title: Ectopic fat deposition and global cardiometabolic risk: new paradigm in cardiovascular medicine.
abstract: The obesity epidemic is a global public health concern that increases the likelihood of morbidity and mortality of metabolic and cardiovascular disease (CVD) and threatens to reduce life expectancy around the world. The concept of the metabolic syndrome (MetS) takes into account that visceral fat plays an essential role in the development of metabolic and cardiovascular diseases. However, MetS cannot be used to assess global CVD risk but is at best one more modifiable CVD risk factor. Thus, global cardiometabolic risk (the global risk of cardiovascular disease resulting from traditional risk factors combined with the additional contribution of the metabolic syndrome and/or insulin resistance) should be considered individually. There is solid evidence supporting the notion that excess abdominal fat is predictive of insulin resistance and the presence of related metabolic abnormalities currently referred to as MetS. Despite the fact that abdominal obesity is a highly prevalent feature of MetS, the mechanisms by which abdominal obesity is causally related to MetS are not fully elucidated. Besides visceral fat accumulation, ectopic lipid deposition, especially in liver and skeletal muscle, has been implicated in the pathophysiology of diabetes, insulin resistance and obesity-related disorders. Also, ectopic fat deposition could be deteriorated in the heart components such as (1) circulatory and locally recruited fat, (2) intra- and extra-myocellular fat, (3) perivascular fat, and (4) pericardial fat. In this review, the contribution of ectopic lipid deposition to global cardiometabolic risk is reviewed and also discussed are potential underlying mechanisms including adipocytokine, insulin resistance and lipotoxicity.
authors.affiliation: Department of Cardio-Diabetes Medicine, the University of Tokushima Graduate School of Health Biosciences, Tokushima, Japan.
authors.forename: Michio
authors.initials: M
authors.lastname: Shimabukuro
authors.forename: Chisayo
authors.initials: C
authors.lastname: Kozuka
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Taira
authors.forename: Koichi
authors.initials: K
authors.lastname: Yabiku
authors.forename: Munkhbaatar
authors.initials: M
authors.lastname: Dagvasumberel
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Ishida
authors.forename: Sachiko
authors.initials: S
authors.lastname: Matsumoto
authors.forename: Shusuke
authors.initials: S
authors.lastname: Yagi
authors.forename: Daiju
authors.initials: D
authors.lastname: Fukuda
authors.forename: Ken
authors.initials: K
authors.lastname: Yamakawa
authors.forename: Moritake
authors.initials: M
authors.lastname: Higa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Soeki
authors.forename: Hisashi
authors.initials: H
authors.lastname: Yoshida
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Masuzaki
authors.forename: Masataka
authors.initials: M
authors.lastname: Sata
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000188:drug therapy / Q000209:etiology*; D003327:Coronary Disease / Q000209:etiology; D006801:Humans; D007333:Insulin Resistance; D050356:Lipid Metabolism; D024821:Metabolic Syndrome / Q000150:complications*; D012307:Risk Factors