Finally, we noted a higher density of RANKL positive cells in plaques from diabetic patients as compared to non-diabetic ones and a significant positive association between hypertriglyceridemia and BMP-4 expression.
In addition, the splicing of the β-oxidation enzyme, CPT1, was altered in the SF2-RNAi flies potentially promoting the increased triglycerides in these animals.
Deficiency of hepatic Nogo-B receptor (NgBR) expression activates liver X receptor α (LXRα) in an adenosine monophosphate-activated protein kinase α (AMPKα)-dependent manner, thereby inducing severe hepatic lipid accumulation and hypertriglyceridemia.
Furthermore, curcumin repressed the capacity of risperidone to induce the hepatic over expression of enzymes involved in lipid metabolism (LXRα, FAS, ACC1, LPL, PPARγ, ACO, SREBP2) and decreased risperidone-induced glucose intolerance and hypertriglyceridemia.
Systemic administration of STC2 recombinant protein or adenovirus-mediated overexpression of STC2 markedly attenuated hepatosteatosis and hypertriglyceridemia in obese mice.
We enrolled 14 patients with type 2 diabetes and hypertriglyceridemia treated with statins and dipeptidyl peptidase-4 inhibitors with glycated hemoglobin (HbA1c) < 8.0%, LDL-C < 120 mg/dL, and fasting triglyceride ≥150 mg/dL.
This study provides evidence for a role of RTN3 in inducing obesity and triglyceride accumulation and suggests that inhibiting the expression of RTN3 in fat tissue may be a novel therapeutic approach to treat obesity and hypertriglyceridemia.
Deficiency of hepatic Nogo-B receptor (NgBR) expression activates liver X receptor α (LXRα) in an adenosine monophosphate-activated protein kinase α (AMPKα)-dependent manner, thereby inducing severe hepatic lipid accumulation and hypertriglyceridemia.
In multivariate prediction, control subjects with AT1R 1166AC or CC genotype had a higher risk for high triglycerides compared to the AA genotype carriers.
After wholemeal pasta, glucose, triglyceride increased and GLP-1 responses were not different compared to control pasta but insulin response at 30 min (p<0.05) and ghrelin at 60 min (p=0.03) were lower and PYY levels higher (AUC=+44%, p=0.001).
Deficiency of hepatic Nogo-B receptor (NgBR) expression activates liver X receptor α (LXRα) in an adenosine monophosphate-activated protein kinase α (AMPKα)-dependent manner, thereby inducing severe hepatic lipid accumulation and hypertriglyceridemia.
Methods and Results: The clinical examination displayed that miR-377 expression was markedly lower in plasma from patients with hypertriglyceridemia compared with non-hypertriglyceridemic subjects.
Similarly, the highest TTR and HOMA-IR tertiles had greater risk of hypertriglyceridemia at 3.5 (95% CI = 1.30-9.20, p = 0.01) and 3.6 (95% CI = 1.33-9.58, p = 0.01) times higher than the respective lowest tertiles.
Increased IL-13 was extraordinarily well associated with hyperglycemia (<i>r</i> = 0.7362) and hypertriglyceridemia (<i>r</i> = 0.7632) but unexpectedly exhibited no significant correlations with TNF-<i>α</i> (<i>r</i> = 0.2907), IL-10 (<i>r</i> = -0.3882), Mon-CD11c<sup>+</sup>CD206<sup>-</sup> (<i>r</i> = 0.2745) or Mon-CD11c<sup>-</sup>CD206<sup>+</sup> (<i>r</i> = -0.3237).
Angiopoietin-like protein 8(ANGPTL8) and apolipoprotein CIII (apoCIII) were found to inhibit the activity of lipoprotein lipase (LPL) and disrupt the clearance of triglyceride-rich lipoproteins (TRLs), leading to hypertriglyceridemia.
Untargeted analysis of lipid metabolites demonstrated a distinguishable profile in MeCP2-e1 female mutant liver characterized by increased triglycerides.