| 1. |
- Ekman, M J, et al.
(författare)
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6-minute walk test before and after a weight reduction program in obese subjects.
- 2013
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Ingår i: Obesity. - : Wiley. - 1930-739X .- 1930-7381. ; 21:3, s. 236-243
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Tidskriftsartikel (refereegranskat)abstract
- Weight loss and physical activity have shown favorable effects on risks associated with obesity. It is therefore of interest to evaluate exercise capacity and related co-morbidities in obese patients. We present data from obese subjects evaluated by the 6-minute walk test (6MWT) before and after a 7.3 (6.1-8.2) month weight reduction program. 251 subjects completed the test at baseline (BMI 40.6 [36.9-44.6] kg/m(2) ) and 129 (51.4 %) repeated the test after intervention (BMI 35.6 [31.2-38.5] kg/m(2) ). The six minute walking distance (6MWD) at baseline (535 [480-580] m) and at follow up (599 [522-640] m) correlated to several cardiovascular risk markers. Age, weight, height, resting heart rate, smoking status, fP-glucose and use of ß-blockers explained 43 % of the variance in predicted 6MWD at baseline. The effect of smoking status, fP-glucose, ß-blockers and resting heart rate lost significance at follow up. Presence of diabetes and the metabolic syndrome had a negative influence on 6MWD but did not affect the impact of intervention based on percentage increase in walking distance. Gender had no impact on 6MWD. Reported pain during the test was common but decreased after intervention (57.0 % vs. 28.7 %, p<0.001). In conclusion, the 6MWT may be used to evaluate intervention success beyond kilogram weight loss in obese subjects. We present formulas to predict 6MWD and the effect of weight loss on walking distance in clinical practice. Pain is a common problem which has to be considered when giving advice on exercise as a part of weight loss intervention.
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| 2. |
- Johansson, Lovisa, et al.
(författare)
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Differential gene expression in adipose tissue from obese human subjects during weight loss and weight maintenance.
- 2012
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 96:1, s. 196-207
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Differential gene expression in adipose tissue during diet-induced weight loss followed by a weight stability period is poorly characterized. Markers of these processes may provide a deeper understanding of underlying mechanisms. OBJECTIVE: We aimed to identify differentially expressed genes in human adipose tissue during weight loss and weight maintenance after weight loss. DESIGN: RNA from subcutaneous abdominal adipose tissue from 9 obese subjects was analyzed by using a complementary DNA microarray at baseline after weight loss on a low-calorie diet and after weight maintenance. RESULTS: Subjects lost 18.8 ± 1.8% of weight and maintained this loss during weight maintenance (1.1 ± 2.1%; range: -9.3 to 10.6%). Most differentially expressed genes exhibited a reciprocal regulation and returned to baseline after weight loss (2163 genes) and weight maintenance (3175 genes). CETP and ABCG1, both of which participate in the HDL-mediated reverse cholesterol transport (RCT), were among the most upregulated of the 750 genes that were differentially expressed after both processes. Several genes involved in inflammation were downregulated. The use of real-time polymerase chain reaction confirmed or partially confirmed the previously implicated genes TNMD and MMP9 (both downregulated), PNPLA3 (upregulated), and CIDEA and SCD (both reciprocally regulated). CONCLUSIONS: The beneficial effects of weight loss should be investigated after long-term weight maintenance. The processes of weight loss and weight maintenance should be viewed as biologically distinct. CETP and ABCG1 may be important mediators of these effects through HDL-mediated RCT.
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| 3. |
- Wilman, H. R., et al.
(författare)
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Genetic studies of abdominal MRI data identify genes regulating hepcidin as major determinants of liver iron concentration
- 2019
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Ingår i: Journal of Hepatology. - : Elsevier. - 0168-8278 .- 1600-0641. ; 71:3, s. 594-602
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Excess liver iron content is common and is linked to the risk of hepatic and extrahepatic diseases. We aimed to identify genetic variants influencing liver iron content and use genetics to understand its link to other traits and diseases. Methods: First, we performed a genome-wide association study (GWAS) in 8,289 individuals from UK Biobank, whose liver iron level had been quantified by magnetic resonance imaging, before validating our findings in an independent cohort (n = 1,513 from IMI DIRECT). Second, we used Mendelian randomisation to test the causal effects of 25 predominantly metabolic traits on liver iron content. Third, we tested phenome-wide associations between liver iron variants and 770 traits and disease outcomes. Results: We identified 3 independent genetic variants (rs1800562 [C282Y] and rs1799945 [H63D] in HFE and rs855791 [V736A] in TMPRSS6) associated with liver iron content that reached the GWAS significance threshold (p <5 × 10−8). The 2 HFE variants account for ∼85% of all cases of hereditary haemochromatosis. Mendelian randomisation analysis provided evidence that higher central obesity plays a causal role in increased liver iron content. Phenome-wide association analysis demonstrated shared aetiopathogenic mechanisms for elevated liver iron, high blood pressure, cirrhosis, malignancies, neuropsychiatric and rheumatological conditions, while also highlighting inverse associations with anaemias, lipidaemias and ischaemic heart disease. Conclusion: Our study provides genetic evidence that mechanisms underlying higher liver iron content are likely systemic rather than organ specific, that higher central obesity is causally associated with higher liver iron, and that liver iron shares common aetiology with multiple metabolic and non-metabolic diseases. Lay summary: Excess liver iron content is common and is associated with liver diseases and metabolic diseases including diabetes, high blood pressure, and heart disease. We identified 3 genetic variants that are linked to an increased risk of developing higher liver iron content. We show that the same genetic variants are linked to higher risk of many diseases, but they may also be associated with some health advantages. Finally, we use genetic variants associated with waist-to-hip ratio as a tool to show that central obesity is causally associated with increased liver iron content.
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