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Bo Zhou, Huixia Li, Jiali Liu, Lin Xu, Qinyue Guo, Hongzhi Sun and Shufang Wu

( Zhou et al . 2013 a , b ). Measurement of blood parameters Peripheral serum was subject to ELISA using standard kits (R&D Systems, Inc., Minneapolis, MN, USA) for progranulin. Morning blood glucose and insulin levels were measured and glucose tolerance

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Gilberto Paz-Filho, Claudio Alberto Mastronardi, Brian J Parker, Ainy Khan, Antonio Inserra, Klaus I Matthaei, Monika Ehrhart-Bornstein, Stefan Bornstein, Ma-Li Wong and Julio Licinio

/metabolite measurements Circulating leptin levels were determined at the end point using ELISA kits in duplicate (R&D systems, Minneapolis, MN, USA). Insulin levels were determined using an ultrasensitive ELISA (Alpco, Salem, NH, USA). Intraperitoneal glucose tolerance

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Yanyan Cao, Yunsheng Li, Jaekyung Kim, Yulin Ren, Klaus Himmeldirk, Yi Liu, Yanrong Qian, Fengming Liu and Xiaozhuo Chen

measurement of plasma insulin. At the end of the study with HFD-induced T2D mice, 6Cl-TGQ-treated mice were subjected to a glucose tolerance test. Glucose was injected into mice at time zero, and blood glucose levels were monitored for about 3.5 h until blood

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Björn Hansson, Sebastian Wasserstrom, Björn Morén, Vipul Periwal, Petter Vikman, Samuel W Cushman, Olga Göransson, Petter Storm and Karin G Stenkula

experimental analyses conducted included all groups. The protocol was repeated three times, generating three independent experiments. Glucose tolerance test and serum analysis Mice fasted overnight (12 h) were injected intraperitoneally (i

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Ting-Ting Zhou, Fei Ma, Xiao-Fan Shi, Xin Xu, Te Du, Xiao-Dan Guo, Gai-Hong Wang, Liang Yu, Vatcharin Rukachaisirikul, Li-Hong Hu, Jing Chen and Xu Shen

demonstrated that DMT administration efficiently decreased fasting blood glucose and hemoglobin A1c (HbA1c) levels and improved glucose tolerance and pyruvate tolerance tests. To our knowledge, DMT might be the first reported small molecule as a Gαq signaling

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Yueting Dong, Zhiye Xu, Ziyi Zhang, Xueyao Yin, Xihua Lin, Hong Li and Fenping Zheng

the same vehicle treatment by i.p. injection. Body weight was recorded once a week, and food intake was monitored every day. In vivo glucose homeostasis assays After 3 weeks of treatment, intraperitoneal glucose tolerance tests (IPGTT) and

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Li Hu, Fengli He, Meifeng Huang, Meihua Peng, Zhiguang Zhou, Feng Liu and Yan-Shan Dai

, Kusminski et al . 2016 , Deng et al . 2017 ). A number of studies have demonstrated that inhibiting macrophage infiltration in white AT can improve glucose tolerance in the context of obese mice ( Osborn & Olefsky 2012 , Aouadi et al . 2013 ). Also

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Karen Oliva, Gillian Barker, Clyde Riley, Mark J Bailey, Michael Permezel, Gregory E Rice and Martha Lappas

(Heidelberg, Australia) and Ethics Committee and informed consent was obtained from all participating subjects. Human placenta was obtained from lean and obese pregnant women with normal glucose tolerance at the time of term Caesarean section before the onset

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J. U. Weaver, G. A. Hitman and P. G. Kopelman


Obesity is likely to be a multifactorial disease with an important genetic component. Animal models of genetic and experimentally induced obesity suggest that glucocorticoid receptor (GR) activity plays a role in the aetiology and maintenance of the obese state. Glucocorticoid activity appears to be essential for the development of hyperinsulinaemia and subsequent fat deposition. In humans, glucocorticoid excess is associated with central fat distribution. We have therefore investigated the restriction fragment length polymorphisms of the human GR gene locus (GRL) and have sought associations of specific alleles with anthropometric measurements and indices of insulin secretion and resistance in obesity.

Fifty-six extremely obese, unrelated, nondiabetic premenopausal British Caucasian females and 43 age-matched, normal weight controls were studied. The obese subjects were characterized by fat distribution (waist to hip ratio), insulin secretion and insulin resistance (fasting insulin (FI)), an index of insulin resistance (HOMA), stimulated insulin secretion during an oral glucose tolerance test and insulin-mediated glucose disposal, steady-state plasma glucose). A BclI polymorphism (fragments of 4·5 and 2·3 kb) demonstrated significant association with indices of glucose metabolism in obesity; those subjects homozygous for the 4·5 kb fragment had elevated FI (Pc=0·012) and HOMA (Pc=0·012) values. The genotypic and allelic frequencies of the GRL BclI polymorphism were otherwise similar in obese and normal weight subjects. We postulate that the GRL BclI polymorphism may directly affect GR gene expression, or be in linkage disequilibrium with a possible mutation within one of three exons of the GR gene, and thereby modulate GR transcriptional activity on target genes involved in glucose and insulin homeostasis.

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R Perfetti, H Hui, K Chamie, S Binder, M Seibert, J McLenithan, K Silver and JD Walston

The Arg64 beta(3)-adrenergic receptor (beta(3)AR) variant is associated with an earlier age of onset of diabetes and lower levels of insulin secretion in humans. The aims of this study were to investigate whether beta(3)AR is expressed by islet cells, if receptor binding affects insulin secretion and, finally, if the beta(3)AR Arg64 variant induces abnormal insulin secretory activity. Human pancreas extracts were subjected to RT-PCR, Western blotting and immunostaining analyses. DNA sequencing and Western blotting demonstrated that the beta(3)AR gene is transcribed and translated in the human pancreas; immunostaining showed that it is expressed by the islets of Langerhans. Cultured rat beta-cells responded to human beta(3)AR agonists in a dose- and time-dependent manner. Transfection of cultured rat beta-cells with the wild-type human beta(3)AR produced an increased baseline and ligand-dependent insulin secretion compared with parental cells. On the other hand, cells transfected with the Arg64 variant of the beta(3)AR secreted less insulin, both spontaneously and after exposure to human beta(3)AR agonists. Furthermore, while transfection with the wild-type beta(3)AR preserved the glucose-dependent secretion of insulin, expression of the variant receptor rendered the host cells significantly less responsive to glucose. In summary, cells express the beta(3)AR, and its activation contributes to the regulation of insulin secretion. These findings may help explain the low levels of insulin secretion in response to an i.v. glucose tolerance test observed in humans carrying the Arg64 polymorphism.