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Welcome to Diabetologia

Diabetologia publishes original clinical and experimental research within the field of diabetes. We are interested in papers that convey new information or insight into any aspect of the condition, ranging from basic science to clinical applications. These are judged in terms of their scientific quality, novelty, relevance and interest to our broadly based readership.

Angelika Bierhaus 1962–2012

Angelika Bierhaus

Professor Angelika Bierhaus passed away on 15 April 2012 after a long and courageous battle with cancer. Angelika will remain in our memories as an extremely engaged scientist full of passion for her profession.
Angelika served with distinction as an Associate Editor for Diabetologia from January 2008 to December 2011, and was a member of the Advisory Board from January 2012. She hosted the EASD Scientists' Training Course in Heidelberg in 2010 and 2011.
We will miss her very much, and our thoughts are with her family, friends and colleagues. An obituary written by Professor Peter Nawroth will be published in the journal.

Current issue: June 2012

June 2012 cover

Click here to view this month's contents

The cover picture shows a polarised light micrograph of crystals of xylitol, a plant-derived sugar alcohol. Xylitol tastes as sweet as cane sugar, but has one-third fewer kilojoules per gram, and is hence used as a sugar substitute. Recent reports have suggested that xylitol might have favourable metabolic effects. In the present issue of Diabetologia (55: 1808–1812), Kishore et al explore this possibility in a model of acute insulin resistance, induced by raising fatty acid levels in rats. These studies demonstrate that xylitol prevents fat-induced insulin resistance, restoring normal insulin-mediated glucose uptake and glycogen storage in muscle. This suggests that xylitol can improve glucose metabolism and may be beneficial in type 2 diabetes.

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Cover credit: SIDNEY MOULDS/SCIENCE PHOTO LIBRARY

Up front

Juleen Zierath

Competition for publication in Diabetologia is greater than ever, and less than 20% of papers are accepted. Of all the high-quality papers that appear in this month's issue I want to share with you five articles that I find to be of particular interest. These will be featured 'up front' in the print issue and here on our website. Juleen R. Zierath, Editor

Management of hyperglycaemia in type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD)
by S. E. Inzucchi, R. M. Bergenstal, J. B. Buse, M. Diamant, E. Ferrannini, M. Nauck, A. L. Peters, A. Tsapas, R. Wender, D. R. Matthews

Treatment algorithms for type 2 diabetes are necessary but notoriously difficult to produce, and obtaining consensus about details is an almost impossible undertaking. In this issue, representatives of the EASD and ADA present a position statement that is very much different from previous approaches, which—typical of algorithms—were based on specific HbA_1c targets and defined first-line treatment choices as well as alternative choices if these were unsucessful. Instead, the statements presented here are far less algorithmic and prescriptive but truly patient centred, taking into account factors that commonly drive clinical decision-making: patient attitude and expected treatment efforts, risks potentially associated with hypoglycaemia and other adverse events, disease duration, age and life expectancy, comorbidities and vascular complications, available resources and support systems. The scope of this paper ranges from pathophysiology to cardiovascular risk reduction, from the mechanisms of action of all available oral agents to side effects and from lifestyle intervention to short- and long-acting insulins. Given the admitted absence of clinical trials backing every possible scenario, the clinician following the presented concepts must practise the art of clinical medicine, rather than stringently following an algorithm.

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Adipose tissue and fetal programming
by M. E. Symonds, M. Pope, D. Sharkey, H. Budge

Adipose tissue is one of the last fetal organs to appear but has a vital role in ensuring effective adaptation to cold-exposure in the extrauterine environment. This is achieved through the rapid early activation of non-shivering thermogenesis in brown adipose tissue, which gradually declines in later life. Modifications in fetal adipose tissue and its control in response to the maternal nutritional environment could be important modifiable factors in the aetiology of obesity, especially in children. In their review in this issue, Symonds et al consider the impact of maternal metabolism on the growth and development of fetal white and brown fat. This is discussed in conjunction with its contribution to later obesity and diabetes through the differential growth of fat depots in defined anatomical locations. These adaptations may ultimately determine whether brown or white fat characteristics dominate in later life.

