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Source: Archives of Biochemistry and Biophysics
Condition: Metabolic Syndrome

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Total 2 results found since Jan 2013.

Hydrogen sulfide regulates circadian-clock genes in C2C12 myotubes and the muscle of high-fat-diet-fed mice.
We examined whether H2S has any effect on CCG in the skeletal muscle of mice fed a high-fat diet (HFD) and in myotubes. In the muscle of HFD-mice, the expression of H2S biosynthesis enzyme genes (CSE, CBS, and 3-Mpst) along with antioxidant genes (GCLC, GCLM, GSS, and GSR) involved in GSH biosynthesis and recycling were reduced significantly, but the oxidative stress (OS) increased. Expression of the CCG (Bmal1, Clock, RORα, Cry2, Per2) and clock-controlled genes (PPARγ, PGC-1α, RXRα) was downregulated, whereas the levels of PPARα mRNA were upregulated. Similar to that in the muscle of HFD-mice, in vitro myotubes expo...
Source: Archives of Biochemistry and Biophysics - July 23, 2019 Category: Biochemistry Authors: Parsanathan R, Jain SK Tags: Arch Biochem Biophys Source Type: research

Glucose-6-phosphate dehydrogenase deficiency increases cell adhesion molecules and activates human monocyte-endothelial cell adhesion: Protective role of l-cysteine.
Abstract Glucose-6-phosphate dehydrogenase is a major enzyme that supplies the reducing agent nicotinamide adenine dinucleotide phosphate hydrogen (NADPH), which is required to recycle oxidized/glutathione disulfide (GSSH) to reduced glutathione (GSH). G6PD-deficient cells are susceptible to oxidative stress and a deficiency of GSH. Endothelial dysfunction is characterized by the loss of nitric oxide (NO) bioavailability, which regulates leukocyte adhesion to endothelium. G6PD-deficient endothelial cells (EC) demonstrate a reduced expression of endothelial nitric oxide synthase (eNOS) and NO levels along with redu...
Source: Archives of Biochemistry and Biophysics - December 21, 2018 Category: Biochemistry Authors: Parsanathan R, Jain SK Tags: Arch Biochem Biophys Source Type: research