Diabetes (DIABETES)

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
  • Classification
    ​ blue

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Administration of lipids into the upper intestine of rats has been shown to acutely decrease endogenous glucose production in the pre-absorptive state, postulated to act through a gut-brain-liver axis involving accumulation of long-chain fatty acyl CoA, release of cholecystokinin and subsequent neuronal signaling. It remains unknown, however, whether a similar gut-brain-liver axis is operative in humans. Here we infused 20% Intralipid (a synthetic lipid emulsion) or saline intraduodenally for 90 min at 30 ml/h, 4 to 6 weeks apart, in random order, in nine healthy men. Endogenous glucose production was assessed under pancreatic clamp conditions with stable isotope enrichment techniques. Under these experimental conditions, intraduodenal infusion of Intralipid, compared with saline, did not affect plasma glucose concentration or endogenous glucose production throughout the study period. We conclude that Intralipid infusion into the duodenum at this rate does not elicit detectable effects on glucose homeostasis or endogenous glucose production in healthy men, which may reflect important interspecies differences between rodents and humans with respect to the putative gut-brain-liver axis.
    Diabetes 03/2015;
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    ABSTRACT: Vascular endothelial growth factor (VEGF) blockers have been developed for the treatment of proliferative diabetic retinopathy (PDR), the leading cause of visual impairments in the working-age population in the Western world. However, limitations to anti-VEGF therapies may exist because of the local production of others pro-angiogenic factors that may cause resistance to anti-VEGF interventions. Thus, novel therapeutic approaches targeting additional pathways are required. Here, we identified a sulfated derivative of the E. coli polysaccharide K5 [K5-N,OS(H)] as a multi-target molecule highly effective in inhibiting VEGF-driven angiogenic responses in different in vitro, ex vivo and in vivo assays, including a murine model of oxygen-induced retinopathy. Furthermore, K5-N,OS(H) binds a variety of heparin-binding angiogenic factors upregulated in PDR vitreous humor besides VEGF, thus inhibiting their biological activity. Finally, K5-N,OS(H) hampers the angiogenic activity exerted in vitro and in vivo by human vitreous fluid samples collected from PDR patients. Together, the data provide compelling experimental evidence that K5-N,OS(H) represents an anti-angiogenic multi-target molecule with potential implications for the therapy of pathologic neovessel formation in the retina of PDR patients. © 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 02/2015; DOI:10.2337/db14-1378
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    ABSTRACT: Obesity arises from a combination of genetic, environmental, and behavioral factors. However, the processes that regulate white adipose tissue (WAT) expansion at the level of the adipocyte are not well understood. The Hedgehog (HH) pathway plays a conserved role in adipogenesis, inhibiting fat formation in vivo and in vitro, but it has not been shown that mice with reduced HH pathway activity have enhanced adiposity. We report that mice lacking the HH coreceptor BOC displayed age-related overweight and excess WAT. They also displayed alterations in some metabolic parameters, but normal food intake. Furthermore, they had an exacerbated response to a high fat diet, including enhanced weight gain and adipocyte hypertrophy, livers with greater fat accumulation, and elevated expression of genes related to adipogenesis, lipid metabolism, and adipokine production. Cultured Boc(-/-) mouse embryo fibroblasts showed enhanced adipogenesis relative to Boc(+/+) cells, and they expressed reduced levels of HH pathway target genes. Therefore, a loss-of-function mutation in a HH pathway component is associated with WAT accumulation and overweight in mice. Variant alleles of such HH regulators may contribute to WAT accumulation in human individuals with additional genetic or lifestyle-based predisposition to obesity. © 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 01/2015; DOI:10.2337/db14-1017
  • Diabetes 01/2015; DOI:10.2337/db15-0107
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    ABSTRACT: Accumulation evidence links obesity-induced inflammation as an important contributor to the development of insulin resistance which plays a key role in the pathophysiology of obesity-related diseases such as type 2 diabetes mellitus and non- alcoholic fatty liver disease. Cyclooxygenase (COX)-1 and -2 catalyze the first step in prostanoid biosynthesis. Since adult hepatocytes fail to induce COX-2 expression regardless of the pro-inflammatory stimuli used, we have evaluated whether this lack of expression under mild pro-inflammatory conditions might constitute a permissive condition for the onset of insulin resistance. Our results show that constitutive expression of human COX-2 (hCOX-2) in hepatocytes protects against adiposity, inflammation, and hence insulin resistance induced by high fat diet as demonstrated by decreased hepatic steatosis, adiposity, plasmatic and hepatic triglycerides and free fatty acids, increased adiponectin/leptin ratio and decreased levels of pro-inflammatory cytokines together with an enhancement of insulin sensitivity and glucose tolerance. Furthermore, hCOX-2 transgenic mice exhibited increased whole body energy expenditure due in part by induction of thermogenesis and fatty acid oxidation. The analysis of hepatic insulin signaling revealed an increase in insulin receptor-mediated Akt phosphorylation in hCOX-2-Tg. In conclusion, our results point to COX-2 as a potential therapeutic target against obesity-associated metabolic dysfunction.
