Diabetes Journal Impact Factor & Information

Publisher: American Diabetes Association, American Diabetes Association

Journal description

Diabetes publishes original research about the physiology and pathophysiology of diabetes mellitus. Submitted manuscripts can report any aspect of laboratory, animal, or human research. Emphasis is on investigative reports focusing on areas such as the pathogenesis of diabetes and its complications, normal and pathologic pancreatic islet function and intermediary metabolism, pharmacological mechanisms of drug and hormone action, and biochemical and molecular aspects of normal and abnormal biological processes. Studies in the areas of diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus are not published.

Current impact factor: 8.10

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 8.095
2013 Impact Factor 8.474
2012 Impact Factor 7.895
2011 Impact Factor 8.286
2010 Impact Factor 8.889
2009 Impact Factor 8.505
2008 Impact Factor 8.398
2007 Impact Factor 8.261
2006 Impact Factor 7.955
2005 Impact Factor 8.028
2004 Impact Factor 8.848
2003 Impact Factor 8.298
2002 Impact Factor 8.256
2001 Impact Factor 7.7
2000 Impact Factor 7.715
1999 Impact Factor 9.019
1998 Impact Factor 8.459
1997 Impact Factor 8.675
1996 Impact Factor 7.616
1995 Impact Factor 6.248
1994 Impact Factor 6.26
1993 Impact Factor 5.256
1992 Impact Factor 5.861

Impact factor over time

Impact factor

Additional details

5-year impact 8.44
Cited half-life 8.80
Immediacy index 2.49
Eigenfactor 0.09
Article influence 3.04
Website Diabetes website
Other titles Diabetes
ISSN 0012-1797
OCLC 1566563
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Diabetes Association

