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Learning Objective 1: The learner will learn at least three involuntary pathways capable of disrupting energy intake, storage, and expenditure and promoting obesity.
Learning Objective 2: The learner will be able to discuss at least two emerging areas of nursing research into obesity based on the Pathways to Obesity Model.
Methods: Theory synthesis was utilized to organize research findings of adipogenic factors into a model of obesity pathophysiology. A literature review based on search terms “obesity etiology,” “obesity pathophysiology,” and “adipogenesis” was conducted to identify defects in energy homeostasis which may account for excess fat accumulation.
Results: Three pathways were identified by which energy homeostasis may be involuntarily disrupted through genetic and epigenetic influences. Adipose cell dysfunction includes excess adipose cell proliferation due to activation of gene transcription factors (thiazolidinediones, adenovirus-36, fatty acids), and impaired fatty acid liberation and thermogenesis due to beta-adrenergic receptor polymorphisms, and decreased brown fat mass. Neuroendocrine hunger and satiety pathways may be disrupted due to factors including hyperinsulinemia, melanocortin receptor polymorphisms and anti-melanocortin receptor autoantibodies, stress, sleep deprivation, and medications (antihistamines, antipsychotic drugs). Mitochondrial impairment in converting food substrates into cellular energy may result from impaired beta-oxidation of fatty acids, disruption of the tricarboxcylic acid cycle by medications (certain beta adrenergic blockers, tricyclic antidepressants), and environmental exposures (atrazine, dioxin, persistent organic pollutants). The Pathways to Obesity Model was constructed to show the inter-relationships between these patterns of obesity etiology.
Conclusion: The model provides a new framework for assessing patients and for designing and researching different approaches to obesity prevention and management based on the underlying etiology and pathophysiology.