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Metabolic dysfunction has reemerged as an essential hallmark of tumorigenesis, and metabolic phenotypes are increasingly being integrated into pre-clinical models of disease.
As a mechanism of sorafenib-induced liver injury, metabolic dysfunction has been reported [9].
The potentially central role of preadipocytes in genesis of fat tissue inflammation and metabolic dysfunction has not received much attention.
Notably, the effect of obesity on the stomach tissue and the role of the stomach in metabolic dysfunction has been largely overlooked.
Metabolic dysfunction has been implicated in a wide variety of human diseases such as obesity, diabetes, inborn errors of metabolism, neurodegenerative diseases, and cancer.
Because the muscle of patients with T2DM contain ~30% fewer mitochondria than those with normal insulin sensitivity (He et al., 2001; Kelley et al., 2002), the notion that 'mitochondrial deficiency' is causally linked to metabolic dysfunction has become popular.
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Negative, interlinked consequences of prolonged stress, inflammation and metabolic dysfunction have been well-documented in mammalian models [ 72, 73].
Likewise, therapies aimed at managing the symptoms of metabolic dysfunction have shown limited efficacy in slowing the progression of diabetic retinopathy; diabetic complications develop in ∼20% of patients under strict glycemic or blood-pressure control (Antonetti et al., 2012).
Poor development of the outer muscle layer, atherosclerosis and metabolic dysfunction have been related to under-dimensioned hearts and reduced cardiac function in Atlantic salmon aquaculture, consequently resulting in increased mortality [ 16].
Several pathways, in particular related to metabolic dysfunctions, have been proposed to explain the progressive liver pathologies associated with obesity.
Studies of OCN levels in patients with metabolic dysfunctions have revealed a close correlation with perturbed OCN levels [ 1, 2].
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