triglyceride/hypoxia

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Positive cross-talk between hypoxia inducible factor-1α and liver X receptor α induces formation of triglyceride-loaded foam cells.

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OBJECTIVE Atherosclerosis is a chronic and progressive inflammatory disease of the arteries that is characterized by subendothelial accumulation of lipid-rich macrophages, called foam cells. We sought to identify the molecular details of cross-talk between liver X receptor α (LXRα) and

[Effect of perinatal hypoxia on blood triglycerides and total cholesterol including high density lipoproteins].

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Cholesterol, low/high density lipoprotein cholesterol (LDLc, HDLc), triglycerides and phospholipids plasma concentrations were measured in arterial (UA) and venous (UV) cord blood samples collected at birth in 22 healthy newborn infants (G-I) in 24 intrapartum stressed newborn infants (G-II) and in

Myocardial triglycerides increased by fasting. Effects of hypoxia on contractility and enzymatic release.

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The effect of fasting on the mechanics of contraction was studied in the isolated perfused rat heart, in oxygenated and hypoxic conditions. Animals were subjected to 48 h of fasting, a condition which produces augmented endogenous triglycerides (TG). Normal and fasted rats were submitted to a 10-min

Hypoxia worsens the impact of intracellular triglyceride accumulation promoted by electronegative low-density lipoprotein in cardiomyocytes by impairing perilipin 5 upregulation.

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Plasma lipoproteins are a source of lipids for the heart, and the proportion of electronegative low density lipoprotein [LDL(-)] is elevated in cardiometabolic diseases. Perilipin 5 (Plin5) is a crucial protein for lipid droplet management in the heart. Our aim was to assess the effect of LDL(-) on

[Effects of hypobaric hypoxia and erucic acid on mitochondrial triglycerides in rat heart].

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At normal atmospheric pressure, an erucic acid-supplemented diet produces an increase of heart mitochondrial triglycerides. With the same quantity of erucic acid, hypoxia emphasizes the triglyceride overload in rat heart mitochondria. Thus, hypoxia increases the risk caused by rapeseed-oil. In

Modest hypoxia significantly reduces triglyceride content and lipid droplet size in 3T3-L1 adipocytes.

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BACKGROUND A previous study has demonstrated that endurance training under hypoxia results in a greater reduction in body fat mass compared to exercise under normoxia. However, the cellular and molecular mechanisms that underlie this hypoxia-mediated reduction in fat mass remain uncertain. Here, we

Transient hypoxia reprograms differentiating adipocytes for enhanced insulin sensitivity and triglyceride accumulation.

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OBJECTIVE To investigate the impact of transient (2-4 h) hypoxia on metabolic reprogramming of adipocytes. METHODS The impact of transient hypoxia on metabolic reprogramming was investigated in 3T3-L1 cells before and after differentiation. Glucose uptake, fatty acid oxidation, lipolysis and

Hypoxia-inducible lipid droplet-associated protein inhibits adipose triglyceride lipase.

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Elaborate control mechanisms of intracellular triacylglycerol (TAG) breakdown are critically involved in the maintenance of energy homeostasis. Hypoxia-inducible lipid droplet-associated protein (HILPDA)/hypoxia-inducible gene-2 (Hig-2) has been shown to affect intracellular TAG levels, yet, the

The Lipid Droplet Protein Hypoxia-inducible Gene 2 Promotes Hepatic Triglyceride Deposition by Inhibiting Lipolysis.

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The liver is a major site of glucose, fatty acid, and triglyceride (TG) synthesis and serves as a major regulator of whole body nutrient homeostasis. Chronic exposure of humans or rodents to high-calorie diets promotes non-alcoholic fatty liver disease, characterized by neutral lipid accumulation in

Effect of chronic intermittent hypoxia on triglyceride uptake in different tissues.

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Chronic intermittent hypoxia (CIH) inhibits plasma lipoprotein clearance and adipose lipoprotein lipase (LPL) activity in association with upregulation of an LPL inhibitor angiopoietin-like protein 4 (Angptl4). We hypothesize that CIH inhibits triglyceride (TG) uptake via Angptl4 and that an

No effect of acute normobaric hypoxia on plasma triglyceride levels in fasting healthy men.

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Circulating fatty acids are a major systemic energy source in the fasting state as well as a determinant of hepatic triglycerides (TG)-rich very-low-density lipoprotein production. Upon acute hypoxia, sympathetic arousal induces adipose tissue lipolysis, resulting in an increase in circulating

The Effect of Acute Continuous Hypoxia on Triglyceride Levels in Constantly Fed Healthy Men.

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Elevated plasma triglyceride (TG) concentrations are an important contributor to deleterious metabolic alterations. Evidence in animals suggest that acute exposure to an environment with reduced oxygen inhibits plasma TG clearance and causes important rise in plasma TG, especially in

Intermittent hypoxia inhibits clearance of triglyceride-rich lipoproteins and inactivates adipose lipoprotein lipase in a mouse model of sleep apnoea.

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Identifikohuni Regjistrohu

OBJECTIVE Delayed lipoprotein clearance is associated with atherosclerosis. This study examined whether chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnoea (OSA), can lead to hyperlipidaemia by inhibiting clearance of triglyceride rich lipoproteins (TRLP). RESULTS Male

Hypoxia-inducible lipid droplet-associated (HILPDA) is a novel peroxisome proliferator-activated receptor (PPAR) target involved in hepatic triglyceride secretion.

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Peroxisome proliferator-activated receptors (PPARs) play major roles in the regulation of hepatic lipid metabolism through the control of numerous genes involved in processes such as lipid uptake and fatty acid oxidation. Here we identify hypoxia-inducible lipid droplet-associated (Hilpda/Hig2) as a

Hypoxia causes triglyceride accumulation by HIF-1-mediated stimulation of lipin 1 expression.

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Identifikohuni Regjistrohu

Adaptation to hypoxia involves hypoxia-inducible transcription factors (HIFs) and requires reprogramming of cellular metabolism that is essential during both physiological and pathological processes. In contrast to the established role of HIF-1 in glucose metabolism, the involvement of HIFs and the

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