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's personal website, institutional repository or funding body's repository
    • Post-prints must include the set statement (see copyright assignment information)
    • Must link to publisher version
    • Must be identical to final accepted version
    • Authors may make erratum at any time
    • Publisher's version/PDF cannot be used
    • Publisher last reviewed on 21/04/2015
  • Classification
    ​ blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Concentric left ventricular (LV) remodelling is associated with adverse cardiovascular events and is frequently observed in patients with type 2 diabetes mellitus (T2DM). Despite this, the cause of concentric remodelling in diabetes, per se, is unclear, but may be related to cardiac steatosis and impaired myocardial energetics. Thus, we investigated the relationship amongst myocardial metabolic changes and LV remodelling in T2DM. Forty-six non-hypertensive T2DM patients and twenty matched controls underwent cardiovascular magnetic resonance to assess LV remodelling (LV mass to LV end diastolic volume ratio-LVMVR), function, pre- and post-contrast tissue characterisation using T1 mapping, (1)H-, (31)P-magnetic resonance spectroscopy for myocardial triglyceride content (MTG) and phosphocreatine to ATP ratio (PCr/ATP) respectively. When compared to body mass index and blood pressure matched controls, diabetes was associated with: concentric LV remodelling, higher MTG, impaired myocardial energetics and impaired systolic strain indicating a subtle contractile dysfunction. Importantly, cardiac steatosis independently predicted concentric remodelling and systolic strain. Extracellular volume fraction was unchanged, indicating absence of fibrosis. In conclusion, cardiac steatosis may contribute to LV concentric remodelling and contractile dysfunction in diabetes. As cardiac steatosis is modifiable, strategies aimed at reducing myocardial triglyceride may be beneficial in reversing concentric remodelling and improving contractile function in the diabetic heart.
    Diabetes 10/2015; DOI:10.2337/db15-0627
  • Diabetes 10/2015; 64(10):3353-3354. DOI:10.2337/dbi15-0003
  • Diabetes 10/2015; 64(10):3350-3352. DOI:10.2337/db15-0746
  • Diabetes 10/2015; 64(10):e35-e36. DOI:10.2337/db15-0649
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    ABSTRACT: Class IIa histone deacetylases (HDACs), such as HDAC4, HDAC5, and HDAC7 provide critical mechanisms for regulating glucose homeostasis. Here we report HDAC9, another class IIa HDAC, regulates hepatic gluconeogenesis via deacetylation of a Forkhead box O (FoxO) family transcription factor, FoxO1, together with HDAC3. Specifically, HDAC9 expression can be strongly induced upon hepatitis C virus (HCV) infection. HCV-induced HDAC9 upregulation enhances gluconeogenesis by promoting the expression of gluconeogenic genes, including phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, indicating a major role for HDAC9 in the development of HCV-associated exaggerated gluconeogenic responses. Moreover, HDAC9 expression levels and gluconeogenic activities were elevated in livers from HCV-infected patients and persistent HCV-infected mice, emphasizing the clinical relevance of these results. Our results suggest HDAC9 is involved in glucose metabolism and HCV-induced abnormal glucose homeostasis and type-2 diabetes.
    Diabetes 09/2015; DOI:10.2337/db15-0197
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    ABSTRACT: From 27-29 October 2014, more than 100 people gathered in Chicago, IL, to participate in a research symposium titled "Diabetes and the Microbiome," jointly sponsored by the American Diabetes Association and JDRF. The conference brought together international scholars and trainees from multiple disciplines, including microbiology, bioinformatics, endocrinology, metabolism, and immunology, to share the current understanding of host-microbe interactions and their influences on diabetes and metabolism. Notably, this gathering was the first to assemble specialists with distinct expertise in type 1 diabetes, type 2 diabetes, immunology, and microbiology with the goal of discussing and defining potential pathophysiologies linking the microbiome and diabetes. In addition to reviewing existing evidence in the field, speakers presented their own original research to provide a comprehensive view of the current understanding of the topics under discussion.Presentations and discussions throughout the conference reflected a number of important concepts. The microbiota in any host represent a complex ecosystem with a high degree of interindividual variability. Different microbial communities, comprising bacteria, archaea, viruses, and fungi, occupy separate niches in and on the human body. Individually and collectively, these microbes provide benefits to the host-including nutrient harvest from food and protection against pathogens. They are dynamically