International Journal of Obesity Impact Factor & Information

Publisher: International Association for the Study of Obesity, Nature Publishing Group

Journal description

Multi-disciplinary forum for research describing: basic clinical and applied studies in biochemistry, physiology, genetics and nutrition, molecular, metabolic, psychological and epidemiological aspects of obesity and related disorders.

Current impact factor: 5.00

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 5.004
2013 Impact Factor 5.386
2012 Impact Factor 5.221
2011 Impact Factor 4.691
2010 Impact Factor 5.125
2009 Impact Factor 4.343
2008 Impact Factor 3.64
2007 Impact Factor 3.56
2006 Impact Factor 4.055
2005 Impact Factor 4.482
2004 Impact Factor 3.459
2003 Impact Factor 2.794
2002 Impact Factor 2.363
2001 Impact Factor 2.196
2000 Impact Factor 2.982
1999 Impact Factor 3.199
1998 Impact Factor 3.003
1997 Impact Factor 2.476
1996 Impact Factor 1.759
1995 Impact Factor 1.832
1994 Impact Factor 1.568
1993 Impact Factor 1.776
1992 Impact Factor 1.607

Impact factor over time

Impact factor

Additional details

5-year impact 5.28
Cited half-life 8.60
Immediacy index 1.11
Eigenfactor 0.03
Article influence 1.82
Website International Journal of Obesity website
Other titles International journal of obesity
ISSN 0307-0565
OCLC 26074170
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Published source must be acknowledged and DOI cited
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • On author's personal website and institutional repository
    • If funding agency rules apply, authors may post authors version to their relevant funding body's archive, 6 months after publication
    • This policy is an exception to the default policies of 'Nature Publishing Group'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND/OBJECTIVES: Both genetic and dietary factors contribute to the metabolic syndrome (MetS) in humans and animal models. Characterizing their individual roles as well as relationships among these factors is critical for understanding MetS pathogenesis and developing effective therapies. By studying phenotypic responsiveness to high-risk versus control diet in two inbred mouse strains and their derivatives, we estimated the relative contributions of diet and genetic background to MetS, characterized strain-specific combinations of MetS conditions, and tested genetic and phenotypic complexity on a single substituted chromosome. METHODS: Ten measures of metabolic health were assessed in susceptible C57BL/6 J and resistant A/J male mice fed either a control or a high-fat, high-sucrose (HFHS) diet, permitting estimates of the relative influences of strain, diet, and strain-diet interactions for each trait. The same traits were measured in a panel of C57BL/6 J (B6)-ChrA/J chromosome substitution strains (CSSs) fed the HFHS diet, followed by characterization of interstrain relationships, covariation among metabolic traits, and quantitative trait loci (QTLs) on Chromosome 10. RESULTS: We identified significant genetic contributions to nine of ten metabolic traits and significant dietary influence on eight. Significant strain-diet interaction effects were detected for four traits. Although a range of HFHS-induced phenotypes was observed among the CSSs, significant associations were detected among all traits but one. Strains were grouped into three clusters based on overall phenotype, and specific CSSs were identified with distinct and reproducible trait combinations. Finally, several Chr10 regions were shown to control severity of MetS conditions. CONCLUSIONS: Generally strong genetic and dietary effects validate these CSSs as a multifactorial model of MetS. Although traits tended to segregate together, considerable phenotypic heterogeneity suggests that underlying genetic factors influence their co-occurrence and severity. Identification of multiple QTLs within and among strains highlights both the complexity of genetically-regulated, diet-induced MetS and the ability of CSSs to prioritize candidate loci for mechanistic studies.
    International Journal of Obesity 09/2015; DOI:10.1038/ijo.2015.184
