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      Ectopic adiposity and cardiometabolic health in COPD

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          Abstract

          Rationale

          Obesity/overweight is the most prevalent body composition abnormality in COPD. However, little is known about the impact of fat distribution on cardiometabolic health in COPD.

          Objective

          To study the associations between ectopic adiposity, cardiometabolic health, and COPD.

          Methods

          A total of 263 subjects (166 males; age=65±9 years) were randomly selected from the general population. Subjects were classified as non-COPD controls and COPD, according to the Global initiative for chronic Obstructive Lung Disease (GOLD) classification, and the presence of cardiometabolic comorbidities was recorded. Ectopic fat accumulation was documented from computed tomography measurements of visceral adipose tissue cross-sectional areas and muscle mean attenuation, assessed at L4–L5. Blood glucose, lipid, and adipokine profiles were also evaluated.

          Results

          After correcting for age, sex, and tobacco exposure, visceral adipose tissue cross-sectional area was higher in GOLD 2+ compared to GOLD 1 individuals. Consistent with this, mean muscle tissue attenuation was lower in GOLD 2+ vs GOLD 1 and non-COPD controls ( P<0.001). In multiple regression models, visceral adipose tissue cross-sectional area was strongly associated with hypertension ( P<0.001) and diabetes ( P<0.001), while muscle attenuation was associated with coronary artery disease ( P<0.001). Blood glucose, lipid, and adipokine profiles were similar across groups with the exception of leptin level which was higher in GOLD 2+ subjects compared to GOLD 1 and controls.

          Conclusion

          GOLD 2+ COPD was associated with ectopic fat accumulation which modulated cardiometabolic health.

          Related collections

          Most cited references 28

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          Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men.

          We determined whether interindividual variation in hepatic insulin sensitivity could be attributed to variation in liver fat content (LFAT) independent of obesity. We recruited 30 healthy nondiabetic men whose LFAT (determined by proton spectroscopy); intraabdominal, sc, and total (determined by magnetic resonance imaging) fat; and insulin sensitivity of endogenous glucose rate of production (R(a)) and suppression of serum FFA [euglycemic insulin clamp combined with [3-(3)H]glucose (0-300 min); insulin infusion rate, 0.3 mU/kg.min, 120-300 min] were measured. The men were divided into groups of low (mean +/- SD, 1.7 +/- 0.2%) and high (10.5 +/- 2.0%) LFAT based on their median fat content. The low and high LFAT groups were comparable with respect to age (44 +/- 2 vs. 42 +/- 2 yr), body mass index (25 +/- 1 vs. 26 +/- 1 kg/m(2) ), waist to hip ratio (0.953 +/- 0.013 vs. 0.953 +/- 0.013), maximal oxygen uptake (35.6 +/- 1.5 vs. 33.5 +/- 1.5 ml/kg.min), and intraabdominal, sc, and total fat. The high compared with the low LFAT group had several features of insulin resistance, including fasting hyperinsulinemia (7.3 +/- 0.6 vs. 5.3 +/- 0.6 mU/liter; P < 0.02, high vs. low LFAT) hypertriglyceridemia (1.4 +/- 0.2 vs. 0.9 +/- 0.1 mmol/liter; P < 0.02), a low high density lipoprotein (HDL) cholesterol concentration (1.4 +/- 0.1 vs. 1.6 +/- 0.1 mmol/liter; P < 0.05), and a higher ambulatory 24-h systolic blood pressure (130 +/- 3 vs. 122 +/- 3 mm Hg; P < 0.05). Basal glucose R(a) and serum FFA were comparable between the groups, whereas insulin suppression of glucose R(a) [51 +/- 8 vs. 20 +/- 12 mg/m(2).min during 240-300 min (P < 0.05) or -55 +/- 7 vs. -85 +/- 12% below basal (P < 0.05, high vs. low LFAT)] and of serum FFA (299 +/- 33 vs. 212 +/- 13 micromol/liter; 240-300 min; P < 0.02) were impaired in the high compared with the low LFAT group. Insulin stimulation of glucose Rd were comparable in the men with high LFAT (141 +/- 12 mg/m(2).min) and those with low LFAT (156 +/- 14 mg/m(2).min; P = NS). Fat accumulation in the liver is, independent of body mass index and intraabdominal and overall obesity, characterized by several features of insulin resistance in normal weight and moderately overweight subjects.
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            Can comorbidity be measured by questionnaire rather than medical record review?

