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Metabolic - U.S. Department of Veterans Affairs

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Last Updated: 15 April 2022

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Metabolic benefits of methionine restriction in adult mice do not require functional methionine sulfoxide reductase A (MsrA).

Although there are growing reports that methionine redox regulation of certain aspects of cell function, regulatory control of certain aspects of physiological function is in place, interactions with MR are largely unexplored. We investigated the role of the ubiquitously expressed methionine repair enzyme methionine reductase A in mice's metabolic benefits. We investigated the extent to which MsrA is essential for metabolic reactions of MR in adult mice using mice that lack MsrA. Overall, our findings show that MsrA is not required for the metabolic benefits of MR in adult mice.

Source link: https://doi.org/10.1038/s41598-022-08978-4


Hexokinase 1 cellular localization regulates the metabolic fate of glucose.

We produced mice lacking the HK1 MBD to clarify the effect of HK1 mitochondrial dissociation on cell metabolism. In addition, there was reduced glucose flux below the level of GAPDH and elevated upstream flux through the PPP. The glycolytic block below GAPDH is mediated by the binding of cytosolic HK1 with S100A8/A9, which results in GAPDH nitrosylation by iNOS. Through regulation of GAPDH, HK1 mitochondrial binding alters glucose metabolism, according to our findings.

Source link: https://doi.org/10.1016/j.molcel.2022.02.028


Monosodium urate crystals regulate a unique JNK-dependent macrophage metabolic and inflammatory response.

In vivo without prior priming, monosodium urate crystals cause inflammation, boosting the likelihood of an initial cell-autonomous phase. The initiating inflammatory responses in acute gout flares are controlled by a steady increase in JUN's promoter of target genes via JNK signaling, but not P38-in a process that is different from post-LPS stimulation and independent of inflammasome activation. In animal models of acute gouty inflammation, pharmacological JNK inhibition limits MSUc-induced inflammation.

Source link: https://doi.org/10.1016/j.celrep.2022.110489


Sex and genetic background define the metabolic, physiologic, and molecular response to protein restriction.

Despite facts that sex and genetic history are important factors in the response to diet, most protein intake studies focus on a single strain and sex of mice. We find that metabolic health in reaction to reduced dietary protein rises strongly depend on sex and strain. Our findings reveal the importance of sex and genetic history in dietary protein levels as well as the potential of a personalized medicine approach to dietary interventions.

Source link: https://doi.org/10.1016/j.cmet.2021.12.018


Peripheral versus central insulin and leptin resistance: Role in metabolic disorders, cognition, and neuropsychiatric diseases.

Insulin and leptin are commonly thought of as peptide hormones that play important roles in metabolism. Although the consequences of these disorders are well-known, the CNS difficulties of leptin and insulin resistance have come into sharper focus. Insulin and leptin resistance have been linked to cognitive deficits and neuropsychiatric disorders such as depression, according to both preclinical and clinical studies. This report will explore insulin and leptin's peripheral and central functions in various metabolic disorders, cognition, and neuropsychiatric disorders in light of these findings.

Source link: https://doi.org/10.1016/j.neuropharm.2021.108877

* 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