Exploration d'une anomalie lipidique

Résumé

L'exploration d'une anomalie lipidique (EAL) ou bilan lipidique est un examen biologique permettant de déterminer le profil lipidique d'un individu. Il porte sur les taux sanguins des lipides comme le cholestérol, le HDL, le LDL et les triglycérides. Usage Dosage de la concentration sanguine des lipoprotéines pour le dépistage ou le suivi des dyslipidémies. Méthode Le bilan lipidique se fait à partir d’une prise de sang à jeun depuis au moins 12h. Le prélèvement se fait traditionnellement sur tube sec pour permettre un dosage du sérum sanguin. Pour simplifier le prélèvement, en permettant d'autre dosages sanguins de routine sur le même échantillon, les fabricants de réactifs préconisent souvent l'usage d'un tube hépariné conduisant à un dosage du plasma. L’anticoagulant peut cependant influencer les résultats obtenus, en particulier en abaissant la cholestérolémie. Mesures Aspect du sérum C'est un examen visuel du sérum sanguin débarra

Source officielle

https://fr.wikipedia.org/wiki/Exploration_d'une_anomalie_lipidique

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Reduced ech-6 expression attenuates fat-induced lifespan shortening in C. elegans

Wen Gao, Richardus Houtkooper, Yan Liu

Deregulated energy homeostasis represents a hallmark of aging and results from complex gene-by-environment interactions. Here, we discovered that reducing the expression of the gene ech-6 encoding enoyl-CoA hydratase remitted fat diet-induced deleterious effects on lifespan in Caenorhabditis elegans, while a basal expression of ech-6 was important for survival under normal dietary conditions. Lipidomics revealed that supplementation of fat in ech-6-silenced worms had marginal effects on lipid profiles, suggesting an alternative fat utilization for energy production. Transcriptomics further suggest a causal relation between the lysosomal pathway, energy production, and the longevity effect conferred by the interaction between ech-6 and fat diets. Indeed, enhancing energy production from endogenous fat by overexpressing lysosomal lipase lipl-4 recapitulated the lifespan effects of fat diets on ech-6-silenced worms. Collectively, these results suggest that the gene ech-6 is potential modulator of metabolic flexibility and may be a target for promoting metabolic health and longevity.

NATURE PORTFOLIO2022

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Niacin: an old lipid drug in a new NAD(+) dress

Johan Auwerx, Dina Hofer, Elena Katsyuba, Mario Romani

Niacin, the first antidyslipidemic drug, has been at the center stage of lipid research for many decades before the discovery of statins. However, to date, despite its remarkable effects on lipid profiles, the clinical outcomes of niacin treatment on cardiac events is still debated. In addition to its historically well-defined interactions with central players of lipid metabolism, niacin can be processed by eukaryotic cells to synthesize a crucial cofactor, NAD(+). NAD(+) acts as a cofactor in key cellular processes, including oxidative phosphorylation, glycolysis, and DNA repair. More recently, evidence has emerged that NAD(+) also is an essential cosubstrate for the sirtuin family of protein deacylases and thereby has an impact on a wide range of cellular processes, most notably mitochondrial homeostasis, energy homeostasis, and lipid metabolism. NAD(+) achieves these remarkable effects through sirtuin-mediated deacetylation of key transcriptional regulators, such as peroxisome proliferator-activated receptor gamma coactivator 1-alpha, LXR, and SREBPs, that control these cellular processes. Here, we present an alternative point of view to explain niacin's mechanism of action, with a strong focus on the importance of how this old drug acts as a control switch of NAD(+)/sirtuin-mediated control of metabolism.

AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC2019

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Long noncoding RNA SNHG12 integrates a DNA-PK-mediated DNA damage response and vascular senescence

Johan Auwerx, Lei Chen, Norman Lionel Moullan

Long noncoding RNAs (lncRNAs) are emerging regulators of biological processes in the vessel wall; however, their role in atherosclerosis remains poorly defined. We used RNA sequencing to profile lncRNAs derived specifically from the aortic intima of Ldlr(-/-) mice on a high-cholesterol diet during lesion progression and regression phases. We found that the evolutionarily conserved lncRNA small nucleolar host gene-12 (SNHG12) is highly expressed in the vascular endothelium and decreases during lesion progression. SNHG12 knockdown accelerated atherosclerotic lesion formation by 2.4-fold in Ldlr(-/-) mice by increased DNA damage and senescence in the vascular endothelium, independent of effects on lipid profile or vessel wall inflammation. Conversely, intravenous delivery of SNHG12 protected the tunica intima from DNA damage and atherosclerosis. LncRNA pulldown in combination with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis showed that SNHG12 interacted with DNA-dependent protein kinase (DNA-PK), an important regulator of the DNA damage response. The absence of SNHG12 reduced the DNA-PK interaction with its binding partners Ku70 and Ku80, abrogating DNA damage repair. Moreover, the anti-DNA damage agent nicotinamide riboside (NR), a clinical-grade small-molecule activator of NAD(+), fully rescued the increases in lesional DNA damage, senescence, and atherosclerosis mediated by SNHG12 knockdown. SNHG12 expression was also reduced in pig and human atherosclerotic specimens and correlated inversely with DNA damage and senescent markers. These findings reveal a role for this lncRNA in regulating DNA damage repair in the vessel wall and may have implications for chronic vascular disease states and aging.

AMER ASSOC ADVANCEMENT SCIENCE2020

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