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    ABSTRACT: BACKGROUND/OBJECTIVE:Genome-wide-association studies have identified numerous BMI-associated variants, but it is unclear how these relate to weight gain in adults at different ages. METHODS: We examined the association of a genetic risk score (GRS), consisting of 31 BMI-associated variants, with an annual weight gain (AWG) and a substantial weight gain (SWG) of 10% by comparing self-reported weight at 20 years (y) with baseline weight (mean: 58 y; standard deviation (s.d.): 8y) in 21407 participants from the Malmö Diet and Cancer Study (MDCS), and comparing baseline weight to weight at follow-up (mean: 73y; s.d.: 6y) among 2673 participants. Association between GRS and AWG and SWG was replicated in 4327 GLACIER participants (mean: 45y; s.d.: 7y) with 10y follow-up. Cohort-specific results were pooled by fixed-effect meta-analyses. RESULTS: In MDCS, the GRS was associated with increased AWG (β: 0.003; s.e: 0.01; P: 7 × 10-8) and increased odds for SWG (odds ratio (OR) 1.01 (95% confidence interval (CI): 1.00, 1.02); P: 0.013) per risk-allele from age 20y, but unexpectedly with decreased AWG (β: -0.006; s.e: 0.002; P: 0.009) and decreased odds for SWG OR 0.96 (95% CI: 0.93, 0.98); P: 0.001) between baseline and follow-up. Effect estimates from age 20y to baseline differed significantly from those from baseline to follow-up (P: 0.0002 for AWG and P: 0.0001 for SWG). Similar to MDCS, the GRS was associated with decreased odds for SWG OR 0.98 (95% CI: 0.96, 1.00); P: 0.029) from baseline to follow-up in GLACIER. In meta-analyses (n=7000), the GRS was associated with decreased AWG (β: -0.005; s.e: 0.002; P: 0.002) and decreased odds for SWG OR 0.97 (95% CI: 0.96, 0.99); P: 0.001) per risk-allele. CONCLUSION: Our results provide convincing evidence for a paradoxical inversed relationship between a high number of BMI-associated risk-alleles and less weight gain during and after middle-age, in contrast to the expected increased weight gain seen in younger age.
    International Journal of Obesity 09/2015; 10.1038/ijo.2015.180. DOI:10.1038/ijo.2015.180
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    ABSTRACT: South Asians are a high risk group for type 2 diabetes and coronary heart disease. We sought to determine ethnic differences in newborn adiposity comparing South Asians (SA) to white Caucasians (whites). 790 pregnant women (401 SA, 389 whites) and their full term offspring from two birth cohorts in Canada were analyzed. Pregnant women completed a health assessment including a 75 gram oral glucose tolerance test to assess for dysglycemia. Birthweight, length, waist and hip circumference, and triceps and subscapular skinfold thickness (a surrogate measure of body adiposity) were measured in all newborns. Multivariate regression was used to identify maternal factors associated with newborn skin fold measurements. South Asian women were younger (30.1 vs 31.8 years, P<0.001), their pre-pregnancy body mass index was lower (23.7 vs 26.2, P<0.0001), and gestational diabetes was substantially higher (21 vs 13%, P=0.005) compared to whites. Among full-term newborns, South Asians were lower birthweight (3283 vs 3517 g, P=0.0001), had greater skinfold thickness (11.7 vs 10.6 mm; P=0.0001) and higher waist circumference (31.1 vs 29.9 cm, P=0.0001) compared to whites. Risk factors for newborn skinfold thickness included South Asian ethnicity (standardized estimate (SE): 0.24; P<0.0001), maternal glucose (SE: 0.079; P=0.04), and maternal body fat (SE: 0.14; P=0.0002). South Asian newborns are lower birth weight and have greater skinfold thickness, compared to white newborns, and this is influenced by maternal body fat and glucose. Interventions aimed at reducing body fat prior to pregnancy and gestational diabetes during pregnancy in South Asians may favourably alter newborn body composition and require evaluation.International Journal of Obesity accepted article preview online, 28 August 2015. doi:10.1038/ijo.2015.171.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.171
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    ABSTRACT: Inflammation, oxidative stress, and dysregulation of adipokines are thought to be pathophysiological mechanisms linking obesity to the development of insulin resistance and atherosclerosis. In adults, bariatric surgery reduces inflammation and oxidative stress, and beneficially changes levels of several adipokines, but little is known about post-surgical changes among adolescents. In two separate longitudinal cohorts we evaluated change from baseline of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), monocyte chemo-attractant protein-1 (MCP-1), oxidized LDL cholesterol (oxLDL), adiponectin, leptin, and resistin up to 12 months following elective laparoscopic roux en Y gastric bypass (RYGB) or vertical sleeve gastrectomy (VSG) surgery in adolescents with severe obesity. In cohort 1, which consisted of 39 adolescents (mean age 16.5±1.6; 29 females) undergoing either RYGB or VSG, IL-6 (baseline: 2.3±3.4 pg/ml vs 12 months: 0.8±0.6 pg/ml, P<0.01), leptin (baseline: 178±224 ng/ml vs 12 months: 41.4±31.9 ng/ml, P<0.001), and oxLDL (baseline: 41.6±11.6 U/l vs 12 months: 35.5±11.1 U/l, P=0.001) significantly decreased and adiponectin significantly increased (baseline: 