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Bo Zhu, Yumei Chen, Fang Xu, Xiaolu Shen, Xuanyu Chen, Jieqiang Lv, and Songying Zhang

that reflects their physiological function as proinsulin maturation and insulin secretion, and disruption of ER homeostasis in β cells affect their physiological function and result in excessive amount of insulin in circulation, hyperinsulinemia, which

Open access

Kaisa K Ivaska, Maikki K Heliövaara, Pertti Ebeling, Marco Bucci, Ville Huovinen, H Kalervo Väänänen, Pirjo Nuutila, and Heikki A Koistinen

circulating levels on ucOC and the controversy regarding the optimal assay design for ucOC (28) . It is also unclear whether changes in osteoblast function and bone metabolism can be observed in response to hyperinsulinemia in humans in vivo . Here, we

Open access

Zi-Di Xu, Wei Zhang, Min Liu, Huan-Min Wang, Pei-Pei Hui, Xue-Jun Liang, Jie Yan, Yu-Jun Wu, Yan-Mei Sang, Cheng Zhu, and Gui-Chen Ni

after admission to the hospital. The specific diagnostic criteria are as follows: (1) hyperinsulinemia (plasma insulin >2 µIU/mL); (2) hypolipidemia (plasma free fatty acid <1.5 mmol/L); (3) hypoketonemia (serum β-hydroxybutyric acid <2.0 mmol/L); (4

Open access

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

measured in cells derived from primary PCa tumors (22) . The fact that hyperinsulinemia is a pathological hallmark of type 2 diabetes, along with the structural and functional homology between INSR and IGF1R, prompted us to further investigate the

Open access

Esben Thyssen Vestergaard, Morten B Krag, Morten M Poulsen, Steen B Pedersen, Niels Moller, Jens Otto Lunde Jorgensen, and Niels Jessen

(RBP4) concentrations at baseline and in response to hyperinsulinemia and hyperinsulinemia combined with ghrelin infusions in hypopituitary men. Serum RBP4 levels decreased in response to hyperinsulinemia, whereas ghrelin infusion abrogates the

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Meena Asmar, Ali Asmar, Lene Simonsen, Flemming Dela, Jens Juul Holst, and Jens Bülow

hyperglycemia and hyperinsulinemia increases ATBF and stimulates glucose uptake and triacylglycerol (TAG) deposition in adipose tissue in lean humans ( 7 ). In contrast, in these experiments neither GIP nor hyperinsulinemia per se had any effect on ATBF

Open access

Neil R Chappell, Beth Zhou, Amy K Schutt, William E Gibbons, and Chellakkan S Blesson

glucose intolerance in the lean PCOS group when compared to the controls ( Fig. 2B , control 1891 ± 53.81 mmol/L × 180 min vs lean PCOS 2121 ± 39.56 mmol/L × 180 min, P  < 0.01). The lean PCOS group showed evidence of hyperinsulinemia at the 30 min ( Fig

Open access

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

). However, the mechanism(s) linking low SHBG to these metabolic disorders remains incompletely understood. Early studies established a relationship between hyperinsulinemia and low SHBG ( 14 ). Polymorphisms in the SHBG gene ( 15 ) and experiments using SHBG

Open access

Jana Ernst, Katharina Gert, Frank Bernhard Kraus, Ulrike Elisabeth Rolle-Kampczyk, Martin Wabitsch, Faramarz Dehghani, and Kristina Schaedlich

gain during pregnancy and diabetes (type 1, type 2 or gestational) are among the adverse influences put forward by this hypothesis ( 3 , 4 , 5 ). Obesity and hyperinsulinemia are major causes for female hyperandrogenemia. The thereby elevated

Open access

Anastasia P Athanasoulia-Kaspar, Kathrin H Popp, and Gunter Karl Stalla

altered metabolic profile with hyperinsulinemia, increased body weight and increased prevalence of diabetes mellitus in comparison to healthy individuals and patients with non-functioning pituitary adenomas. Treatment with dopamine agonists in these