Basal metabolic rate in morbidly obese patients with non-alcoholic fatty liver disease

Department of Clinical and Experimental Medicine, Federico II University Medical School of Naples, Italy.
Clinical and investigative medicine. Medecine clinique et experimentale (Impact Factor: 1.23). 01/2008; 31(1):E24-9.
Source: PubMed

ABSTRACT Non-Alcoholic Fatty Liver Disease occurs mainly in severly obese patients and its relationship to Metabolic Syndrome is increasingly recognized. The aim of this study was to determine energy production-utilization by measuring the Basal Metabolic Rate in severely obese patients, characterized by NAFLD, with or without Metabolic Syndrome. Then, the role of systemic inflammation was assessed.
Twenty severly obese men with Metabolic Syndrome were compared with a well-matched cohort of patients without Metabolic Syndrome. All showed hepatic steatosis at UltraSonography. Basal Metabolic Rate was measured by indirect calorimetry using a canopy system and single-frequency bio-impedance analysis. Serum Interleukin-6 and fibrinogen levels were measured as markers of inflammation
Basal Metabolic Rate was higher in severely obese patients with Metabolic Syndrome than in those without it: 2,496+/-358 kcal/d vs 2,126+/-253 kcal/d, P = 0 .001. Laboratory findings of concurrent chronic inflammation were also higher in these patients, i.e., Il6 4.35+/-1.34 pg/ml vs 6.23+/-2.1 pg/ml, P = 0.034; fibrinogenemia 285+/-40 mg/dL vs 376+/-91 mg/dL, P = 0.020; these of of cytonecrosis, i.e., AlaninaminoTransferase, equally behaved 32.3+/-7.9 UI vs 65.7+/-28.2 UI, P < 0.001. Visceral adiposity and arterial hypertension were more frequently detected in patients with Metabolic Syndrome.
Increased energy expenditure, observed in morbidly obese patients as a consequence of a systemic, low-grade, inflammatory process, may explain progression from obesity to Metabolic Syndrome, independent of the presence of NAFLD. In this context, increased Basal Metabolic Rate may be a clue of Metabolic Syndrome.

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Available from: Giovanni Tarantino, Sep 26, 2015
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    • "After a 15–20 min adaptation to the instrument, oxygen consumption and carbon dioxide production were determined for 45 min. Energy expenditure was derived from CO2 production and O2 consumption with the appropriate Weir formula neglecting protein oxidation [14]. BMR, expressed as kcal/24 h, was adjusted for changes in fat-free mass (FFM), which was evaluated by single-frequency bioimpedance analysis obtaining a RMR/FFM ratio, expressed as kcal/24 h∗kg of body [15]. "
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    ABSTRACT: The present study shows low circulating levels of SIRT4 in obese patients with nonalcoholic fatty liver disease mirroring its reduced mitochondrial expression in an attempt to increase the fat oxidative capacity and then the mitochondrial function in liver and in muscle. SIRT4 modulates the metabolism of free fatty acids reducing their high circulating levels but, unfortunately, increasing ROS production. Great concentration of free fatty acids, released by adipose tissue, coupled with oxidative stress, directly results in endothelial dysfunction, early atherosclerosis, and coronary artery disease risk factor.
    Oxidative medicine and cellular longevity 06/2014; 2014:920676. DOI:10.1155/2014/920676 · 3.36 Impact Factor
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    • "However, cases had significantly lower basal metabolic rate than controls. Contrary to this, one study reported higher BMR in morbidly obese subjects with MS.[15] "
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    ABSTRACT: The clustering of cardiovascular risk factors is termed the metabolic syndrome (MS), which strongly predict risk of diabetes and cardiovascular disease. Many studies implicate insulin resistance (IR) in the development of diabetes, but ignore the contribution of beta-cell dysfunction. Hence, we studied beta-cell function, as assessed by HOMA model, in subjects with MS. We studied 50 subjects with MS diagnosed by IDF criteria and 24 healthy age- and sex-matched controls. Clinical evaluation included anthropometry, body fat analysis by bioimpedance, biochemical, and insulin measurement. IR and secretion were calculated by HOMA model. Subjects with MS had more IR (HOMA-IR) than controls (3.35 ± 3.14 vs. 1.76 ± 0.53, P = 0.029) and secreted less insulin (HOMA-S) than controls (66.80 ± 69.66 vs. 144.27 ± 101.61, P = 0.0003), although plasma insulin levels were comparable in both groups (10.7 ± 10.2 vs. 8.2 ± 2.38, P = 0.44). HOMA-IR and HOMA-S were related with number of metabolic abnormalities. HOMA-IR was positively associated with body mass index, waist hip ratio, body fat mass, and percent body fat. HOMA-S was negatively associated with waist hip ratio, fasting plasma glucose and total cholesterol and positively with basal metabolic rate. Percent body fat was an independent predictor of HOMA-IR and waist hip ratio of HOMA-S in multiple regression analysis. Subjects with MS have increased IR and decreased insulin secretion compared with healthy controls. Lifestyle measures have been shown to improve IR, insulin secretion, and various components and effects of MS. Hence, there is an urgent need for public health measures to prevent ongoing epidemic of diabetes and cardiovascular disease.
    07/2011; 15(Suppl 1):S44-9. DOI:10.4103/2230-8210.83059
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    ABSTRACT: The estimated prevalence of NonAlcoholic Fatty Liver Disease in the general population in western countries is about 30%, but it is higher among obese and diabetic people. It is likely that more sophisticated approaches are required to understand its pathogenesis and to develop drug targets. In the meantime, the range of associations between NAFLD and other illnesses broadens. Although association does not mean causation, the link between some diseases and NAFLD suggests a common mechanism.
    Clinical and investigative medicine. Medecine clinique et experimentale 02/2008; 31(5):E290-5. · 1.23 Impact Factor
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