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Destabilization of atherosclerotic plaque by bilirubin deficiency

ABSTRACT: The rupture of atherosclerotic plaque contributes significantly to cardiovascular disease (CVD). Plasma concentrations of bilirubin, a by-product of heme catabolism, inversely associate with risk of CVD, although the link between bilirubin and atherosclerosis remains unclear.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Roland Stocker

PROVIDER: PXD040314 | JPOST Repository | Thu Feb 22 00:00:00 GMT 2024

REPOSITORIES: jPOST

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			Action	DRS
	Px_07.wiff	Wiff
	Px_07.wiff.scan	Wiff
	Px_08.wiff	Wiff
	Px_08.wiff.scan	Wiff
	Px_09.wiff	Wiff

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Project description:We evaluated the potential importance of adipose tissue (AT) oxygenation on AT biology and insulin sensitivity in people. AT oxygen partial pressure (pO2), branched chain amino acid (BCAA) catabolism and marker of inflammation were determined in three groups stratified by adiposity and insulin sensitivity: 1) metabolically-healthy lean (MHL); 2) metabolically-healthy obese (MHO); and 3) metabolically-unhealthy obese (MUO). AT pO2 progressively declined from the MHL to the MHO to the MUO group, and was positively associated with hepatic and whole-body insulin sensitivity. AT pO2 was positively associated with AT expression of genes involved in BCAA catabolism and negatively associated with plasma BCAA concentrations. Although AT pO2 was negatively associated with AT markers of inflammation, it was not associated with plasma adipokine concentrations. These results support the notion that reduced AT pO2 in people with obesity contributes to insulin resistance by decreasing AT BCAA catabolism and thereby increasing plasma BCAA concentrations.

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