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AMPK phosphorylates and inhibits SREBP activity to attenuate hepatic steatosis and atherosclerosis in diet-induced insulin-resistant mice.
TLDR
It is demonstrated that AMPK interacts with and directly phosphorylates sterol regulatory element binding proteins (SREBP-1c and -2) and AMPK-dependent phosphorylation of SREBP may offer therapeutic strategies to combat insulin resistance, dyslipidemia, and atherosclerosis. Expand
SIRT1 Regulates Hepatocyte Lipid Metabolism through Activating AMP-activated Protein Kinase*
TLDR
It is shown that polyphenols, including resveratrol and the synthetic polyphenol S17834, increase SIRT1 deacetylase activity, LKB1 phosphorylation at Ser428, and AMPK activity, which suggests that Sirt1 functions as a novel upstream regulator for L KB1/AMPK signaling and plays an essential role in the regulation of hepatocyte lipid metabolism. Expand
Endothelial dysfunction in diabetes
TLDR
Correcting the principal mediators of hyperglycaemia‐induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non‐enzymatic glycation and oxidative stress, as well as administration of ACE inhibitors and folate has been shown to improve endothelium‐dependent vasodilation in diabetes. Expand
Polyphenols Stimulate AMP-Activated Protein Kinase, Lower Lipids, and Inhibit Accelerated Atherosclerosis in Diabetic LDL Receptor–Deficient Mice
TLDR
It is revealed that inactivation of hepatic AMPK is a key event in the pathogenesis of hyperlipidemia in diabetes, point to a novel mechanism of action of polyphenols to lower lipids by activating AMPK, and emphasize a new therapeutic avenue to benefit hyper Lipidemia and atherosclerosis specifically in diabetes. Expand
Endothelium‐dependent contractions in SHR: a tale of prostanoid TP and IP receptors
TLDR
Because EDCFs converge to activate TP receptors, selective antagonists of this receptor, by preventing endothelium‐dependent contractions, curtail the endothelial dysfunction in diseases such as hypertension and diabetes. Expand
In SHR aorta, calcium ionophore A-23187 releases prostacyclin and thromboxane A2 as endothelium-derived contracting factors.
TLDR
Results indicate that in the aorta of SHR and WKY, the endothelium-dependent contractions involve the release of thromboxane A(2) and prostacyclin with a most likely concomitant contribution of PGH(2). Expand
The thromboxane receptor antagonist S18886 but not aspirin inhibits atherogenesis in apo E-deficient mice: evidence that eicosanoids other than thromboxane contribute to atherosclerosis.
TLDR
Comparisons of the effects of aspirin and the TP receptor antagonist S18886 suggest that blockade of TP receptors inhibits atherosclerosis by a mechanism independent of platelet-derived TxA(2), perhaps by preventing the expression of adhesion molecules whose expression is stimulated by eicosanoids other than Tx a(2). Expand
Altered thrombus formation in von Willebrand factor-deficient mice expressing von Willebrand factor variants with defective binding to collagen or GPIIbIIIa.
TLDR
Observations suggest that targeting the VWF-collagen orVWF-GPIIbIIIa interactions could be an interesting alternative for new antithrombotic strategies. Expand
Increased TIMP/MMP ratio in varicose veins: a possible explanation for extracellular matrix accumulation
TLDR
It is demonstrated that varicose veins are characterized by a higher than normal TIMP/MMP ratio, which may facilitate extracellular matrix accumulation in the diseased venous wall. Expand
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