Advanced searches left 3/3

Metabolic - Wiley Online Library

Summarized by Plex Scholar
Last Updated: 15 May 2022

* If you want to update the article please login/register

Mid‐upper arm circumference is associated with liver steatosis and fibrosis in patients with metabolic‐associated fatty liver disease: A population based observational study

Metabolic-associated fatty liver disease is a group of liver diseases based on liver steatosis and metabolic disorders. We investigated the value of mid-upper arm circumference in assessing liver steatosis and fibrosis in patients with MAFLD in this research. In every multivariate linear regression model, a weighted generalized additive model, and smooth curve fitting using R. MUAC was positively correlated with liver steatosis and fibrosis, and this positive relationship was consistent in both men and women, as well as other ethnic groups. On the other hand, MUAC was positively related to liver fibrosis in every multivariate linear regression model, and this positive correlation remained strong in both men and women, as well as among non-Hispanic White and Black populations. Patients with MAFLD had increased MUAC, liver steatosis, and fibrosis.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/hep4.1990


The role of ERNDIM Diagnostic Proficiency Schemes in improving the quality of diagnostic testing for Inherited Metabolic Diseases

External quality control is also required to monitor and improve biochemical genetic testing's quality. Laboratory experiments' ability is being used by laboratories to correctly identify and interpret anomalies in authentic urine samples from a variety of IMDs. Diagnostic proficiency varied widely: amino acid disorders, range 33-100%, mean 84%; organic acid disorders, spectrum 14–100%, mean 74%; miscellaneous disorders, range 19–90%, mean 85 percent; no IMD, mean 85 percent; and cardiovascular disorders, range 33–100%, mean 84%; and autism disorders; mean 84%; and hypososomal storage disorders; and obesity syndromes, affecting 85%; no IMD, mean 85 percent; and When a sample of the same disorder was distributed in a subsequent research, results improved in 75 percent, with no change seen in 32 percent, indicating overall improvement of results. Diagnostic proficiency testing by ERNDIM is a valuable tool that can help to analyze laboratory results, identify methodological/technical issues, be transparent during quality audits, and contribute to a greater clinical appreciation of diagnostic uncertainty.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/jimd.12523


Metabolic bone disease in a white‐faced saki (Pithecia pithecia)

Non-human New World primates are identified as particularly vulnerable to metabolic bone disease. Inadequate dietary vitamin D exposure and/or inadequate dietary intake can contribute to poor bone formation and skeletal mineralization deficiencies. Ensure proper calcium control and prevention of sequela related to low calcium and vitamin D levels are important issues for individuals living indoors and during periods of growth, since inconsistent feeding habits and seasonality are suspected of contributing to rickets in this individual, as well as ample UV light exposure and adequate vitamin D levels are likely to result in this individual's growth.

Source link: https://onlinelibrary.wiley.com/doi/10.1002/vrc2.393


SLC3A2 N‐glycosylation and alternate evolutionary trajectories for amino acid metabolism

SLC3A2, an adaptor to amino acid transporters SLC7A511, 13, which maintains cell surface permanence, has been found in a search for additional glycoproteins that link metabolism, Nglycosylation, and signaling. SLC3A2*SLC7A5 exchanger imports essential AA that promotes signaling and anabolic metabolism, while SLC3A2*SLC7A11 supports glutathione production and reduction of oxidative stress. Analysis of SLC3A2 Nglycans published stable site-specific profiles of Golgi remodeling, with the exception of the conserved N365, where branching and polyNacetyllactosamine information were crucial to the incorporation of lost ancestral sites and to HBP. The Nglycans are poised to encourage galectin-mediated clustering within Nglycosylated Na++/AA symporters and increase diffusionlimited flux between exchangers and AA /Na+ symporters. These genes in Primates, Neoaves, and Naked mole rat reveal the nexus between metabolic rates and oxidative stress that control lifestyle and longevity.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.0I108


