Energy Expenditure Due to Physical Activity Is Not Increased to Achieve Intended Weight Loss

Reduced physical activity and almost unlimited availability of food are major contributors to the development of obesity. With the decline of strenuous work, energy expenditure due to spontaneous physical activity has attracted increasing attention. Our aim was to assess changes in energy expenditure, physical activity patterns and nutritional habits in obese subjects aiming at self-directed weight loss. Methods: Energy expenditure and physical activity patterns were measured with a portable armband device. Nutritional habits were assessed with a food frequency questionnaire. Results: Data on weight development, energy expenditure, physical activity patterns and nutritional habits were obtained for 105 patients over a six-month period from an initial cohort of 160 outpatients aiming at weight loss. Mean weight loss was −1.5 ± 7.0 kg (p = 0.028). Patients with weight maintenance (n = 75), with substantial weight loss (>5% body weight, n = 20) and with substantial weight gain (>5% body weight, n = 10) did not differ in regard to changes of body weight adjusted energy expenditure components (total energy expenditure: −0.2 kcal/kg/day; non-exercise activity thermogenesis: −0.3 kcal/kg/day; exercise- related activity thermogenesis (EAT): −0.2 kcal/kg/day) or patterns of physical activity (duration of EAT: −2 min/day; steps/day: −156; metabolic equivalent unchanged) measured objectively with a portable armband device. Self-reported consumption frequency of unfavorable food decreased significantly (p = 0.019) over the six-month period. Conclusions: An increase in energy expenditure or changes of physical activity patterns (objectively assessed with a portable armband device) are not employed by obese subjects to achieve self-directed weight loss. However, modified nutritional habits could be detected with the use of a food frequency questionnaire

Serum bile acids and leptin interact with glucose metabolism in patients with liver cirrhosis

<p>Background & aims: We investigated possible involvements of bile acids (BA) and leptin in hepatogenous insulin resistance being present in up to 90% of cirrhotic patients.</p><p>Methods: Blood was analysed in 10 cirrhotic patients (8m/2f, 48 +/- 10.4 yrs) and 10 controls (8m/2f, 43 +/- 9.3 yrs) after oral nutrition and during 1 h of parenteral feeding. In patients, leptin was additionally analysed from mesenteric and arterial blood.</p><p>Results: Cirrhosis patients showed typical signs of hepatogenous insulin resistance (hyperinsulinaemia, normoglycaemia, hyperglucagonaemia). Both fasting BA (r = .714, p = 0.047) and fasting leptin (r = .867, p = 0.001) correlated to HOMA and predicted insulin response after oral feeding (R(2)adj = .783, p = 0.002). But during parenteral nutrition only leptin predicted insulin response (p = 0.005). The prandial glucose response was negatively correlated to the BA increase after oral nutrition (r = -.733, p = 0.028) and to the change in leptin during parenteral nutrition (r = -.738, p = 0.037) pointing towards a nutritional route-dependent positive impact on glucose tolerance of both substances. Prandial glucagon response was correlated to BA under both feeding conditions (p</p><p>Conclusion: Our results suggest a substantial involvement of BA and leptin by improving postprandial glucose tolerance related to liver cirrhosis. (C) 2012 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.</p>

Plasma bile acids are associated with energy expenditure and thyroid function in humans

Background/Aims: Animal studies implicate a role of bile acids (BA) in thyroid-regulated energy expenditure (EE) via activation of the TGR-5/adenylate cyclase/deiodinase type 2 pathway. Here we investigated these possible associations in humans. Methods: EE, BA, and thyroid hormone status were assessed in 10 healthy subjects and eight patients with liver cirrhosis at baseline and after oral nutrition. In cirrhosis, blood was additionally sampled from the mesenteric vein and the radial artery. Results: At baseline, BA and EE related positively (r = 0.648, P = 0.048 in healthy subjects; r = 0.833, P = 0.010 in cirrhosis; r = 0.556, P = 0.017 in all), with the highest correlation with deoxycholic acid levels. The respiratory quotient associated negatively to baseline BA (all, r = -0.639, P = 0.004). Postprandially, serum TSH decreased in both groups (P <0.05 each). In cirrhosis, the decrease of TSH after 60 min correlated to the meal-stimulated BA increase (r = -0.762, P = 0.028). To assess the mechanism involved, we studied a single human TSHoma and T alpha T1 mouse thyrotrope cells. In TSHoma cells, TGR-5 was predominantly expressed cytoplasmically, and in vitro stimulation with BA did not substantially alter cAMP or deiodinase type 2. Conclusions: Our data support a role of BA in human energy metabolism and in thyroid hormone control. Even though no convincing response to BA was demonstrated in TSHoma and T alpha T1 cells, the TSH decrease after a nutritional challenge suggests an interaction of BA on the set point of the thyroid axis. (J Clin Endocrinol Metab 97:535-542, 2012