regulated by both host genes and the environment, and they critically influence both physiology and lifelong health. The objective of the symposium was to discuss the relationship between the host and the microbiome-the combination of microbiota and their biomolecular environment and ecology-specifically with regard to metabolic and immunological systems and to define the critical research needed to understand and potentially target the microbiome in the prevention and treatment of diabetes. In this report, we present meeting highlights in the following areas: 1) relationships between diabetes and the microbiome, 2) bioinformatic tools, resources, and study design considerations, 3) microbial programming of the immune system, 4) the microbiome and energy balance, 5) interventions, and 6) limitations, unanswered questions, and resource and policy needs.
    Diabetes 09/2015; DOI:10.2337/db15-0597
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    ABSTRACT: IGF2 produced and secreted by adult β cells, functions as an autocrine activator of the β cell IGF1R signaling pathway. Whether this autocrine activity of IGF2 plays a physiological role in β cell and whole body physiology is not known. Here, we studied mice with β cell-specific inactivation of Igf2 (βIGF2KO mice) and assessed β cell mass and function in ageing, pregnancy, and acute induction of insulin resistance. We showed that glucose-stimulated insulin secretion (GSIS) was markedly reduced in old female βIGF2KO mice; glucose tolerance was, however, normal because of increased insulin sensitivity. On high fat diet, both male and female βIGF2KO mice displayed lower GSIS as compared to control mice but reduced β cell mass was observed only in female βIGF2KO mice. During pregnancy, there was no increase in β cell proliferation and mass in βIGF2KO mice. Finally, β cell mass expansion in response to acute induction of insulin resistance was lower in βIGF2KO than in control mice. Thus, the autocrine action of IGF2 regulates adult β cell mass and function to preserve in vivo GSIS in ageing, and to adapt β cell mass in response to metabolic stress, pregnancy hormones, and acutely induced insulin resistance.
    Diabetes 09/2015;
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    ABSTRACT: Protein kinase C (PKC) δ has been shown to be increased in liver in obesity and plays an important role in the development of hepatic insulin resistance in both mice and humans. In the present study, we explored the role of PKCδ in skeletal muscle in the control of insulin sensitivity and glucose metabolism by generating mice in which PKCδ was deleted specifically in muscle using Cre-lox recombination. Deletion of PKCδ in muscle improved insulin signaling in young mice, especially at low insulin doses, however, this did not change glucose tolerance or insulin tolerance tests done with pharmacological levels of insulin. Likewise, in young mice, muscle-specific deletion of PKCδ did not rescue high-fat diet induced insulin resistance or glucose intolerance. However, with an increase in age, PKCδ levels in muscle increased, and by 6- to 7-months of age, muscle-specific deletion of PKCδ improved whole body insulin sensitivity and muscle insulin resistance, and by 15 months of age, improved the age-related decline in whole body glucose tolerance. At 15 months of age, M-PKCδKO mice also exhibited decreased metabolic rate and lower levels of some proteins of the OXPHOS complex suggesting a role for PKCδ in the regulation of mitochondrial mass at older age. These data indicate an important role of PKCδ in the regulation of insulin sensitivity and mitochondrial homeostasis in skeletal muscle with aging. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 08/2015; DOI:10.2337/db14-1891
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    ABSTRACT: Adipokines play important roles in metabolic homeostasis and disease. We have recently identified a novel adipokine Metrnl, also known as Subfatin for its high expression in subcutaneous fat. Here, we demonstrate a pro-differentiation action of Metrnl in white adipocytes. Adipocyte-specific knockout of Metrnl exacerbates insulin resistance induced by high fat diet, while adipocyte-specific transgenic overexpression of Metrnl prevents insulin resistance induced by high fat diet or leptin deletion. Body weight and adipose content are not changed by adipocyte Metrnl. Consistently, no correlation is found between serum Metrnl level and body mass index in humans. Metrnl promotes white adipocyte differentiation, expandability, lipid metabolism and inhibits adipose inflammation to form functional fat, which contributes to its activity against insulin resistance. The insulin sensitization of Metrnl is blocked by PPARγ inhibitors or knockdown. However, Metrnl does not drive white adipose browning. Acute intravenous injection of recombinant Metrnl has no hypoglycemic effect, and one-week intravenous administration of Metrnl is unable to rescue insulin resistance exacerbated by adipocyte Metrnl deficiency. Our results suggest adipocyte Metrnl controls insulin sensitivity at least via its local autocrine/paracrine action through PPARγ pathway. Adipocyte Metrnl is an inherent insulin-sensitizer and may become a therapeutic target for insulin resistance. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 08/2015; DOI:10.2337/db15-0274
