Individual variations in energy utilized for biomechanical processes and molecular mobility account for diverse susceptibility to obesity.
To explain why subjects vary in body fat content despite similar nutrient intake and physical activity, a hypothesis is proposed invoking individual variability in the potentially vast quantities of energy utilizable for such biomechanical functions as cellular motility processes, and for protein mobility. The collective term "biomechanical-mobile" activity is introduced. The hypothesis explains variation without differences in external energy losses. After utilization for indispensable metabolic needs and the variable "biomechanical-mobile" activity, excess energy is mainly transduced to anabolic processes, and eventually stored as chemical energy, mostly as adipocyte triglycerides. At one extreme, are subjects with the least degrees of "biomechanical-mobile" activity, the consequently largest surfeits of energy for chemical storage, and thus the greatest susceptibility to massive obesity. The converse applies to inordinate leanness. Between the extremes, the almost infinite individual variability is due to a "continuous" distribution of "biomechanical-mobile" activity inversely related to the quantity remaining for chemical storage. While the extremes may result from mutations, the intervening continuum is ascribed to genetic polymorphism and to novel endocrine-neural mechanisms. In addition, such environmental influences as diet and drugs might modulate "biomechanical-mobile" activity. This hypothesis is extrapolated to all living systems.
D000273:Adipose Tissue / Q000378:metabolism; D001696:Biomechanical Phenomena; D002465:Cell Movement; D004734:Energy Metabolism; D006801:Humans; D008954:Models, Biological; D009765:Obesity / Q000209:etiology* / Q000378:metabolism; D011110:Polymorphism, Genetic; D013851:Thinness / Q000209:etiology / Q000378:metabolism