Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1α
AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity
It is demonstrated that AMPK controls the expression of genes involved in energy metabolism in mouse skeletal muscle by acting in coordination with another metabolic sensor, the NAD+-dependent type III deacetylase SIRT1.
Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity
It is reported that S6K1-deficient mice are protected against obesity owing to enhanced β-oxidation, however on a high fat diet, levels of glucose and free fatty acids still rise in S6k1- deficient mice, resulting in insulin receptor desensitization.
Molecular basis for feedback regulation of bile acid synthesis by nuclear receptors.
Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation
It is shown that the administration of BAs to mice increases energy expenditure in brown adipose tissue, preventing obesity and resistance to insulin, and indicates that BAs might be able to function beyond the control of BA homeostasis as general metabolic integrators.
Sirt5 Is a NAD-Dependent Protein Lysine Demalonylase and Desuccinylase
It is found that Sirt5 is an efficient protein lysine desuccinylase and demalonylase in vitro and may represent a posttranslational modification that can be reversed by Sirt 5 in vivo.
PGC-1α, SIRT1 and AMPK, an energy sensing network that controls energy expenditure
Metabolic sensors such as AMPK and SIRT1, gatekeepers of the activity of the master regulator of mitochondria, PGC-1α, are vital links in a regulatory network for metabolic homeostasis and understanding the mechanisms by which they act could guide us to identify and improve preventive and therapeutic strategies for metabolic diseases.
TGR5-mediated bile acid sensing controls glucose homeostasis.
Mechanism of action of fibrates on lipid and lipoprotein metabolism.
- B. Staels, J. Dallongeville, J. Auwerx, K. Schoonjans, E. Leitersdorf, J. Fruchart
- 10 November 1998
Both enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL underlie the hypotriglyceridemic effect of fibrates, whereas their effect on HDL metabolism is associated with changes in HDL apolipoprotein expression.
Bile acids lower triglyceride levels via a pathway involving FXR, SHP, and SREBP-1c.
The results suggest that strategies aimed at increasing FXR activity and the repressive effects of SHP should be explored to correct hypertriglyceridemia.