Introduction Type 2 diabetes is characterized by accelerated atherosclerosis ( Hobb 2006 ). Elevated tumour necrosis factor α (TNF) levels and hyperglycaemia are implicated in diabetes-associated endothelial cell dysfunction and may be causal in
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Hongbin Liu, Anthony E Dear, Lotte B Knudsen, and Richard W Simpson
Antonia Hufnagel, Laura Dearden, Denise S Fernandez-Twinn, and Susan E Ozanne
impairments such as T2D after a GDM-complicated pregnancy ( Dickens & Thomas 2019 ). Maternal obesity and GDM are closely intertwined, with both characterised by metabolic derangements such as hyperglycaemia, inflammation, hyperinsulinaemia, hyperleptinaemia
G Üçkaya, P Delagrange, A Chavanieu, G Grassy, M-F Berthault, A Ktorza, E Cerasi, G Leibowitz, and N Kaiser
diabetes with moderate obesity, insulin resistance, marked hyperglycaemia and hyperlipidaemia ( Kalderon et al. 1986 ). Hyperglycaemia in P. obesus is associated with marked depletion of islet insulin content and increased β-cell apoptosis ( Donath et
Alex Rafacho, Henrik Ortsäter, Angel Nadal, and Ivan Quesada
effects, including peripheral insulin resistance (IR) and glucose intolerance as well as overt hyperglycaemia and diabetes. These side effects are observed particularly in susceptible individuals such as pregnant women, obese subjects, IR individuals or
Paul W Caton, Nanda K Nayuni, Julius Kieswich, Noorafza Q Khan, Muhammed M Yaqoob, and Roger Corder
Introduction Prevalence of type 2 diabetes mellitus (T2DM) has increased dramatically over the past four decades. T2DM is characterised by insulin resistance, hyperinsulinaemia and hyperglycaemia. Increased glucose production through abnormally
Yasushi Kirino, Youichi Sato, Takayuki Kamimoto, Kazuyoshi Kawazoe, Kazuo Minakuchi, and Yutaka Nakahori
4 activity in vivo . Considering these clinical findings, it may be complicated to define the correlation of DPP4 activity to the severity of hyperglycaemia because of the diverse clinical background; therefore, experimental diabetic models with
Salvatore P Mangiafico, Shueh H Lim, Sandra Neoh, Helene Massinet, Christos N Joannides, Joseph Proietto, Sofianos Andrikopoulos, and Barbara C Fam
) resulting in inappropriately elevated endogenous glucose production (EGP; Lamont et al . 2003 ), will cause glucose intolerance and fasting hyperglycaemia, as observed in T2D ( Consoli et al . 1989 , Nurjhan et al . 1992 , Perriello et al . 1997
Sofianos Andrikopoulos, Barbara C Fam, Anita Holdsworth, Sherley Visinoni, Zheng Ruan, Maria Stathopoulos, Anne W Thorburn, Christos N Joannides, Michael Cancilla, Lois Balmer, Joseph Proietto, and Grant Morahan
Introduction Type 2 diabetes (T2D) is a complex and progressive metabolic disorder characterised by a chronic elevation of blood glucose levels. Although it is accepted that impaired insulin action is an initiating defect, hyperglycaemia only ensues
Jon G Mabley, Pal Pacher, Kanneganti G K Murthy, William Williams, Garry J Southan, Andrew L Salzman, and Csaba Szabo
spontaneous non-obese diabetic (NOD) mouse model. The MLDS model of diabetes is characterized by a progressive hyperglycaemia and an insulitis similar to that observed in human subjects with recent-onset type I diabetes ( Like & Rossini 1976 , Rossini et al
Stuart A Lanham, Dominique Blache, Richard O C Oreffo, Abigail L Fowden, and Alison J Forhead
sheep, hypoinsulinaemia induced either by pancreas removal or streptozocin treatment is associated with hyperglycaemia and decreases in umbilical glucose uptake (both absolute and relative to fetal body weight), fetal glucose utilization and the fraction
