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 Archer (Creator)

James O. Hill (Creator)

Carl J. Lavie (Creator)

Samantha McDonald (Creator)

Gregory Pavela (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 compete\r\nfor calories (i.e., nutrient-energy). Axiomatically, cell-types with competitive advantages\r\nacquire a greater number of consumed calories, and when possible, increase in\r\nsize and/or number. Thus, it is logical and parsimonious to posit that obesity is the\r\ncompetitive advantages of fat-cells (adipocytes) driving a disproportionate acquisition\r\nand storage of nutrient-energy. Accordingly, we introduce two conceptual frameworks.\r\nAsymmetric Nutrient-Energy Partitioning describes the context-dependent, cell-specific\r\ncompetition for calories that determines the partitioning of nutrient-energy to oxidation,\r\nanabolism, and/or storage\; and Effective Caloric Intake which describes the number\r\nof calories available to constrain energy-intake via the inhibition of the sensorimotor\r\nappetitive cells in the liver and brain that govern ingestive behaviors. Inherent in\r\nthese frameworks is the independence and dissociation of the energetic demands\r\nof metabolism and the neuro-muscular pathways that initiate ingestive behaviors and\r\nenergy intake. As we demonstrate, if the sensorimotor cells suffer relative caloric\r\ndeprivation via asymmetric competition from other cell-types (e.g., skeletal muscle- or\r\nfat-cells), energy-intake is increased to compensate for both real and merely apparent\r\ndeficits in energy-homeostasis (i.e., true and false signals, respectively). Thus, we\r\nposit that the chronic positive energy balance (i.e., over-nutrition) that leads to obesity\r\nand metabolic diseases is engendered by apparent deficits (i.e., false signals) driven\r\nby the asymmetric inter-cellular competition for calories and concomitant differential\r\npartitioning of nutrient-energy to storage. These frameworks, in concert with our\r\nprevious theoretic work, the Maternal Resources Hypothesis, provide a parsimonious\r\nand rigorous explanation for the rapid rise in the global prevalence of increased body\r\nand fat mass, and associated metabolic dysfunctions in humans and other mammals\r\ninclusive of companion, domesticated, laboratory, and feral animals.

Additional Information

Publication

Other

Language: English

Date: 2023

Subjects

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

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