity), reproductive dysfunction (infertility, menstrual irregularity, miscarriage, pregnancy complications) and metabolic complications ( 6 , 7 ). Metabolic features include insulin resistance (IR), compensatory hyperinsulinaemia and

Open access

Min Li, Ying Chen, Jingjing Jiang, Yan Lu, Zhiyi Song, Shengjie Zhang, Chao Sun, Hao Ying, Xiaofang Fan, Yuping Song, Jialin Yang, and Lin Zhao

adipokine profile ( 17 , 18 ). In contrast, mice depleted of Nrg4 or ErbB4 developed metabolic disorders as shown by development of obesity, dyslipidemia, hepatic steatosis, hyperglycemia, hyperinsulinemia and insulin resistance ( 14 , 19 ). Considering

Open access

Lilit Egshatyan, Daria Kashtanova, Anna Popenko, Olga Tkacheva, Alexander Tyakht, Dmitry Alexeev, Natalia Karamnova, Elena Kostryukova, Vladislav Babenko, Maria Vakhitova, and Sergey Boytsov

formula: (concentration of fasting blood glucose (mmol/l))×(concentration of fasting blood insulin (mU/l))/22.5. Insulin resistance (IR) was diagnosed if HOMA-IR >2.5 (11) . A 75 g OGTT was performed with blood glucose measurement before glucose intake

Open access

Doron Weinstein, Rive Sarfstein, Zvi Laron, and Haim Werner

are effectively used in clinical settings (2, 4) . The insulin-like growth factor (IGF) system has an important role in the normal growth and development of the prostate gland (5) . In addition to its physiological role, epidemiological, clinical

Open access

Stavroula A Paschou, Nektaria Papadopoulou-Marketou, George P Chrousos, and Christina Kanaka-Gantenbein

information on the pathogenesis of T1DM. We will present genetic, environmental and immunologic factors ( Table 1 ) that eventually destroy β cells of the endocrine pancreas and lead to insulin deficiency. Table 1 Contributing factors in type 1 diabetes

Open access

Ling Hu, Ying Hu, and Ting Li

Objective: The purpose of this study was to explore the prevalence of thyroid nodules (TN) and metabolic syndrome (MS) and to analyze the correlation between TN and the components of MS.

Methods: A total of 1526 subjects were divided into two groups: a TN group and a non-thyroid nodules (NTN) group. The height, weight, blood pressure, fasting blood glucose level, fasting plasma insulin level, serum lipid profile, uric acid level, serum thyroid-stimulating hormone (TSH) level, free triiodothyronine (FT3) level, and free thyroxine (FT4) level of each patient were measured. Insulin resistance (IR) was estimated by homeostasis model assessment of insulin resistance (HOMA-IR). Fatty liver and TN were detected by color Doppler ultrasonography.

Results: (1) The overall prevalence of TN was 39.5%; it was significantly higher in women than in men (P<0.01) and progressively increased with age in both sexes. (2) The overall prevalence of MS was 25.6%; it was significantly higher in men than in women (P<0.01) and progressively increased with age in both sexes. (3) FT3 was significantly lower in the TN group than in the NTN group (P<0.01). (4) Body mass index, triglycerides, and HOMA-IR were higher in the TN group than in the NTN group (P<0.05). (5) The existence of TN was significantly associated with overweight/obesity (OR = 1.03, 95% CI = 1.024 - 1.089), and with insulin resistance (IR) (OR = 1.98, 95% CI = 1.645 - 2.368), after adjusting for age and sex.

Conclusions: The prevalence of thyroid nodules and metabolic syndrome in the Nanchang area increases with age, and overweight/obesity and IR in patients are associated with thyroid nodules.

Open access

Stephen J. Winters, Charles R. Scoggins, Duke Appiah, and Dushan T Ghooray

Low plasma levels of sex hormone binding globulin (SHBG) are a marker for obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes. The transcription factor HNF4α is a major determinant of hepatic SHBG expression and thereby serum SHBG levels, and mediates in part the association of low SHBG with hyperinsulinemia and hepatic steatosis. We analyzed the lipidome in human liver specimens from a cohort of patients who underwent hepatic resection as a treatment for cancer, providing insight into hepatic lipids in those without extreme obesity or the clinical diagnosis of NAFLD or non-alcoholic steatohepatitis. Both steatosis and high HOMA-IR were associated with higher levels of saturated and unsaturated FA, other than arachidonic, with the most dramatic rise in 18:1 oleate, consistent with increased stearoyl-Co A desaturase activity. Individuals with low HOMA-IR had low levels of total hepatic fatty acids while both low and high fatty acid levels characterized the high HOMA-IR group. Both insulin resistance and high levels of hepatic fat were associated with low expression levels of HNF4α and thereby SHBG, but expression of these genes was also low in the absence of these determinants, implying additional regulatory mechanisms that remain to be determined.

Open access

Xiaolei Hu and Fengling Chen

). It was first reported by Berson and coworkers ( 2 ) that clinical hypersensitivity and insulin resistance were associated with circulating insulin antibodies (IAs) in patients receiving exogenous animal insulin therapy. Over the past few decades, with

Open access

Ling Zhou, Ruixue Zhang, Shuangyan Yang, Yaguang Zhang, and Dandan Shi

Background: Our previous study revealed that astragaloside IV (AS-IV) effectively improved gestational diabetes mellitus (GDM) by reducing hepatic gluconeogenesis. Due to the importance of placental oxidative stress, we further explored the protective role of AS-IV on placental oxidative stress in GDM.

Methods: First, non-pregnant mice were orally administrated with AS-IV to evaluate its safety and effect. Then GDM mice were orally administered with AS-IV for 20 days and its effect on the symptoms of GDM, placental oxidative stress, secretions of inflammatory cytokines, as well as toll-like receptor 4 (TLR4)/NF-κB signaling pathway, were evaluated.

Results: AS-IV had no adverse effect on non-pregnant mice. On the other hand, AS-IV significantly attenuated the GDM-induced hyperglycemia, glucose intolerance, insulin resistance, placental oxidative stress, productions of inflammatory cytokines and the activation of TLR4/NF-κB pathway.

Conclusion: AS-IV effectively protected against GDM by alleviating placental oxidative stress and inflammation, in which TLR4/NF-κB might be involved.