5.4±2.4 μg/ml vs 12 months: 13.5±8.9 μg/ml, P<0.001). In cohort 2, which consisted of 13 adolescents (mean age 16.5±1.6 years; 10 females) undergoing RYGB, results were similar: IL-6 (baseline: 1.7±0.9 pg/ml/ml vs 12 months: 0.4±0.9 pg/ml, P<0.05) and leptin (baseline: 92.9±31.3 ng/ml vs 12 months: 37.3±33.4 ng/ml, P<0.001) significantly decreased and adiponectin significantly increased (baseline: 6.1±2.9 μg/ml vs 12 months: 15.4±8.0 μg/ml, P<0.001). When the cohorts were combined to evaluate changes at 12 months, oxLDL also significantly decreased (baseline: 39.8±16.7 U/l vs 12 months: 32.7±11.9 U/l, P=0.03). Bariatric surgery produced robust improvements in markers of inflammation, oxidative stress, and several adipokines among adolescents with severe obesity, suggesting potential reductions in risk for type 2 diabetes and cardiovascular disease.International Journal of Obesity accepted article preview online, 28 August 2015. doi:10.1038/ijo.2015.174.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.174
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    ABSTRACT: Activation of Notch signaling pathologically enhances lipogenesis and gluconeogenesis in the liver causing non-alcoholic fatty liver disease (NAFLD) and diabetes. Delta-like 1 homolog (DLK1), an imprinted gene that can modulate adipogenesis and muscle development in mice, was found as an inhibitory regulator of Notch signaling. Therefore, we investigated the metabolic effect of exogenous DLK1 in vitro and in vivo. A soluble DLK1 peptide was generated with fusion between a human Fc fragment and extracellular domain of DLK1. Male db/db mice were randomly assigned to two groups: vehicle-treated and DLK1-treated group (25 mg/kg, intraperitoneal injection, twice a week for 4 weeks). Primary mice hepatocytes and HepG2 cells were used for in vitro experiments. After 4 weeks of DLK1 administration, hepatic triglyceride content and lipid droplets in liver tissues, as well as serum levels of liver enzymes, were markedly decreased in db/db mice. DLK1 treatment induced phosphorylation of AMPK and ACC and suppressed nuclear expression of SREBP-1c in the mouse liver or hepatocytes, indicating regulation of fatty acid oxidation and synthesis pathways. Furthermore, DLK1-treated mice showed significantly lower levels of fasting and random glucose, with improved glucose and insulin tolerance compared to the vehicle-treated group. Macrophage infiltration and proinflammatory cytokine levels in the epididymal fat were decreased in DLK1-treated db/db mice. Moreover, DLK1 suppressed glucose production from hepatocytes, which was blocked after co-administration of an AMPK inhibitor, compound C. DLK1-treated hepatocytes and mouse liver tissues showed lower PEPCK and G6Pase expression. DLK1 triggered AKT phosphorylation followed by cytosolic translocation of FOXO1 from the nucleus in hepatocytes. The present study demonstrated that exogenous administration of DLK1 reduced hepatic steatosis and hyperglycemia via AMPK activation in the liver. This result suggests that DLK1 may be a novel therapeutic approach for treating NAFLD and diabetes.International Journal of Obesity accepted article preview online, 28 August 2015. doi:10.1038/ijo.2015.173.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.173
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    ABSTRACT: In response to luminal food stimuli during meals, enteroendocrine cells release gastrointestinal (GI) peptides that have long been known to control secretory and motor functions of the gut, pancreas and liver. Glucagon-like peptide-1 (GLP-1) has emerged as one of the most important GI peptides because of a combination of functions not previously ascribed to any other molecule. GLP-1 potentiates glucose-induced insulin secretion, suppresses glucagon release, slows gastric emptying and may serve as a satiation signal, although the physiological status of the latter function has not been fully established yet. Here we review the available evidence for intestinal GLP-1 to fulfill a number of established empirical criteria for assessing whether a hormone inhibits eating by eliciting physiological satiation in man and rodents.International Journal of Obesity accepted article preview online, 28 August 2015. doi:10.1038/ijo.2015.172.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.172
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    ABSTRACT: Objectives: Increased energy expenditure (EE) has been proposed as an important mechanism for weight loss following Roux-en-Y gastric bypass (RYGB). However, this has never been investigated in a controlled setting independent of changes in energy balance. Similarly, only few studies have investigated the effect of RYGB on glycaemic control per se. Here, we investigated the effect of RYGB on EE, appetite, glycaemic control and specific signalling molecules compared with a control group in comparable negative energy balance.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.162