            Comorbidity generally is measured by medical record abstraction, which is expensive and often impractical. The aim of this study was to assess the reproducibility and validity of a comorbidity questionnaire. The authors developed a brief comorbidity questionnaire that included items corresponding to each element of the medical record-based Charlson index. The questionnaire was administered to 170 inpatients. Charlson scores were abstracted from these patients' medical records. We assessed test-retest reliability of the questionnaire and the Charlson index, the correlation between the questionnaire and the Charlson index, and correlations between each comorbidity measure and indicators of health resource utilization including medication use, hospitalizations in the past year, and hospital charges. Test-retest reliability, assessed with the intraclass correlation coefficient, was 0.91 for the questionnaire and 0.92 for the chart-based Charlson index. The Spearman correlation between these two measures was 0.63. The correlation between comorbidity measures was weaker in less educated patients. Correlations with indicators of resource utilization were similar for the two comorbidity instruments. The authors found that a questionnaire version of the Charlson index is reproducible, valid, and offers practical advantages over medical record-based assessments.
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              Physical inactivity in patients with COPD, a controlled multi-center pilot-study.

              Physical activity (PA) has been reported to be reduced in severe chronic obstructive pulmonary disease (COPD). Studies in moderate COPD are currently scarce. The aim of the present study was to investigate physical activity in daily life in patients with COPD (n=70) and controls (n=30). A multi-center controlled study was conducted. PA was assessed using a multisensor armband device (SenseWear, BodyMedia, Pittsburgh, PA) and is reported as the average number of steps per day, and the time spent in mild and moderate physical activity. Patients suffered from mild (n=9), moderate (n=28), severe (n=23) and very severe (n=10) COPD. The time spent in activities with mild (80 + or - 69 min vs 160 + or - 89 min, p<0.0001) and moderate intensity (24 + or - 29 min vs 65 + or - 70 min; p<0.0036) was reduced in patients compared to controls. The number of steps reached 87 + or - 34%, 71 + or - 32%, 49 + or - 34% and 29 + or - 20% of control values in GOLD-stages I to IV respectively. The time spent in activities at moderate intensity was 53 + or - 47%, 41 + or - 45%, 31 + or - 47% and 22 + or - 34% of the values obtained in controls respectively with increasing GOLD-stage. These differences reached statistical significance as of GOLD stage II (p<0.05). No differences were observed among centers. Physical activity is reduced early in the disease progression (as of GOLD-stage II). Reductions in physical activities at moderate intensity seem to precede the reduction in the amount of physical activities at lower intensity. Copyright 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2018
                15 October 2018
                : 13
                : 3331-3340
                Affiliations
                [1 ]Centre de Recherche, Institut Universitaire de Cardiologie et de Pneumologie de Québec-Université Laval, Québec, QC, Canada, francois.maltais@ 123456fmed.ulaval.ca
                [2 ]University of British Columbia, Vancouver, BC, Canada
                [3 ]Institut de Recherches Cliniques de Montréal, Département de Nutrition et Service d’Endocrinologie, Centre Hospitalier de l’Université de Montréal, Montréal, QC, Canada
                [4 ]Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Centre, Montreal, QC, Canada
                Author notes
                Correspondence: François Maltais, Centre de Pneumologie, Institut Universitaire de Cardiologie et de Pneumologie de Québec, 2725 Chemin Sainte-Foy, Québec (QC), G1V 4G5, Canada, Tel +1 418 656 4762, Email francois.maltais@ 123456fmed.ulaval.ca
                Article
                copd-13-3331
                10.2147/COPD.S168963
                6197246
                © 2018 Coats et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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