Abstract
Session presented on: Tuesday, July 23, 2013:
Purpose: Obesity is recognized as a global health problem. The calories in-calories out paradigm of obesity has been only marginally successful in preventing or treating obesity, and fails to explain why some people overeat or under-exercise. The purpose of the research was to identify and organize a new conceptual model of factors associated with the development and progression of obesity based on the pathophysiological bases for these associations.
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.
Sigma Membership
Iota Mu
Type
Presentation
Format Type
Text-based Document
Study Design/Type
N/A
Research Approach
N/A
Keywords:
Nursing Research, Obesity, Pathophysiology
Recommended Citation
Rogge, Mary Madeline, "Pathways to obesity: Implications of a shifting obesity paradigm for nursing research" (2013). INRC (Congress). 86.
https://www.sigmarepository.org/inrc/2013/presentations_2013/86
Conference Name
24th International Nursing Research Congress
Conference Host
Sigma Theta Tau International
Conference Location
Prague, Czech Republic
Conference Year
2013
Rights Holder
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Acquisition
Proxy-submission
Pathways to obesity: Implications of a shifting obesity paradigm for nursing research
Prague, Czech Republic
Session presented on: Tuesday, July 23, 2013:
Purpose: Obesity is recognized as a global health problem. The calories in-calories out paradigm of obesity has been only marginally successful in preventing or treating obesity, and fails to explain why some people overeat or under-exercise. The purpose of the research was to identify and organize a new conceptual model of factors associated with the development and progression of obesity based on the pathophysiological bases for these associations.
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.
