Levine, James

Background Physical activity is important in obesity, metabolic and cardiovascular diseases and cancer prevention. Several cell phone platforms integrate an accelerometer onto the motherboard. We wrote a software application to access the on board accelerometer from the iPhone (Apple Computer, Cupertino, CA) to measure and quantify physical activity. Here we tested the validity of the cell phone accelerometer to assess physical activity in a controlled laboratory setting. Methods 31 subjects wore the cell phone along with the validated Physical Activity Monitoring System (PAMS) with different body postures and during graded walking at 7 velocities. Energy expenditure was measured using indirect calorimetry. Data were also collected from 7346 users who downloaded the “Walk n’ Play” application from the internet. Results In all the 31 subjects, the cell phone accelerometer distinguished sedentary and walking activity reliably even with ½ mph increments in walking and was accurate and precise compared to the PAMS, with an intra‐class correlation coefficient (r 2 > 0.98). The cell phone accelerometer showed excellent sequential increases with increased in walking velocity and energy expenditure (r 2 >0.9). The data from the 7346 free‐living people demonstrated that most daily activity detected with the cell phone accelerometer occurs in the low intensity. Conclusions An accelerometer embedded into a cell phone was shown to be accurate and reliable in measuring and quantifying physical activity in the laboratory setting. Before a comprehensive integrated physical activity promoting and weight loss platform can be deployed, free‐living evaluation is necessary.

ABSTRACT Obesity is one of the major health problems of our times. Elucidating the signaling mechanisms by which high‐fat caloric diet induces obesity is critical for the understanding of this condition and for the development of therapeutic strategies for its treatment. Here, we demonstrate a novel role for protein CD38 as a regulator of body weight during a high‐fat diet. CD38 is a ubiquitous enzyme that catalyzes the synthesis of second messengers and has been implicated in the regulation of a wide variety of signaling pathways. We report that CD38‐deficient mice are pro‐tected against high‐fat diet‐induced obesity owing to enhanced energy expenditure. In fact, calorimetric studies indicate that CD38‐deficient animals have a higher metabolic rate compared to control mice. Analysis of the mechanism revealed that this resistance to diet‐induced obesity is mediated at least in part via a NAD‐dependent activation of SIRT‐PGC1α axis, a well‐established cascade, involved in the regulation of mito‐chondrial biogenesis and energy homeostasis. Thus, together these results identify a novel pathway regulating body weight and clearly show that CD38 is a nearly obligatory component of the cellular cascade that led to diet‐induced obesity.—Barbosa, M. T. P., Soares, S. M., Novak, C. M., Sinclair, D., Levine, J. A., Aksoy, P., Chini, E. N. The enzyme CD38 (a NAD glycohydrolase, EC 3.2.2.5) is necessary for the development of diet‐induced obesity. FASEB J. 21, 3629–3639 (2007)