    Diabetes 11/2014; DOI:10.2337/db14-0979
  • Diabetes 11/2014;
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    ABSTRACT: Besides their role in facilitating lipid absorption, bile acids are increasingly being recognized as signaling molecules that activate cell-signaling receptors. Targeted disruption of sterol 12α- hydroxylase gene (Cyp8b1) results in complete absence of cholic acid (CA) and its derivatives. Here we investigate the impact of Cyp8b1 deletion on glucose homeostasis. Absence of Cyp8b1 results in improved glucose tolerance, insulin sensitivity and β-cell function, mediated by absence of CA in Cyp8b1(-/-) mice. In addition, we show that reduced intestinal fat absorption in the absence of biliary CA leads to increased free fatty acids reaching the ileal L-cells. This correlates with increased secretion of the incretin hormone glucagon like peptide-1 (GLP-1). GLP-1 in turn increases the biosynthesis and secretion of insulin from β-cells, leading to the improved glucose tolerance observed in the Cyp8b1(-/-) mice. Thus, our data elucidate the importance of Cyp8b1 inhibition on regulation of glucose metabolism.
    Diabetes 10/2014; DOI:10.2337/db14-0716
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    ABSTRACT: Hyperglycemia-induced inflammation and apoptosis have important roles in the pathogenesis of diabetic cardiomyopathy. We recently found that a novel curcumin derivative, C66, is able to reduce the high glucose (HG)-induced inflammatory response. This study was designed to investigate the protective effects on diabetic cardiomyopathy and its underlying mechanisms. Pretreatment with C66 significantly reduced HG-induced overexpression of inflammatory cytokines via inactivation of nuclear factor-kappa B in both H9c2 cells and neonatal cardiomyocytes. Furthermore, we showed that the inhibition of Jun NH2-terminal kinase (JNK) phosphorylation contributed to the protection of C66 from inflammation and cell apoptosis, which was validated by the use of SP600125 and dominant-negative JNK. The molecular docking and kinase activity assay confirmed direct binding of C66 to and inhibition of JNK. In mice with type 1 diabetes, the administration of C66 or SP600125 at 5 mg/kg significantly decreased the levels of plasma and cardiac tumor necrosis factor-alpha, accompanied by decreasing cardiac apoptosis, and, finally, improved histological abnormalities, fibrosis, and cardiac dysfunction without affecting hyperglycemia. Thus, this work demonstrated the therapeutic potential of the JNK-targeting compound C66 for the treatment of diabetic cardiomyopathy. Importantly, we indicated a critical role of JNK in diabetic heart injury, and suggested that JNK inhibition may be a feasible strategy for treating diabetic cardiomyopathy.
    Diabetes 09/2014; 63(10):3497-3511. DOI:10.2337/db13-1577
  • [Show abstract] [Hide abstract]
    ABSTRACT: We previously reported that continuous 24-month costimulation blockade by abatacept significantly slows the decline of beta-cell function after diagnosis of type 1 diabetes. In a mechanistic extension of that study, we evaluated peripheral blood immune cell subsets (CD4, CD8-naive, memory and activated subsets, myeloid and plasmacytoid dendritic cells, monocytes, B lymphocytes, CD4(+)CD25(high) regulatory T cells, and invariant NK T cells) by flow cytometry at baseline and 3, 6, 12, 24, and 30 months after treatment initiation to discover biomarkers of therapeutic effect. Using multivariable analysis and lagging of longitudinally measured variables, we made the novel observation in the placebo group that an increase in central memory (CM) CD4 T cells (CD4(+)CD45R0(+)CD62L(+)) during a preceding visit was significantly associated with C-peptide decline at the subsequent visit. These changes were significantly affected by abatacept treatment, which drove the peripheral contraction of CM CD4 T cells and the expansion of naive (CD45R0(-)CD62L(+)) CD4 T cells in association with a significantly slower rate of C-peptide decline. The findings show that the quantification of CM CD4 T cells can provide a surrogate immune marker for C-peptide decline after the diagnosis of type 1 diabetes and that costimulation blockade may exert its beneficial therapeutic effect via modulation of this subset.
    Diabetes 09/2014; 63(10):3449-3457. DOI:10.2337/db14-0047
  • Diabetes 09/2014; 63(12). DOI:10.2337/db14-1366