Epigenetic Mediators of Risk for Metabolic Disease Across Generations

The belief that the maternal perinatal environment influences childhood chronic diseases is well-recognized. Epigenetic tags are altered in sperm from rodents exposed to prenatal undernutrition, postnatal hunger, and other stimuli, according to We and others. While human results are more limited, paternal BMI at the time of pregnancy is connected to infant birth weight and DNA methylation of infant cord blood; differential DNA methylation at some loci persisted to age 7. T2D also modifies the sperm methylome, according to our latest preliminary results.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.0I167


A novel NSC small molecule inhibitor inhibits proliferation of triple‐negative breast cancer cells through metabolic reprograming

Patients with triplenegative breast cancer have been resistant to therapy due to a lack of well-defined molecular targets and high invasive and proliferative capabilities of these cells. Here, we discovered a new small molecule inhibitor with potent anti-tumor activity against TNBC cells. Methods NSC small molecule inhibitor was determined by 2D and 3D culture cell proliferation assays. TNBC cells' proliferation was reduced by a new NSC small molecule inhibitor, according to this article. In addition, we found that treatment with NSC small molecule inhibitor decreased glycolysis and oxidative phosphorylation by altering the activity of metabolic regulator enzymes. Conclusions NSC Small molecule inhibitor (British): Conclusions: Overall, our results indicate that the NSC small molecule inhibitor may have anti-tumor activity in TNBC cells, providing a justification for further investigation into the potential of NSC small molecule inhibitor as a popular therapeutic drug for TNBC.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.0R273


Sex‐Specific Arrhythmias Caused by Cardiac Sodium Channel Nav1.5 Mutation Alters Cardiomyocyte Metabolism

The activation of cardiac Nav1. 5 sodium channels sparks the intervention potential in the heart to promote coordinated contraction. Function Arg222Gln mutation in Nav1. 5 disrupts structural interactions during channel activation, resulting in an abnormal pore leading to increased cations entering the cardiomyocyte. The chronic arrhythmia that resultes from Arg222Gln puts the heart under intense strain, which may lead to premature metabolic reprogramming. We have created a mouse model that carries the human Arg222Gln gene, where the males display a significant arrhythmia burden, while females appear to be shielded. Methods The Arg222Gln mutation was converted into the equivalent mouse locus under the endogenous promoter. LCLC mass spectrometry was used to perform complete heart lysate proteomics of total heart lysate. With isolated adult primary CMs from the Seahorse XFe Analyzer, cellular metabolism was determined. The isolated CMs in all four groups remained unchanged, however, arg222Gln males' maximum respiratory capacity was significantly lower than those that were not compared to the wild type males. There were no differences between wild-type females and Arg222Gln females surveyed. Conclusions In a mouse model of arrhythmia owing to a rise-of-function Nav1. 5 mutation, we report sex-specific proteomic changes. Our results indicate that metabolic reprogramming may be involved in female cardioprotection or a compensatory risk factor in males carrying the Arg222Gln mutation. Future experiments will explore how sex affects cardiac function in the context of Arg222Gln, specifically focusing on specific roles of sex hormones.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.0R302


Regulation of NAD Metabolism in Diastolic Dysfunction Induced by Metabolic Stress

DIO also promoted cardiac hypertrophy, which was reduced by SARM1 deficiency. Only one of the lipid metabolites showed a marginal decline in SARM1KO plasma when comparing the 84 metabolites with diabetic WT and diabetic SARM1KO plasma. According to the reversal of cardiac pathogenic mechanisms, WT and SARM1KO hearts experienced similar metabolic stress, and that the rise in diastolic dysfunction in SARM1 deficiency was due to cardiac pathogenic mechanisms. To determine how SARM1 deficiency affected cardiac NAD metabolism, transcript levels of genes involved in NAD metabolic pathways were determined. Expressions of Bst1 and Cd38 NAD hydrolases in SARM1KO hearts did not change in SARM1KO hearts, implying that SARM1 deficiency did not cause compensatory changes in expression of the other NAD hydrolases. Hearts from SARM1KO hearts had lower expressions in several other NAD-consuming genes and NAD synthes genes.

Source link: https://onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.0R366

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions