Pathways to Obesity: Implications of a Taxonomy of Obesity Pathophysiology for Nursing Research and Practice

2.50
Hdl Handle:
http://hdl.handle.net/10755/308440
Category:
Abstract
Type:
Presentation
Title:
Pathways to Obesity: Implications of a Taxonomy of Obesity Pathophysiology for Nursing Research and Practice
Author(s):
Rogge, Mary Madeline
Lead Author STTI Affiliation:
Iota Mu
Author Details:
Mary Madeline Rogge, PhD, RN, FNP, BC, mary.rogge@ttuhsc.edu
Abstract:

Session presented on: Monday, November 18, 2013

Purpose:  The calories in-calories out (gluttony and sloth) paradigm of obesity, has been only marginally effective in preventing or managing this global health problem, 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 excess adipose accumulation.

Methods:  Theory synthesis was utilized to organize research findings of adipogenic factors into a taxonomy of obesity pathophysiology.   A literature review based on search terms “obesity etiology,” “obesity pathophysiology,” and “adipogenesis” was conducted to identify defects in energy homeostasis associated with excess fat accumulation.

Results:  Four pathways were identified by which energy homeostasis can 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), impaired fatty acid thermogenesis due to beta-adrenergic receptor polymorphisms, and decreased brown fat mass.  Neuroendocrine hunger and satiety pathways can be disrupted due to factors including hyperinsulinemia, melanocortin receptor polymorphisms and anti-melanocortin receptor autoantibodies, sleep deprivation, and common medications.  Impaired mitochondrial conversion of food substrates into cellular energy may involve impaired beta-oxidation of fatty acids, disruption of the tricarboxcylic acid cycle by medications and environmental exposures (beta adrenergic blockers, atrazine, dioxin, persistent organic pollutants).  Chronic inflammation (gastrointestinal flora, high fat diet) has been shown to promote adipogenesis through lipopolysaccharide activation of nuclear factor kappa-B (NF-kB) and toll-like receptors in macrophages and adipocytes. 

Conclusion:   The Pathways to Obesity Model was constructed to show the inter-relationships between these patterns of obesity pathophysiology.  The model provides a new taxonomy for a multi-pronged approach to assessing obese patients and new avenues for investigating targeted interventions to prevent and manage the disease.

Keywords:
adipogenesis; pathophysiology; obesity
Repository Posting Date:
19-Dec-2013
Date of Publication:
19-Dec-2013
Conference Date:
2013
Conference Name:
42nd Biennial Convention
Conference Host:
Sigma Theta Tau International, the Honor Society of Nursing
Conference Location:
Indianapolis, Indiana, USA
Description:
42nd Biennial Convention 2013 Theme: Give Back to Move Forward. Held at the JW Marriott

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_GB
dc.type.categoryAbstracten_GB
dc.typePresentationen_GB
dc.titlePathways to Obesity: Implications of a Taxonomy of Obesity Pathophysiology for Nursing Research and Practiceen_GB
dc.contributor.authorRogge, Mary Madelineen_GB
dc.contributor.departmentIota Muen_GB
dc.author.detailsMary Madeline Rogge, PhD, RN, FNP, BC, mary.rogge@ttuhsc.eduen_GB
dc.identifier.urihttp://hdl.handle.net/10755/308440-
dc.description.abstract<p>Session presented on: Monday, November 18, 2013</p><b>Purpose:  </b>The calories in-calories out (gluttony and sloth) paradigm of obesity, has been only marginally effective in preventing or managing this global health problem, 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 excess adipose accumulation. <p><b>Methods: </b> Theory synthesis was utilized to organize research findings of adipogenic factors into a taxonomy of obesity pathophysiology.   A literature review based on search terms “obesity etiology,” “obesity pathophysiology,” and “adipogenesis” was conducted to identify defects in energy homeostasis associated with excess fat accumulation. <p><b>Results:</b>  Four pathways were identified by which energy homeostasis can 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), impaired fatty acid thermogenesis due to beta-adrenergic receptor polymorphisms, and decreased brown fat mass.  Neuroendocrine hunger and satiety pathways can be disrupted due to factors including hyperinsulinemia, melanocortin receptor polymorphisms and anti-melanocortin receptor autoantibodies, sleep deprivation, and common medications.  Impaired mitochondrial conversion of food substrates into cellular energy may involve impaired beta-oxidation of fatty acids, disruption of the tricarboxcylic acid cycle by medications and environmental exposures (beta adrenergic blockers, atrazine, dioxin, persistent organic pollutants).  Chronic inflammation (gastrointestinal flora, high fat diet) has been shown to promote adipogenesis through lipopolysaccharide activation of nuclear factor kappa-B (NF-kB) and toll-like receptors in macrophages and adipocytes.  <p><b>Conclusion:</b>   The Pathways to Obesity Model was constructed to show the inter-relationships between these patterns of obesity pathophysiology.  The model provides a new taxonomy for a multi-pronged approach to assessing obese patients and new avenues for investigating targeted interventions to prevent and manage the disease.en_GB
dc.subjectadipogenesisen_GB
dc.subjectpathophysiologyen_GB
dc.subjectobesityen_GB
dc.date.available2013-12-19T17:31:23Z-
dc.date.issued2013-12-19-
dc.date.accessioned2013-12-19T17:31:23Z-
dc.conference.date2013en_GB
dc.conference.name42nd Biennial Conventionen_GB
dc.conference.hostSigma Theta Tau International, the Honor Society of Nursingen_GB
dc.conference.locationIndianapolis, Indiana, USAen_GB
dc.description42nd Biennial Convention 2013 Theme: Give Back to Move Forward. Held at the JW Marriotten_GB
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