One third of the U.S. population over the age of 20 (58 million individuals) is obese. The prevalence of obesity in children is approximately 20% and rates of obesity are disproportionately high among Black and Hispanic women. Hypertension, stroke, diabetes and disordered blood lipids have been clearly related to obesity. The widely recognized failure of obesity treatments results not from inability to achieve weight reduction, but from inability to maintain weight loss. We are investigating the metabolic basis for this phenomenon. Recently completed studies have shown that changes in the quantity of stored calories (adipose tissue) above or below that which is """"""""normative"""""""" or usual for a given individual, whether lean or obese, are accompanied by changes in energy metabolism in the compartment of non-resting energy expenditure (skeletal muscle). Obese and non-obese individuals have similar responses to experimentally induced changes in caloric storage, """"""""defending"""""""" adipose tissue depots of different size by the same metabolic mechanisms. Candidate systems for effecting these changes in energy metabolism include skeletal muscle and the autonomic nervous system. In obese, never-obese, and formerly-obese subjects, measurements will be made of components of 1.) Systemic energy metabolism (indirect calorimetry, caloric requirement to maintain body weight, differential excretion of isotopes of heavy water, thermic effect of feeding); 2.) Skeletal muscle physiology (oxygen consumption measurements during graded exercise; in vivo metabolic measures of skeletal muscle; muscle biopsies for fiber morphology, capillary density, oxidative and glycolytic enzyme content; 3.) Autonomic nervous system activity (heart rate response to serial blockade of cardiac parasympathetic and sympathetic receptors); 4.) Body composition (hydrodensitometry, water space by isotope dilution, dual photon beam absorptiometry). These measures will be repeated under circumstances of weight stability at weight plateaus equal to, above, and below initial weight. The goal is to identify the cellular and molecular mechanism(s) responsible for the changes in energy metabolism which accompany weight perturbation.
| Rosenbaum, Michael; Leibel, Rudolph L (2014) 20 years of leptin: role of leptin in energy homeostasis in humans. J Endocrinol 223:T83-96 |
| Goldsmith, Rochelle; Joanisse, Denis R; Gallagher, Dympna et al. (2010) Effects of experimental weight perturbation on skeletal muscle work efficiency, fuel utilization, and biochemistry in human subjects. Am J Physiol Regul Integr Comp Physiol 298:R79-88 |
| Rosenbaum, Michael; Kissileff, Harry R; Mayer, Laurel E S et al. (2010) Energy intake in weight-reduced humans. Brain Res 1350:95-102 |
| Rosenbaum, Michael; Hirsch, Jules; Gallagher, Dympna A et al. (2008) Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight. Am J Clin Nutr 88:906-12 |
| Rosenbaum, Michael; Vandenborne, Krista; Goldsmith, Rochelle et al. (2003) Effects of experimental weight perturbation on skeletal muscle work efficiency in human subjects. Am J Physiol Regul Integr Comp Physiol 285:R183-92 |
| Campfield, L Arthur; Smith, Francoise J (2003) Blood glucose dynamics and control of meal initiation: a pattern detection and recognition theory. Physiol Rev 83:25-58 |
| Rosenbaum, Michael; Murphy, Ellen M; Heymsfield, Steven B et al. (2002) Low dose leptin administration reverses effects of sustained weight-reduction on energy expenditure and circulating concentrations of thyroid hormones. J Clin Endocrinol Metab 87:2391-4 |
| Willett, Walter C; Leibel, Rudolph L (2002) Dietary fat is not a major determinant of body fat. Am J Med 113 Suppl 9B:47S-59S |
| Leibel, Rudolph L (2002) The role of leptin in the control of body weight. Nutr Rev 60:S15-9; discussion S68-84, 85-7 |
| Mietus, J E; Peng, C-K; Henry, I et al. (2002) The pNNx files: re-examining a widely used heart rate variability measure. Heart 88:378-80 |
Showing the most recent 10 out of 49 publications