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    ABSTRACT: Human adenovirus 36 (Adv36) increases adiposity and is more prevalent in overweight and obese children. Dietary intake in animal models is comparable regardless of Adv36 status. The effects of Adv36 on obesity treatment outcomes have not been clarified. The aim of the study is to investigate the pre-treatment dietary intake and the response to a 4-week in-patient weight management in 184 obese adolescent girls aged 13.0-17.9 years with respect to the presence of Adv36 antibodies. Evaluation of 3-day dietary records did not show any difference in daily intake of energy and essential nutrients between Adv36 antibody positive and negative girls. After the intervention Adv36 positive girls presented with significantly greater decrease of waist circumference (P=0.020), z-score of waist circumference (P=0.024), waist-to-hip ratio (P=0.007) and weight-to-height ratio (P=0.019) compared to Adv36 negative girls. On the contrary, the sum of four skinfolds decreased significantly more in Adv36 negative than in Adv36 positive individuals (P=0.013). Neither body fat percentage nor metabolic and hormonal parameters showed any significant relevance to Adv36 status in response to weight loss intervention. In conclusion energy restriction in Adv36 antibody positive girls was associated with greater decrease of abdominal obesity and preservation of subcutaneous fat tissue than in those antibody negative.International Journal of Obesity accepted article preview online, 25 August 2015. doi:10.1038/ijo.2015.167.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.167
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    ABSTRACT: Background/Objective Weight misperception is common among adolescents with obesity, but it is not known whether weight perception is related to future weight gain. The objective of the study was to examine the prospective association between accurate weight perception versus weight misperception and weight change among youth who are overweight or obese.Subjects/Methods Using a subsample of The National Longitudinal Study of Adolescent to Adult Health Wave II cohort, we used linear regression modeling (adjusted for age, baseline BMI, parental education, household percent federal poverty level, depression, race, and ethnicity) to examine the prospective association between weight misperception (i.e., perceiving oneself to be under or normal weight) among 2738 overweight and obese youth and subsequent BMI change from Wave II (1996) to Wave IV (2008-2009). Mean age at baseline (Wave II) was 15.9 (0.1).ResultsFifty-seven percent of males and 80% of females accurately perceived themselves as overweight. In fully adjusted models, weight misperception was associated with less BMI gain among youth who were overweight and obese. Specifically, youth who perceived themselves to be at a healthy weight had lower BMI gains (males: β=-1.43, 95% CI=[-2.26, -0.60], P=0.001; females: β=-1.35, 95% CI=[-2.59, -0.11], P=0.035) from Wave II to IV relative to those who accurately perceived themselves as overweight or obese.Conclusions Contrary to commonly held assumptions, weight misperception among a non-clinical sample of youth who were overweight or obese predicted lower future weight gain. Efficacy of efforts to correct weight misperception should be rigorously examined to assess for both intended and unintended consequences.International Journal of Obesity accepted article preview online, 25 August 2015. doi:10.1038/ijo.2015.166.
    International Journal of Obesity 08/2015; DOI:10.1038/ijo.2015.166
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    ABSTRACT: Background: Obesity is a complex disease caused by the interplay of genetic and lifestyle factors, but identification of gene-lifestyle interactions in obesity has remained challenging. Few large-scale studies have reported use of genome-wide approaches to investigate gene-lifestyle interactions in obesity. Methods: In the PROMIS study, a cross-sectional study based in Pakistan, we calculated BMI variance estimates (square of the residual of inverse-normal transformed BMI z-score) in 14 131 participants and conducted genome-wide heterogeneity of variance analyses (GWHVA) for this outcome. All analyses were adjusted for age, age2, sex and genetic ancestry. Results: The GWHVA analyses yielded a genome-wide significance (P-value=3.1 × 10-8) association of the rs140133294 variant at FLJ33534 with BMI