In conclusion, the protein p66Shc exerts an inhibitory effect on β-cell insulin signaling and can mediate the ability of SFAs and excess body fat to cause β-cell IR, which results in both reduced survival and impaired secretory function.
Upregulation of p66Shc in human ECs is linked to a significant reduction of the antioxidant enzyme SOD2, suggesting that p66Shc mediates mitochondrial ROS production and promotes downregulation of scavenging enzymes, leading to unopposed ROS accumulation in vascular ECs.
TUDCA is available OTC. Brand most effective =? Dosage? I have it on order to hopefully treat diaphragm weakness - TUDCA apparently lowers cPLA2.
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Marnie
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Difference between men and women with regards to UDCA (women produce LESS bile acids):
Furthermore, the mean concentration of total bile acids was 51% higher in men than in women...
? OspA – Bb’s p66 she - which is inhibited by SIRT1
TUDCA upregulated SIRT1-FXR activity, which inhibited expression and acetylation of NF-κB and p53 and increased FoxM1 expression, leading to decreased inflammatory response and apoptosis and increased proliferative capacity in hepatocytes, and attenuation of liver injury.
The carbon storage regulator A (CsrA) is a protein responsible for the
repression of a variety of stationary-phase genes in bacteria.
CsrA negatively regulates gluconeogenesis, glycogen biosynthesis and catabolism, and biofilm formation (14, 23, 25).
Additionally, CsrA can activate glycolysis, acetate metabolism, and flagellum biosynthesis (25-27).
CsrA acts posttranscriptionally by repressing gene expression of essential enzymes in carbohydrate metabolism, like ADP-glucose pyrophosphorylase (glgC), glycogen synthase (glgA), glycogen branching enzyme (glgB), and glycogen phosphorylase (glgP).
CsrA destabilizes target mRNAs by binding in a region within the −18 and +31 nucleotides of the coding region, which includes the ribosome-binding site (18).
This prevents translation of the corresponding mRNA and promotes its degradation by endogenous RNases.
As a result, a decrease in the intracellular levels of the glycogen biosynthetic enzymes and decreased synthesis of intracellular glycogen are observed.
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