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How much does screening bring forward the diagnosis of type 2 diabetes and reduce complications? Twelve year follow-up of the Ely cohort
by M. Rahman, R. K. Simmons, S. H. Hennings, N. J. Wareham, S. J. Griffin

While modelling studies suggest that diabetes screening may be an efficient use of resources, and screening has been advocated by a number of organisations, there are several outstanding uncertainties. One of these is the duration of the 'lead time' by which screening brings forward the diagnosis of diabetes. The length of the lead time is important for policy decisions about whether or not to screen for diabetes as, in general, the benefits of screening will lessen as lead time shortens. In this issue, Rahman et al show that in a population offered screening for diabetes, people were diagnosed on average 3.3 years earlier than individuals clinically diagnosed in an unscreened population. This difference is significantly shorter than previous estimates. Health outcomes were similar in the screened and unscreened groups after 12 years of follow-up, suggesting that earlier diagnosis did not lead to health benefits. Further evidence is needed to justify the introduction of population-based screening. This article is the subject of a commentary in this issue by Sawicki.

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Intrapancreatic delivery of human umbilical cord blood aldehyde dehydrogenase-producing cells promotes islet regeneration
by G. I. Bell, D. M. Putman, J. M. Hughes-Large, D. A. Hess

The availability of donor pancreas tissue limits the use of islet transplantation for diabetes. Therefore, the derivation of transplantable beta cells from an unlimited source or the establishment of novel methods to regenerate damaged islets within the pancreas is highly sought. With the recent establishment of national registries, human umbilical cord blood represents a readily available source of stem and progenitor cells with putative islet-regenerative capacity. However, recruitment of regenerative cells to the pancreas after transplantation is inefficient and limits the exposure of endogenous islets to regenerative stimuli. In this issue, Bell et al demonstrate that umbilical cord blood progenitor cells possess potent islet-regenerative capacity, and that transplantation of these cells directly into the murine pancreas reverses established hyperglycaemia by stimulating cell proliferation and revascularisation within islets. Uncovering the regenerative factors secreted by umbilical cord blood progenitor cells may aid the development of future cellular or drug-based islet-regenerative therapies.

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Carbohydrate response element-binding protein (ChREBP) plays a pivotal role in beta cell glucotoxicity
by N. Poungvarin, J. K. Lee, V. K. Yechoor, M. V. Li, T. Assavapokee, P. P. Suksaranjit, J. J. Thepsonwajja, P. K. Saha, K. Okka, L. Chan

Progressive beta cell failure marks the clinical course of patients with type 2 diabetes. In these individuals, hyperglycaemia is a consequence of impaired insulin secretion and is an inducer of incremental beta cell dysfunction, setting in motion a vicious cycle of ↓insulin→hyperglycaemia→↑beta cell failure→↓insulin→hyperglycaemia that characterises the inexorable progressive nature of type 2 diabetes. The deleterious effects of hyperglycaemia on the beta cell, known as glucotoxicity, encompass multiple defects, including lipid accumulation, increased oxidative stress, impaired insulin transcription/secretion and enhanced beta cell apoptosis. Using in vitro and in vivo observations in mice and human pancreatic tissue samples, in this issue, Poungvarin et al show that the chronic hyperglycaemia-activated transcription factor known as carbohydrate response element-binding protein (ChREBP) mediates the myriad manifestations of glucotoxicity and the progressively worsening beta cell function in diabetes. Some of these effects of ChREBP involve activation of thioredoxin-interacting protein, a direct ChREBP target. These findings highlight the role of ChREBP as a potential drug target for preserving beta cell function in type 2 diabetes.

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Inside this issue

Reviews

Adipose tissue and fetal programming
M. E. Symonds, M. Pope, D. Sharkey and H. Budge

Diabetes and cancer (1): evaluating the temporal relationship between type 2 diabetes and cancer incidence
J. A. Johnson, B. Carstensen, D. Witte, S. L. Bowker and L. Lipscombe, et al

Diabetes and cancer (2): evaluating the impact of diabetes on mortality in patients with cancer
A. G. Renehan, H.-C. Yeh, J. A. Johnson, S. H. Wild and E. A. M. Gale, et al

Clinical Science and Care

Microvascular autoregulation in children and adolescents with type 1 diabetes mellitus
O. Schlager, A. Hammer, A. Willfort-Ehringer, M. Fritsch and B. Rami-Merhar, et al

Fenofibrate-associated changes in renal function and relationship to clinical outcomes among individuals with type 2 diabetes: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) experience
D. E. Bonds, T. E. Craven, J. Buse, J. R. Crouse and R. Cuddihy, et al

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Epidemiology

How much does screening bring forward the diagnosis of type 2 diabetes and reduce complications? Twelve year follow-up of the Ely cohort
M. Rahman, R. K. Simmons, S. H. Hennings, N. J. Wareham and S. J. Griffin

