Type 2 diabetes mellitus (DM) is a complicated metabolic disorder with no definite treatment. Different species of the genus Tamarix (tamarisk) are used by local people to treat DM. Tamarix stricta Boiss. is an endemic species to Iran with several traditional therapeutic uses in Persian Medicine. This study aimed to assess the antidiabetic activity of T. stricta.

Hydroethanolic extract of the plant was prepared and analyzed by High-performance liquid chromatography (HPLC). The protective effect of the extract was evaluated in streptozotocin (STZ)-induced toxicity and markers of autophagy in pancreatic RIN-5F cells. The effect of intragastric 10 or 20mg/kg of the extract was compared with negative control (water) or positive control (metformin) treatment during four weeks of administration in high-fat diet+STZ-induced DM in Balb/c mice.

Results showed the presence of 8.436mg of gallic acid in each gram of the extract. A significant cytoprotective effect was observed by T. stricta in STZ-induced toxicity in RIN-5F cells, partially due to the modulation of autophagy. Also, animals treated with the extract showed a significant improvement in glycemic and lipid profiles, liver function, and histopathologic features of pancreas and liver compared with the negative control.

T. stricta demonstrated beneficial effects in animal model of DM; though, further studies are recommended to confirm the clinical use of this plant in DM.

T. stricta demonstrated beneficial effects in animal model of DM; though, further studies are recommended to confirm the clinical use of this plant in DM.Cumulative evidence indicates that excessive consumption of calories from saturated fat contributes to the development of Alzheimer’s disease (AD). Here, we assess the triggering and progression of AD pathology induced by a high-fat diet (HFD), and the effects of resveratrol, a polyphenol found in common dietary sources with pleiotropic neuroprotective activities. Over 16 weeks, male wild type (WT) and AD transgenic 5XFAD mice were fed a control diet, HFD (60% kcal from fat), or HFD supplemented with 0.1% resveratrol. Resveratrol protected against HFD-induced memory loss in WT mice and prevented memory loss in 5XFAD mice. Resveratrol also reduced the amyloid burden aggravated by HFD in 5XFAD, and protected against HFD-induced tau pathology in both WT and 5XFAD strains. At the mechanistic level, resveratrol inhibited the HFD-increased amyloidogenic processing of the amyloid precursor protein in both strains; it also restored abnormal high levels in the proteolytic activity of the ubiquitin-proteasome system induced by HFD, suggesting the presence of a compensatory mechanism to counteract the accumulation of aberrant proteins. Thus, our data suggest that resveratrol can correct the harmful effects of HFD in the brain and may be a potential therapeutic agent against obesity-related disorders and AD pathology.Scavenger receptor BI (SR-BI) has been suggested to modulate adipocyte function. To uncover the potential relevance of SR-BI for the development of obesity and associated metabolic complications, we compared the metabolic phenotype of wild-type and SR-BI deficient mice fed an obesogenic diet enriched in fat. check details Both male and female SR-BI knockout mice gained significantly more weight as compared to their wild-type counterparts in response to 12 weeks high fat diet feeding (1.5-fold; P less then .01 for genotype). Plasma free cholesterol levels were ~2-fold higher (P less then .001) in SR-BI knockout mice of both genders, whilst plasma cholesteryl ester and triglyceride concentrations were only significantly elevated in males. Strikingly, the exacerbated obesity in SR-BI knockout mice was paralleled by a better glucose handling. In contrast, only SR-BI knockout mice developed atherosclerotic lesions in the aortic root, with a higher predisposition in females. Biochemical and histological studies in male mice revealed that SR-BI deficiency was associated with a reduced hepatic steatosis degree as evident from the 29% lower (P less then .05) liver triglyceride levels. Relative mRNA expression levels of the glucose uptake transporter GLUT4 were increased (+47%; P less then .05), whilst expression levels of the metabolic PPARgamma target genes CD36, HSL, ADIPOQ and ATGL were reduced 39%-58% (P less then .01) in the context of unchanged PPARgamma expression levels in SR-BI knockout gonadal white adipose tissue. In conclusion, we have shown that SR-BI deficiency is associated with a decrease in adipocyte PPARgamma activity and a concomitant uncoupling of obesity development from hepatic steatosis and glucose intolerance development in high fat diet-fed mice.Nutrient starvation and inactivation of target of rapamycin complex 1 (TORC1) protein kinase elicits nucleophagy degrading nucleolar proteins in budding yeast. After TORC1 inactivation, nucleolar proteins are relocated to sites proximal to the nucleus-vacuole junction (NVJ), where micronucleophagy occurs, whereas ribosomal DNA (rDNA encoding rRNA) escapes from the NVJ. Condensin-mediated rDNA condensation promotes the repositioning and nucleophagic degradation of nucleolar proteins. However, the molecular mechanism of TORC1 inactivation-induced chromosome condensation is still unknown. Here, we show that Cdc14 protein phosphatase and topoisomerase II (Topo II), which are engaged in rDNA condensation in mitosis, facilitate rDNA condensation after TORC1 inactivation. rDNA condensation after rapamycin treatment was compromised in cdc14-1 and top2-4 mutants. In addition, the repositioning of rDNA and nucleolar proteins and nucleophagic degradation of nucleolar proteins were impeded in these mutants. Furthermore, Cdc14 and Topo II were required for the survival of quiescent cells in prolonged nutrient-starved conditions. This study reveals that these factors are critical for starvation responses.Gliomas are the most frequent tumors of the central nervous system (CNS) and include the highly malignant glioblastoma (GBM). Characteristically, gliomas have translational control deregulation related to overactivation of signaling pathways such as PI3K/AKT/mTORC1 and Ras/ERK1/2. Thus, mRNA translation appears to play a dominant role in glioma gene expression patterns. The, analysis of genome-wide translated transcripts, together known as the translatome, may reveal important information for understanding gene expression patterns in gliomas. This review provides a brief overview of translational control mechanisms altered in gliomas with a focus on the current knowledge related to the translatomes of glioma cells and murine glioma models. We present an integrative meta-analysis of selected glioma translatome data with the aim of identifying recurrent patterns of gene expression preferentially regulated at the level of translation and obtaining clues regarding the pathological significance of these alterations.