Excess of free fatty acids as a cause of metabolic dysfunction in skeletal muscle

Title:

Excess of free fatty acids as a cause of metabolic dysfunction in skeletal muscle

Creator:

Jana Tůmová, Michal Anděl, and Jan Trnka

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f4e6c962-2dd4-46e2-b4b4-597559c0cd45
uuid:f4e6c962-2dd4-46e2-b4b4-597559c0cd45
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, obezita, inzulinová rezistence, obesity, insulin resistance, free fatty acids, skeletal muscle, mitochondrial function, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Obesity is often associated with metabolic impairments in peripheral tissues. Evidence suggests an excess of free fatty acids (FFA) as one factor linking obesity and related pathological conditions and the impact of FFA overload on skeletal muscle metabolism is described herein. Obesity is associated with dysfunctional adipose tissue unable to buffer the flux of dietary lipids. Resulting increased levels and fluxes of plasma FFA lead to ectopic lipid deposition and lipotoxicity. FFA accumulated in skeletal muscle are associated with insulin resistance and overall cellular dysfunction. Mechanisms supposed to be involved in these conditions include the Randle cycle, intracellular accumulation of lipid metabolites, inflammation and mitochondrial dysfunction or mitochondrial stress. These mechanisms are described and discussed in the view of current experimental evidence with an emphasis on conflicting theories of decreased vs. increased mitochondrial fat oxidation associated with lipid overload. Since different types of FFA may induce diverse metabolic responses in skeletal muscle cells, this review also focuses on cellular mechanisms underlying the different action of saturated and unsaturated FFA., J. Tumova, M. Andel, J. Trnka., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:2

Harvested from:

CDK

Metadata only:

false