variance. In explicit tests of gene × lifestyle interaction, smoking was found to significantly modify the effect of rs140133294 on BMI (Pinteraction=0.0005), whereby the minor allele (T) was associated with lower BMI in current smokers, while positively associated with BMI in never-smokers. No interactions with physical activity were observed. Analyses of ENCODE data at the FLJ33534 locus revealed features indicative of open chromatin and high confidence DNA-binding motifs for several transcription factors, providing suggestive biological support for a mechanism of interaction. Conclusion: In summary, we have identified a novel interaction between smoking and variation at the FLJ33534 locus in relation to BMI in people from Pakistan.
    International Journal of Obesity 08/2015; 10.1038/ijo.2015.152. DOI:10.1038/ijo.2015.152
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    ABSTRACT: Objective: To investigate whether children's perceptions of neighborhood safety are associated with their weight status and weight-related behaviors, independently of their parents' perceptions. Methods: Data were from the baseline wave (collected in 2005-2008) of the Quebec Adipose and Lifestyle Investigation in Youth (QUALITY), an ongoing prospective study of 630 children aged 8-10 years (from Quebec, Canada) at risk of obesity. Weight and height were measured, and WHO age- and sex-specific BMI z-scores were computed. Physical activity was measured by accelerometry, and time spent watching television, playing computer and video games during week and weekend days was self-reported. Structural equation modeling was used to simultaneously estimate the associations between parent and child perceived safety, with children's BMI z-score, physical activity, and screen time. Results: The results suggest that, when parent perceived safety was at the mean, children who perceived their neighborhood as being safest had nearly an additional 70 daily activity counts-per-minute (representing an approximate 10% increase in overall physical activity level) compared to children who perceived it as being least safe. Among children who perceived a mean level of safety, those whose parents perceived their neighborhood as being safest spent approximately an hour less per day in front of screens compared to those whose parents perceived their neighborhood as being least safe. Parent and child perceptions of safety both indirectly contribute to children's weight status by differentially impacting weight-related behaviors. Conclusion: Findings indicate that targeting both parent and child perceived neighborhood safety could bolster efforts to promote healthy weight and weight-related behaviors among children.
    International Journal of Obesity 05/2015; DOI:10.1038/ijo.2015.98
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    ABSTRACT: Epidemics of obesity and diabetes are escalating. High-calorie/high-fat food is a major cause for these global health issues, but molecular mechanisms underlying high-fat, diet-induced obesity are still not well understood. The aryl hydrocarbon receptor (AhR), a transcription factor that acts as a xenobiotic sensor, mediates environmental toxicant-induced obesity, insulin resistance and development of diabetes. AhR also influences lipid metabolism and diet-induced obesity. The effects of AhR deficiency on diet-induced obesity, hepatic steatosis and insulin resistance were examined. Male wild type (WT), AhR null (AhR(-/-)) and AhR heterozygote (AhR(+/-)) mice were fed a normal chow diet (NCD, 10% kcal from fat) or a high-fat diet (HFD, 60% kcal from fat) for up to 14 weeks. Adiposity, adipose and liver morphology, insulin signaling, metabolic parameters and gene profiles were assessed. AhR deficiency protected against HFD-induced obesity, hepatic steatosis, insulin resistance and inflammation. Moreover, AhR deficiency preserved insulin signaling in major metabolic tissues. These protective effects result from a higher energy expenditure in AhR-deficient mice compared to WT. Levels of transcript for both the thermogenic gene, uncoupling protein 1 (Ucp1), in brown adipose tissue and mitochondrial β-oxidation genes in muscle were significantly higher in AhR(-/-) and AhR(+/-) mice compared to WT. This work documents a physiologically relevant function for AhR in regulation of body weight, hepatic fat deposition, insulin sensitivity and energy expenditure under HFD exposure, suggesting that AhR signaling may be developed as a potential therapeutic target for treatment of obesity and metabolic disorders.International Journal of Obesity accepted article preview online, 24 April 2015. doi:10.1038/ijo.2015.63.
    International Journal of Obesity 04/2015; DOI:10.1038/ijo.2015.63