Body adiposity index, body fat content and incidence of type 2 diabetes
M. B. Schulze, B. Thorand, A. Fritsche, H. U. Häring and F. Schick, et al

Low serum 25-hydroxyvitamin D level predicts progression to type 2 diabetes in individuals with prediabetes but not with normal glucose tolerance
A. Deleskog, A. Hilding, K. Brismar, A. Hamsten and S. Efendic, et al

Arm length is associated with type 2 diabetes mellitus in Japanese-Americans
M. M. Smits, E. J. Boyko, K. M. Utzschneider, D. L. Leonetti and M. J. McNeely, et al

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Genetics

Polymorphism of HMGA1 is associated with increased risk of type 2 diabetes among Chinese individuals
Short Communication
L. Liu, H. Ding, H. R. Wang, Y. J. Xu and G. L. Cui, et al

Induced pluripotent stem cells generated from diabetic patients with mitochondrial DNA A3243G mutation
J. Fujikura, K. Nakao, M. Sone, M. Noguchi and E. Mori, et al

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Islet Studies

Involvement of the RNA-binding protein ARE/poly(U)-binding factor 1 (AUF1) in the cytotoxic effects of proinflammatory cytokines on pancreatic beta cells
E. Roggli, S. Gattesco, A. Pautz and R. Regazzi

The voltage-dependent potassium channel subunit Kv2.1 regulates insulin secretion from rodent and human islets independently of its electrical function
X. Q. Dai, J. E. Manning Fox, D. Chikvashvili, M. Casimir and G. Plummer, et al

Lactogens protect rodent and human beta cells against glucolipotoxicity-induced cell death through Janus kinase-2 (JAK2)/signal transducer and activator of transcription-5 (STAT5) signalling
N. Guthalu Kondegowda, A. Mozar, C. Chin, A. Otero and A. Garcia-Ocaña, et al

Aberrant activation of liver X receptors impairs pancreatic beta cell function through upregulation of sterol regulatory element-binding protein 1c in mouse islets and rodent cell lines
Z. X. Meng, Y. Yin, J. H. Lv, M. Sha and Y. Lin, et al

Control of beta cell function and proliferation in mice stimulated by small-molecule glucokinase activator under various conditions
A. Nakamura, Y. Togashi, K. Orime, K. Sato and J. Shirakawa, et al

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Immunology and Transplantation

Intrapancreatic delivery of human umbilical cord blood aldehyde dehydrogenase-producing cells promotes islet regeneration
Short Communication
G. I. Bell, D. M. Putman, J. M. Hughes-Large and D. A. Hess

Innate stimulation of B1a cells enhances the autoreactive IgM repertoire in the NOD mouse: implications for type 1 diabetes
J. Côrte-Real, N. Duarte, L. Tavares and C. Penha-Gonçalves

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Metabolism

Nasal insulin changes peripheral insulin sensitivity simultaneously with altered activity in homeostatic and reward-related human brain regions
M. Heni, S. Kullmann, C. Ketterer, M. Guthoff and K. Linder, et al

Carbohydrate response element-binding protein (ChREBP) plays a pivotal role in beta cell glucotoxicity
N. Poungvarin, J. K. Lee, V. K. Yechoor, M. V. Li and T. Assavapokee, et al

Serine/threonine protein kinase 25 (STK25): a novel negative regulator of lipid and glucose metabolism in rodent and human skeletal muscle
A. Nerstedt, E. Cansby, C. X. Andersson, M. Laakso and A. Stancáková, et al

Xylitol prevents NEFA-induced insulin resistance in rats
Short Communication
P. Kishore, S. Kehlenbrink, M. Hu, K. Zhang and R. Gutierrez-Juarez, et al

Ghrelin contributes to derangements of glucose metabolism induced by rapamycin in mice
G. Xu, Z. Wang, Y. Li, Z. Li and H. Tang, et al

α-Lipoic acid regulates lipid metabolism through induction of sirtuin 1 (SIRT1) and activation of AMP-activated protein kinase
W.-L. Chen, C.-H. Kang, S.-G. Wang and H.-M. Lee

Pentamethylquercetin generates beneficial effects in monosodium glutamate-induced obese mice and C2C12 myotubes by activating AMP-activated protein kinase
J. Z. Shen, L. N. Ma, Y. Han, J. X. Liu and W. Q. Yang, et al

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