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Angiopoietin-like protein 8 (ANGPTL8) is associated with reduced HDL-cholesterol levels and may contribute to the development of dyslipidemia. Factors regulating ANGPTL8 expression remain poorly understood. Here we analyzed the relationship between miRNA-143-3p and ANGPTL8 in liver cells. Using target prediction algorithms, we identified a putative binding site for miR-143-3p in the ANGPTL8 3′ untranslated region (3’UTR). Exogenous miR-143-3p interacted with the ANGPTL8 3’UTR to downregulate its expression compared to scrambled sequence control. Transfection of HepG2 cells with miR-143-3p mimic or siRNA resulted in decreased or increased ANGPTL8 transcript and protein levels, respectively. Treatment of HepG2 cells with 30?mM glucose, 100?nM insulin, or 75?ng/ml lipopolysaccharide to mimic hyperglycemic, hyperinsulinemic, and proinflammatory conditions corresponded with increased miR-143-3p and ANGPTL8 levels. Inhibition of miR-143-3p amplified ANGPTL8 response to these treatments, suggesting that the miRNA acts to suppress ANGPTL8 expression under metabolically distorted conditions. These results, combined with growing evidence supporting a role for ANGPTL8 in the regulation of HDL-C metabolism, provide a better understanding of the molecular mechanisms underlying ANGPTL8 expression.



Hypertriglyceridemia, insulin resistance and hyperglycemia are risk factors for atherosclerosis in type 2 diabetes. Angiopoietin-like protein 8 (ANGPTL8) is a newly identified liver-derived hormone related to these risk factors. Hence, we aimed to explore the correlations between serum levels of ANGPTL8 and subclinical atherosclerosis in type 2 diabetes.


We measured serum ANGPTL8, blood lipids, blood glucose, common carotid artery Intima-Media Thickness (c-IMT) and calculated homeostasis model assessment of insulin resistance in (1) control subjects (n = 100), (2) type 2 diabetic patients without subclinical atherosclerosis (n = 100), and (3) type 2 diabetic patients with subclinical atherosclerosis (n = 100).


Serum levels of ANGPTL8 and triglyceride (TG) were significantly increased in type 2 diabetic patients with subclinical atherosclerosis as compared with type 2 diabetic patients without subclinical atherosclerosis and control subjects (P < 0.001). ANGPTL8 was positively associated with age, TG, diabetes duration, and c-IMT in type 2 diabetes. Logistic regression analysis revealed that ANGPTL8 had higher odds of having subclinical atherosclerosis [odds ratio (OR) 2.90, 95% confidence interval (CI) 1.48–5.70, P = 0.002] in type 2 diabetes. Mediation analysis indicated that TG acted as a partial mediator in the relationship between ANGPTL8 and c-IMT.


TG partially mediates the positive relationship between ANGPTL8 and c-IMT. Our data provide the first evidence for a strong link between ANGPTL8 and subclinical atherosclerosis, suggesting ANGPTL8 to be a new biomarker for subclinical atherosclerosis in type 2 diabetes.


ANGPTL8 Atherosclerosis Type 2 diabetes Triglyceride Insulin resistance Hyperglycemia



The aim of this study was to analyse the effect of pomegranate juice (POM) supplementation on the levels of selected pro-inflammatory cytokines, hepcidin and markers of iron metabolism in well-trained rowers.


The double-blind placebo-controlled study included 19 members of the Polish Rowing Team. The athletes were randomised into the supplemented group (n = 10), receiving 50 ml of standardised POM daily for two months, or the placebo group (n = 9). The subjects performed a 2000 m test on the rowing ergometer at the start of the project (baseline) and end of follow-up period. Blood samples from the antecubital vein were obtained three times during each trial: prior to the exercise, one minute after the test, and following a 24 h recovery.


