[1] would have detected all molecular sizes of vWF, without diffe

[1] would have detected all molecular sizes of vWF, without differentiating between them. It would be interesting to analyze whether ULvWF multimers and ADAMTS13 also have prognostic significance in these patients. CHUNDAMANNIL E. EAPEN, M.D., D.M.1 JOSHUA E. ELIAS, B.SC., M.B.CH.B.2 IAN MACKIE, B.SC., PH.D., FRCPATH3 ELWYN ELIAS, B.SC., M.D., FRCP4 “
“We read with great interest a recent article published in this journal by Tsuchiya et al.[1] In this study the authors investigated all-trans-retinoic acid (ATRA) effects in different mouse models to explore its anti-insulin resistance

activities and inspected mechanisms engaged in this condition and associated hepato-metabolic disorders. Tsuchiya et al.[1] found that ATRA improved insulin sensitivity and activated the leptin signaling pathway in C57BL/6J mice fed a high-fat, high-fructose (HFHFr) diet and in genetically insulin resistant KK-Ay mice. Furthermore, ATRA selleck chemicals llc retrieved metabolic derangements in both models, counteracting liver steatosis and ballooning in HFHFr animals. The authors suggested a possible interaction between the leptin-mediated

pathway and retinoic acid receptor (RAR)-mediated transcriptional regulation to explain ATRA-dependent insulin sensitivity improvement. However, the role of the RAR/leptin network in regulating the antisteatotic effect of ATRA remains to be verified. We recently reported that high fructose-enriched diets may promote phosphatase and tensin homolog (PTEN) phosphorylation/inactivation inducing nonalcoholic fatty liver disease (NAFLD).[2] Therefore, we hypothesized that retinoids might GSK3235025 ic50 have a positive effect on liver steatosis affecting PTEN signaling, a complex PI3K/AKT regulatory pathway involved in the control of hepatic glucose and lipid metabolism.[3, 4] The role of PTEN in mediating the antisteatotic effect of ATRA is supported by medchemexpress our preliminary data. We studied the effect of ATRA in an in vitro model of hepatic steatosis using HepG2 cells supplemented with combined oleic acid (OA) and palmitic acid (PA) (molar ratio 2:1) at 1 mM final concentration. As shown

in Fig. 1A, after 24 hours OA/PA supplementation induced an increase of intracellular lipid accumulation that was significantly reduced by treatment with 5 μM ATRA for 5 hours. Moreover, neither OA/PA nor ATRA treatments influenced cell viability (Fig. 1B). Importantly, ATRA reduced fatty acid-dependent PTEN phosphorylation/inactivation (Fig. 1C). All these findings suggest that retinoids are potential appropriate therapeutic agents to resolve both metabolic alterations and liver-damage triggered by genetically or a diet-induced insulin resistant state. Tsuchiya et al.[1] demonstrated that the leptin pathway may be crucial for the anti-insulin resistance action of ATRA, and we proposed PTEN as a mediator of its antisteatotic effect.

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