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Pabitra B Pal, Himangshu Sonowal, Kirtikar Shukla, Satish K Srivastava and Kota V Ramana

Introduction Hyperglycemia is a significant risk factor as well as a contributor to endothelial dysfunction and resultant cardiovascular complications frequently associated with diabetes. Generally, endothelial cells maintain the balance of

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Shadab Abadpour, Bente Halvorsen, Afaf Sahraoui, Olle Korsgren, Pål Aukrust and Hanne Scholz

Introduction Prolonged and repeated exposure to elevated glucose level, defined as hyperglycemia, contributes to beta cell dysfunction and has been shown to involve in progression of type 1 and type 2 diabetes mellitus (DM) ( Biarnes et al

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Ping Li, Yan Hao, Feng-Hui Pan, Min Zhang, Jian-Qiang Ma and Da-Long Zhu

dramatically increases under certain pathophysiological conditions, such as glucocorticoid or mineralocorticoid excess, hyperglycemia, cell shrinkage, and ischemia ( Lang & Voelkl 2013 ). Various functions of SGK1 have been identified ( Salker et al . 2011

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Stacey N Walters, Jude Luzuriaga, Jeng Yie Chan, Shane T Grey and D Ross Laybutt

Introduction The deleterious effects of chronic hyperglycemia on pancreatic β-cells, a concept termed as glucotoxicity, have been implicated in the alterations in functional β-cell mass in diabetes and with islet transplantation ( Korsgren et al

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X Fang, R Palanivel, X Zhou, Y Liu, A Xu, Y Wang and G Sweeney

AdipoR expression profile in EDL and L6 myoblasts. In soleus, a very low, and barely detectable, AdipoR2 copy number was observed (Table 1 ). Alteration in AdipoR1 and AdipoR2 expression induced by hyperglycemia and

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Jacques-Antoine Haefliger, Françoise Rohner-Jeanrenaud, Dorothée Caille, Anne Charollais, Paolo Meda and Florent Allagnat

prevalence of type 2 diabetes (T2D) is increasing at an alarming rate due to the combination of aging, urbanization, increasing prevalence of obesity, and physical inactivity ( Wild et al . 2004 ). Chronic hyperglycemia and hyperlipidemia severely impact on

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W Becker, R Kluge, T Kantner, K Linnartz, M Korn, G Tschank, L Plum, K Giesen and HG Joost

New Zealand obese (NZO) mice exhibit severe insulin resistance of hepatic glucose metabolism. In order to define its biochemical basis, we studied the differential expression of genes involved in hepatic glucose and lipid metabolism by microarray analysis. NZOxF1 (SJLxNZO) backcross mice were generated in order to obtain populations with heterogeneous metabolism but comparable genetic background. In these backcross mice, groups of controls (normoglycemic/normoinsulinemic), insulin-resistant (normoglycemic/hyperinsulinemic) and diabetic (hyperglycemic/hypoinsulinemic) mice were identified. At 22 weeks, mRNA was isolated from liver, converted to cDNA, and used for screening of two types of cDNA arrays (high-density filter arrays and Affymetrix oligonucleotide microarrays). Differential gene expression was ascertained and assessed by Northern blotting. The data indicate that hyperinsulinemia in the NZO mouse is associated with: (i) increased mRNA levels of enzymes involved in lipid synthesis (fatty acid synthase, malic enzyme, stearoyl-CoA desaturase) or fatty acid oxidation (cytochrome P450 4A14, ketoacyl-CoA thiolase, acyl-CoA oxidase), (ii) induction of the key glycolytic enzyme pyruvate kinase, and (iii) increased mRNA levels of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase. These effects were enhanced by a high-fat diet. In conclusion, the pattern of gene expression in insulin-resistant NZO mice appears to reflect a dissociation of the effects of insulin on genes involved in glucose and lipid metabolism. The data are consistent with a hypothetical scenario in which an insulin-resistant hepatic glucose production produces hyperinsulinemia, and an enhanced insulin- and substrate-driven lipogenesis further aggravates the deleterious insulin resistance of glucose metabolism.

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Afreen Idris Shariff, Sohail Syed, Rebecca A Shelby, Jeremy Force, Jeffrey Melson Clarke, David D’Alessio and Leonor Corsino

-Medarde 2015 ). While theoretically specific and effective, in practice there is some overlap of the targets of these signaling pathways in cancer cells and normal cells raising the potential for adverse effects including hyperglycemia. For example, the insulin

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Yu-Guang Ma, Liang Liang, Yin-Bin Zhang, Bao-Feng Wang, Yun-Gang Bai, Zhi-Jun Dai, Man-Jiang Xie and Zhong-Wei Wang

, hyperglycemia and hypertension are found to coexist frequently and considered to be the two leading risk factors ( Cheung & Li 2012 ). Clinical trials and animal studies have indicated that certain oral hypoglycemic drugs, such as metformin and gliclazide, are

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Suwattanee Kooptiwut, Melkam Kebede, Sakeneh Zraika, Sherley Visinoni, Kathryn Aston-Mourney, Jenny Favaloro, Chris Tikellis, Merlin C Thomas, Josephine M Forbes, Mark E Cooper, Marjorie Dunlop, Joseph Proietto and Sofianos Andrikopoulos

Introduction Reduced glucose-mediated insulin release is a characteristic feature of type 2 diabetes resulting in hyperglycemia ( Porte 1991 ). Furthermore, both in vivo ( Leahy et al. 1987 , Bedoya & Jeanrenaud 1991 ) and in