The study documented the beneficial effect of supplementation with pomegranate fruit juice on TAC (P < 0.002). During the resting period, TAC level in the supplemented group was significantly higher than in the placebo group (x ± SD, 2.49 ± 0.39 vs. 1.88 ± 0.45, P < 0.05). The ergometric test conducted at baseline demonstrated a significant post-exercise increase in the concentrations of soluble transferrin receptors (P < 0.04), iron (P < 0.002) and IL-6 (P < 0.02), and to a significant post-exercise decrease in TAC. A significant increase in IL-6 concentration was also observed 24 h post-exercise. The exercise test conducted at the end of the follow-up period resulted in a significant decrease in TBIC and a significant increase in UIBC (P < 0.001), observed in both groups, both immediately post-exercise and after the resting period.


Supplementation with POM contributed to a significant strengthening of plasma antioxidant potential in the group of well-trained rowers, but had no effect on iron metabolism markers.


Despite the effectiveness of renin-angiotensin blockade in retarding diabetic nephropathy progression, a considerable number of patients still develop end-stage renal disease. The present investigation aims to evaluate the protective potential of FPS-ZM1, a selective inhibitor of receptor for advanced glycation end products (RAGE), alone and in combination with valsartan, an angiotensin receptor blocker, against glomerular injury parameters in streptozotocin-induced diabetic rats. FPS-ZM1 at 1 mg/kg (i.p.), valsartan at 100 mg/kg (p.o.), and their combination were administered for 4 weeks, starting 2 months after diabetes induction in rats. Tests for kidney function, glomerular filtration barrier, and podocyte slit diaphragm integrities were performed. Combined FPS-ZM1/valsartan attenuated diabetes-induced elevations in renal levels of RAGE and phosphorylated NF-κB p65 subunit. It ameliorated glomerular injury due to diabetes by increasing glomerular nephrin and synaptopodin expressions, mitigating renal integrin-linked kinase (ILK) levels, and lowering urinary albumin, collagen type IV, and podocin excretions. FPS-ZM1 also improved renal function as demonstrated by decreasing levels of serum cystatin C. Additionally, the combination also alleviated indices of renal inflammation as revealed by decreased renal monocyte chemoattractant protein 1 (MCP-1) and chemokine (C-X-C motif) ligand 12 (CXCL12) expressions, F4/80-positive macrophages, glomerular TUNEL-positive cells, and urinary alpha-1-acid glycoprotein (AGP) levels. These findings underline the benefits of FPS-ZM1 added to valsartan in alleviating renal glomerular injury evoked by diabetes in streptozotocin rats and suggest FPS-ZM1 as a new potential adjunct to the conventional renin-angiotensin blockade.

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

Posted by M. Kajta, A. Wnuk, J. Rzemieniec, et al. on 2018-08-23 20:09:42


Triclocarban is a phenyl ether that has recently been classified as a contaminant of emerging concern. Evidence shows that triclocarban is present in human tissues, but little is known about the impact of triclocarban on the nervous system, particularly at early developmental stages. This study demonstrated that triclocarban that was used at environmentally relevant concentrations induced apoptosis in mouse embryonic neurons, inhibited sumoylation, and changed the epigenetic status, as evidenced by impaired activities of HDAC, sirtuins, and DNMT, global DNA hypomethylation, and alterations of methylation levels of bax, bcl2, Ahr, and Car genes. The use of selective antagonists and specific siRNAs, which was followed by the co-localization of aryl hydrocarbon receptor (AHR) and constitutive androstane receptor (CAR) in mouse neurons, points to the involvement of AHR and CAR in triclocarban-induced neurotoxicity. A 24-h treatment with triclocarban enhanced protein levels of the receptors which was paralleled by Car hypomethylation and Ahr hypermethylation. Car hypomethylation is in line with global DNA hypomethylation and explains the increased mRNA and protein levels of CAR in response to triclocarban. Ahr hypermethylation could reflect reduced Ahr mRNA expression and corresponds to lowered protein levels after 3- and 6-h exposures to triclocarban that is likely related to proteasomal degradation of activated AHR. We hypothesize that the triclocarban-induced apoptosis in mouse neurons and the disruption of epigenetic status involve both AHR- and CAR-mediated effects, which may substantiate a fetal basis of the adult onset of neurological diseases; however, the expression of the receptors is regulated in different ways.

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