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    ABSTRACT: Obesity has been posited as an independent risk factor for diabetic kidney disease (DKD), but establishing causality from observational data is problematic. We aimed to test whether obesity is causally related to DKD using Mendelian randomization, which exploits the random assortment of genes during meiosis. In 6049 subjects with type 1 diabetes, we used a weighted genetic risk score (GRS) comprised of 32 validated body mass index (BMI) loci as an instrument to test the relationship of BMI with macroalbuminuria, end stage renal disease (ESRD), or DKD defined as presence of macroalbuminuria or ESRD. We compared these results with cross-sectional and longitudinal observational associations. Longitudinal analysis demonstrated a U-shaped relationship of BMI with development of macroalbuminuria, ESRD, or DKD over time. Cross-sectional observational analysis showed no association with overall DKD, higher odds of macroalbuminuria (for every 1 kg/m(2) higher BMI, odds ratio [OR] 1.05, 95% CI 1.03-1.07, P<0.001), and lower odds of ESRD (OR 0.95, 95% CI 0.93 - 0.97, P<0.001). Mendelian randomization analysis showed a 1 kg/m(2) higher BMI conferring an increased risk in macroalbuminuria (OR 1.28, 95% CI 1.11-1.45, P=0.001), ESRD (OR 1.43, 95% CI 1.20-1.72, P<0.001), and DKD (OR 1.33, 95% CI 1.17-1.51, P<0.001). Our results provide genetic evidence for a causal link between obesity and DKD in type 1 diabetes. As obesity prevalence rises, this finding predicts an increase in DKD prevalence unless intervened upon. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 08/2015; DOI:10.2337/db15-0254
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    ABSTRACT: Pancreatic ß-cells normally produce adequate insulin to control glucose homeostasis, but in obesity-related diabetes there is a presumed deficit in insulin production and secretory capacity. Here, insulin production was assessed directly in obese diabetic mouse models and found that proinsulin biosynthesis was contrastingly increased, coupled with significant expansion of the RER (without ER-stress) and Golgi apparatus, increased vesicular trafficking, and a depletion of mature ß-granules. As such, ß-cells have a remarkable capacity to produce substantial quantities of insulin in obesity, which then made available for immediate secretion in an effort to meet increased metabolic demand, but this comes at the price of insulin secretory dysfunction. Notwithstanding, it is reversible. Upon exposing isolated pancreatic islets of obese mice to normal glucose concentrations, ß-cells revert back to their typical morphology with restoration of regulated insulin secretion. These data demonstrate an unrealized dynamic adaptive plasticity of pancreatic ß-cells and underscores the rationale for transient 'ß-cell rest' as a treatment strategy for obese diabetes. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 08/2015; DOI:10.2337/db15-0792
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    ABSTRACT: Clinically relevant weight loss is achievable through lifestyle modification, but unintentional weight regain is common. We investigated whether recently discovered genetic variants affect weight loss and/or weight regain during behavioral intervention. Participants at high-risk of (Diabetes Prevention Program [DPP]; N=917/907 intervention/comparison) or with (Look AHEAD; N=2,014/1,892 intervention/comparison) type 2 diabetes were from two parallel arm (lifestyle vs. comparison) randomized controlled trials. The associations of 91 established obesity-predisposing loci with weight loss across 4 years, and with weight regain across years-2-4 after a minimum of 3% weight loss, were tested. Each copy of the minor G allele of MTIF3 rs1885988 was consistently associated with greater weight loss following lifestyle intervention over 4-years across DPP and LA. No such effect was observed across comparison arms, leading to a nominally significant SNP × treatment interaction (P=4.3×10-3). However, this effect was not significant at a study-wise significance level (Bonferroni threshold P<5·8×10-4). Most obesity-predisposing gene variants were not associated with weight loss or regain within the DPP and Look AHEAD trials, directly or via interactions with lifestyle.
    Diabetes 08/2015; DOI:10.2337/db15-0441
