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Bacitracin Attenuates Hemolysis-Induced Insulin Degradation during Insulin Sensitivity Testing: Repurposing an Old Drug for Use in Metabolic Research.Hemolysis of serially-collected insulin serum samples frequently causes falsely-low measured concentrations due to release of intracellular insulin degrading enzyme (IDE). We investigated if bacitracin, an in vitro IDE inhibitor, could prevent hemolysis-induced insulin degradation during insulin sensitivity testing.
1401 related Products with: Bacitracin Attenuates Hemolysis-Induced Insulin Degradation during Insulin Sensitivity Testing: Repurposing an Old Drug for Use in Metabolic Research.Rabbit Anti-Insulin Recep Mouse Anti-Insulin(1D4 ) Rat monoclonal anti mouse Rabbit Anti-Insulin Recep Mouse Anti-Insulin(1D4 ) Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Polyc Rabbit Anti-Insulin Polyc Mouse Anti-Insulin(1G11) Rabbit Anti-Insulin Recep Mouse Anti-Insulin(1G11)
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FGF21 induces autophagy-mediated cholesterol efflux to inhibit atherogenesis via RACK1 up-regulation.Fibroblast growth factor 21 (FGF21) acts as an anti-atherosclerotic agent. However, the specific mechanisms governing this regulatory activity are unclear. Autophagy is a highly conserved cell stress response which regulates atherosclerosis (AS) by reducing lipid droplet degradation in foam cells. We sought to assess whether FGF21 could inhibit AS by regulating cholesterol metabolism in foam cells via autophagy and to elucidate the underlying molecular mechanisms. In this study, ApoE mice were fed a high-fat diet (HFD) with or without FGF21 and FGF21 + 3-Methyladenine (3MA) for 12 weeks. Our results showed that FGF21 inhibited AS in HFD-fed ApoE mice, which was reversed by 3MA treatment. Moreover, FGF21 increased plaque RACK1 and autophagy-related protein (LC3 and beclin-1) expression in ApoE mice, thus preventing AS. However, these proteins were inhibited by LV-RACK1 shRNA injection. Foam cell development is a crucial determinant of AS, and cholesterol efflux from foam cells represents an important defensive measure of AS. In this study, foam cells were treated with FGF21 for 24 hours after a pre-treatment with 3MA, ATG5 siRNA or RACK1 siRNA. Our results indicated that FGF21-induced autophagy promoted cholesterol efflux to reduce cholesterol accumulation in foam cells by up-regulating RACK1 expression. Interestingly, immunoprecipitation results showed that RACK1 was able to activate AMPK and interact with ATG5. Taken together, our results indicated that FGF21 induces autophagy to promote cholesterol efflux and reduce cholesterol accumulation in foam cells through RACK1-mediated AMPK activation and ATG5 interaction. These results provided new insights into the molecular mechanisms of FGF21 in the treatment of AS.
1504 related Products with: FGF21 induces autophagy-mediated cholesterol efflux to inhibit atherogenesis via RACK1 up-regulation.Toxoplasma gondii MIC 3 r Analysis Tool for AAR-CYT RDEA-119 (BAY-869766) Mec Glutathione (GSH/GSSG/Tot Rabbit Anti-G protein alp Signal Transduction Anti MMP-1 Inhibitor Screening Cholesterol, 8 x 50 ml Caspase-Family Inhibitor ToughStripeâ„¢ BANDE (S) (+) p Toluenesulfinam Caspase-10 Inhibitor AEVD
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Dietary guanidinoacetic acid improves the growth performance and skeletal muscle development of finishing pigs through changing myogenic gene expression and myofibre characteristics.This study aimed to evaluate the effects of dietary guanidine acetic acid (GAA) supplementation on growth performance, carcass traits and the expression of muscle growth-related genes in finishing pigs. A total of 128 (81.03 ± 1.09 kg body weight) crossbred pigs (Duroc × Landrace ×Yorkshire) were blocked by body weight and allotted to 16 pens (eight pigs per pen), and pens were randomly assigned within blocks to one of five dietary treatments, with a basal diet (control group) or a basal diet supplemented with 0.03%, 0.06% and 0.09% GAA respectively. During the 60-day trial, GAA increased the average dairy gain (ADG) and average daily feed intake (ADFI) (p < .05). The back fat thickness of pigs fed 0.06% GAA was lower than other groups (p < .05). Pigs fed 0.06% GAA had improved lean meat percentage, loin muscle area, shear force and cross-sectional area of muscle fibre in comparison with control group (p < .05). The drop loss and the muscle fibre density in pigs fed 0.06% GAA were lower than control (p < .05). In addition, dietary GAA enhanced the expression of myosin heavy chain gene (MYH4), myogenic determination (Myod) and myogenic factor 5 (Myf5) in longissimus dorsi and carnitine palmitoyltransferase-1(CPT-1) in liver (p < .05). Meanwhile, GAA decreased the expression of Myostatin in longissimus dorsi and fatty acid synthase (FAS) in liver (p < .05). In conclusion, our results showed that appropriate dietary GAA supplementation (0.06%) promotes skeletal muscle development through changing myogenic gene expression and myofibre characteristics.
2630 related Products with: Dietary guanidinoacetic acid improves the growth performance and skeletal muscle development of finishing pigs through changing myogenic gene expression and myofibre characteristics.DNA (cytosine 5) methyltr Androst-4-ene-3,17-dion-1 Androgen Receptor , Mouse Gene Expression: Mouse N 5α-N-Acetyl-2'H-androst- pCAMBIA2200 Vector (No Re Androsta-1,4,6-triene-3,1 Androgen Receptor Antibod Epiandrosterone (3 beta H pCAMBIA0380 Vector (No Re Androstane-3a,17b-diol Gl 4 Androstene 3,17 dione C
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