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: 8.47

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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 8.61
Cited half-life 8.00
Immediacy index 1.54
Eigenfactor 0.10
Article influence 3.03
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: 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
  • 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: Growing body of evidence suggests that activation of NF-κB signaling pathways is among the inflammatory mechanism responsible for various metabolic disorders. Nevertheless, the regulatory roles of NF-κB inhibition in modulating mitochondrial function of the adipose tissues is not well-established. Noting that mitochondrial dysfunction alter oxidative metabolism in adipose tissues, the present study was to investigate the direct effects of NF-κB inhibitor upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. NF-κB inhibitor ameliorated mitochondrial dysfunction induced by commonly used mitochondrial inhibitor, oligomycin by altering mitochondrial fusion and fi ssion in adipocytes. The level of oxidative DNA damage, protein carbonylation, and lipid peroxidation were improved. Further, reduced lipolysis was observed in treated cells with morphology and quantification of intracellular lipid droplets was reduced. The insulin stimulated glucose uptake activity was restored with the enhancement of insulin signaling activity via increased phosphorylation of IRS1, Akt/PKB and AS160 in the adipocytes with mitochondrial dysfunction co-treated with inhibitor. The accumulation of pro-inflammatory mediators TNF-α and IL-1β was markedly depleted. These findings may therefore provide a novel insight into the roles of inflammatory inhibitor as a potential avenue for developing effective therapeutic intervention of mitochondrial dysfunction in the pathogenesis of insulin resistance and type 2 diabetes.
    Diabetes 06/2015; 64(Supp 1):A713. DOI:10.2337/db15-2815-284
  • [Show abstract] [Hide abstract]
    ABSTRACT: Fear of diabetes and major surgery may prohibit referral of young children severely impacted by pancreatitis for total pancreatectomy and islet autotransplant (TPIAT). We evaluated outcomes in our youngest TPIAT recipients, age 3-8 years at surgery. Medical records were reviewed for 17 children (9 female) age <8 years undergoing TPIAT from 2000-2014. Most (14/17) had genetic pancreatitis. Since 2006, TPIAT recipients were followed prospectively with health questionnaires and scheduled HbA1c and mixed meal tolerance tests (6 mL/kg Boost HP) before surgery, and at regular intervals after. Patients are 0.4- 10 years post TPIAT (median 1.5 years). Data are reported as median (25th, 75th percentile). All had relief of pain, with 16/17 off narcotics at most recent follow up, and 1 patient using rare oxycodone (<6 mos post-surgery). Eleven (65%) discontinued insulin, higher than the observed insulin independence rate of 38% in 415 patients >8 years of age undergoing TPIAT over the same interval (p=0.08). Median post-TPIAT HbA1c was 6.0% (5.6, 6.2%). Fasting glucose decreased from 3 months to 1 year (p=0.09, table 1) and was lower than that seen in older patients at 1 year (n=0.007). Very young children with severe refractory chronic pancreatitis may be good candidates for TPIAT, with high rates of pain relief and insulin independence, and excellent glycemic control in the majority
    Diabetes 06/2015;
  • [Show abstract] [Hide abstract]
    ABSTRACT: This is the third in a series of Perspectives on intracellular signaling pathways coupled to proliferation in pancreatic β-cells. We contrast the large knowledge base in rodent β-cells with the more limited human database. With the increasing incidence of type 1 diabetes and the recognition that type 2 diabetes is also due in part to a deficiency of functioning β-cells, there is great urgency to identify therapeutic approaches to expand human β-cell numbers. Therapeutic approaches might include stem cell differentiation, transdifferentiation, or expansion of cadaver islets or residual endogenous β-cells. In these Perspectives, we focus on β-cell proliferation. Past Perspectives reviewed fundamental cell cycle regulation and its upstream regulation by insulin/IGF signaling via phosphatidylinositol-3 kinase/mammalian target of rapamycin signaling, glucose, glycogen synthase kinase-3 and liver kinase B1, protein kinase Cζ, calcium-calcineurin-nuclear factor of activated T cells, epidermal growth factor/platelet-derived growth factor family members, Wnt/β-catenin, leptin, and estrogen and progesterone. Here, we emphasize Janus kinase/signal transducers and activators of transcription, Ras/Raf/extracellular signal-related kinase, cadherins and integrins, G-protein-coupled receptors, and transforming growth factor β signaling. We hope these three Perspectives will serve to introduce these pathways to new researchers and will encourage additional investigators to focus on understanding how to harness key intracellular signaling pathways for therapeutic human β-cell regeneration for 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 05/2015; 64(6):1872-1885. DOI:10.2337/db14-1843
  • Diabetes 05/2015; DOI:10.2337/db14-0893
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    ABSTRACT: Diffuse congenital hyperinsulinism in infancy (CHI-D) arises from mutations inactivating the KATP channel, however, the phenotype is difficult to explain from electrophysiology alone. Here we have studied wider abnormalities in the β-cell and other pancreatic lineages. Islets were disorganized in CHI-D compared to control. PAX4 and ARX expression was decreased. A tendency to increased NKX2.2 expression was consistent with its detection in two-thirds of CHI-D δ-cell nuclei, similar to the fetal pancreas and implying immature δ-cell function. CHI-D δ-cells also comprised 10% of cells displaying nucleomegaly. Increased proliferation in CHI-D was most elevated in duct (5-11 fold) and acinar (7-47 fold) lineages. Increased β-cell proliferation observed in some cases was offset by an increase in apoptosis; in keeping with no difference in INSULIN expression or surface area stained for insulin between CHI-D and control pancreas. However, nuclear localization of CDK6 and P27 was markedly enhanced in CHI-D β-cells compared to cytoplasmic localization in control cells. These combined data support normal β-cell mass in CHI-D, but with G1/S molecules positioned in favor of cell cycle progression. New molecular abnormalities in δ-cells and marked proliferative increases in other pancreatic lineages indicate CHI-D is not solely a β-cell disorder.
    Diabetes 04/2015; DOI:10.2337/db14-1202
  • Diabetes 04/2015; DOI:10.2337/db14-1240
  • Diabetes 04/2015; DOI:10.2337/db15-0107
  • Source
    Diabetes 04/2015; DOI:10.2337/db14-1943