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    ABSTRACT: Free fatty acid receptor 2 (FFA2) is expressed on enteroendocrine L-cells that release glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) when activated by short-chain fatty acids (SCFAs). Functionally GLP-1 and PYY inhibit gut transit, increase glucose tolerance and suppress appetite, thus FFA2 has therapeutic potential for type-2 diabetes and obesity. However, FFA2-selective agonists have not been characterised in vivo.Compound 1 (Cpd 1), a potent FFA2 agonist, was tested for its activity on GLP-1 release, modulation of intestinal mucosal ion transport and transit in wild type (WT) and FFA2-/- tissue, and food intake and glucose tolerance in lean and diet-induced obese (DIO) mice.Cpd 1 stimulated GLP-1 secretion in vivo but this effect was only detected with DPPIV inhibition, while mucosal responses were PYY-, not GLP-1-mediated. Gut transit was faster in FFA2-/- mice, while Cpd 1 slowed WT transit, and reduced food intake and bodyweight in DIO mice. Cpd 1 decreased glucose tolerance and suppressed plasma insulin in lean and DIO mice, despite FFA2-/- mice displaying impaired glucose tolerance.These results suggest that FFA2 inhibits intestinal functions and suppresses food intake via PYY pathways, with limited GLP-1 contribution. Thus FFA2 may be an effective therapeutic target for obesity, but not for type-2 diabetes.
    Diabetes 08/2015; DOI:10.2337/db15-0481
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    ABSTRACT: Small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) that reverse protein modification by SUMO are involved in the control of numerous cellular processes, including transcription, cell division, and cancer development. However, the physiological function of SENPs in energy metabolism remains unclear. Here, we investigated the role of SENP2 in fatty acid metabolism in C2C12 myotubes and in vivo. In C2C12 myotubes, treatment with saturated fatty acids, like palmitate, led to nuclear factor-κB-mediated increase in the expression of SENP2. This increase promoted the recruitment of peroxisome proliferator-activated receptor (PPAR)δ and PPARγ, through desumoylation of PPARs, to the promoters of the genes involved in fatty acid oxidation (FAO), such as carnitine-palmitoyl transferase-1 (CPT1b) and long-chain acyl-CoA synthetase 1 (ACSL1). In addition, SENP2 overexpression substantially increased FAO in C2C12 myotubes. Consistent with the cell culture system, muscle-specific SENP2 overexpression led to a marked increase in the mRNA levels of CPT1b and ACSL1 and thereby in FAO in the skeletal muscle, which ultimately alleviated high-fat diet-induced obesity and insulin resistance. Collectively, these data identify SENP2 as an important regulator of fatty acid metabolism in skeletal muscle and further implicate that muscle SENP2 could be a novel therapeutic target for the treatment of obesity-linked metabolic disorders.
    Diabetes 07/2015; 64(7):db150115. DOI:10.2337/db15-0115
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    ABSTRACT: The prevalence of obesity-induced type 2 diabetes (T2D) is increasing worldwide and new treatment strategies are needed. We recently discovered that obesity activates a previously unknown pathway that promotes both excessive hepatic glucose production (HGP) and defective insulin signaling in hepatocytes, leading to exacerbation of hyperglycemia and insulin resistance in obesity. At the hub of this new pathway is a kinase cascade involving calcium/calmodulin-dependent protein kinase II (CaMKII), p38α mitogen-activated protein kinase, and MAPKAPK2/3 (MK2/3). Genetic-based inhibition of these kinases improves metabolism in obese mice. Here, we report that treatment of obese insulin resistant mice with an allosteric MK2/3 inhibitor, compound (cmpd) 28, ameliorates glucose homeostasis by suppressing excessive HGP and enhancing insulin signaling. The metabolic improvement seen with cmpd 28 is additive with the leading T2D drug, metformin, but it is not additive with dominant-negative MK2, suggesting an on-target mechanism of action. Allosteric MK2/3 inhibitors represent a potentially new approach to T2D that is highly mechanism based, has links to human T2D, and is predicted to avoid certain adverse effects seen with current T2D drugs. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 06/2015; DOI:10.2337/db14-1945
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    ABSTRACT: The patophysiology of metabolic syndrome (MS) comprises a complex adipokine mediated cross-talk between visceral adipocytes and peripheral tissue. Dipeptidyl peptidase-4 (DPP4) was recently proposed as a novel adipokine linked to MS. We aimed to assess the relationship between fasting serum DPP4 activity, MS and its components in type 1 diabetic (T1DM) patients. We showed that higher serum DPP4 activity is associated with lower insulin sensitivity and higher MS prevalence in T1DM patients. The potential role of DPP-4 acitivity in the complex pathophysiology of insulin resistance in T1DM needs to be established in future follow-up studies.
    Diabetes;64 (Suppl. 1): A493-A493; 06/2015