Cell-Specific "Competition for Calories" Drives Asymmetric Nutrient-Energy Partitioning, Obesity, and Metabolic Diseases in Human and Non-human Animals

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Edward,Pavela,Gregory,McDonald,Samantha,Lavie,Carl J.,Hill,James O. Archer (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: The mammalian body is a complex physiologic "ecosystem" in which cells competefor calories (i.e., nutrient-energy). Axiomatically, cell-types with competitive advantagesacquire a greater number of consumed calories, and when possible, increase insize and/or number. Thus, it is logical and parsimonious to posit that obesity is thecompetitive advantages of fat-cells (adipocytes) driving a disproportionate acquisitionand storage of nutrient-energy. Accordingly, we introduce two conceptual frameworks.Asymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specificcompetition for calories that determines the partitioning of nutrient-energy to oxidation,anabolism, and/or storage; and Effective Caloric Intake which describes the numberof calories available to constrain energy-intake via the inhibition of the sensorimotorappetitive cells in the liver and brain that govern ingestive behaviors. Inherent inthese frameworks is the independence and dissociation of the energetic demandsof metabolism and the neuro-muscular pathways that initiate ingestive behaviors andenergy intake. As we demonstrate, if the sensorimotor cells suffer relative caloricdeprivation via asymmetric competition from other cell-types (e.g., skeletal muscle- orfat-cells), energy-intake is increased to compensate for both real and merely apparentdeficits in energy-homeostasis (i.e., true and false signals, respectively). Thus, weposit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesityand metabolic diseases is engendered by apparent deficits (i.e., false signals) drivenby the asymmetric inter-cellular competition for calories and concomitant differentialpartitioning of nutrient-energy to storage. These frameworks, in concert with ourprevious theoretic work, the Maternal Resources Hypothesis, provide a parsimoniousand rigorous explanation for the rapid rise in the global prevalence of increased bodyand fat mass, and associated metabolic dysfunctions in humans and other mammalsinclusive of companion, domesticated, laboratory, and feral animals.

Additional Information

Publication

Other

Language: English

Date: 2018

Keywords

obesity, nutrition, physiology, non-genetic, evolution, competition

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