Open AccessExtension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine‐disrupting chemicals and biophysical laws
Author(s) -
Lee Hong Kyu,
Shim Eun Bo
Publication year - 2013
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/jdi.12048
Subject(s) - hypertriglyceridemia , metabolic syndrome , medicine , endocrine system , mitochondrion , diabetes mellitus , endothelial dysfunction , mechanism (biology) , bioinformatics , endocrinology , biology , microbiology and biotechnology , cholesterol , philosophy , triglyceride , epistemology , hormone
Metabolic syndrome and its component phenotypes, hyperglycemia, hypertension, (abdominal) obesity and hypertriglyceridemia, are major risk factors for atherosclerosis. Recently, associations between exposure to endocrine‐disrupting chemicals ( EDC s), mitochondrial dysfunction, metabolic syndrome and atherosclerosis have been established, suggesting a possible common mechanism underlying these phenomena. Extending a previously proposed mitochondria dysfunction theory of metabolic syndrome and using biophysical laws, such as metabolic scaling, Murray's law and fractal geometry of the vascular branching system, we propose that atherosclerosis could be explained as an ill‐adaptive change occurring in nutrient‐supplying arteries in response to the decreasing tissue energy demand caused by tissue mitochondrial dysfunction. Various aspects of this new hypothesis are discussed.