Hepatic PCSK9 expression is regulated by nutritional status via insulin and sterol regulatory element-binding protein 1c
Philippe Costet,Bertrand Cariou,Gilles Lambert,Florent Lalanne,Bernard Lardeux,Anne Laure Jarnoux,Aldo Grefhorst,Bart Staels,Michel Krempf +8 more
TL;DR: Results show that PCSK9 expression is regulated by nutritional status and insulinemia.
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About: This article is published in Journal of Biological Chemistry. The article was published on 10 Mar 2006. and is currently open access. The article focuses on the topics: Sterol regulatory element-binding protein & Apolipoprotein B.
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Citations
AMPK phosphorylates and inhibits SREBP activity to attenuate hepatic steatosis and atherosclerosis in diet-induced insulin-resistant mice.
Yu Li,Shanqin Xu,Maria M. Mihaylova,Bin Zheng,Xiuyun Hou,Bingbing Jiang,Ogyi Park,Zhijun Luo,Etienne Lefai,John Y.-J. Shyy,Bin Gao,Michel Wierzbicki,Tony Verbeuren,Reuben J. Shaw,Richard A. Cohen,Mengwei Zang +15 more
TL;DR: 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.
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Clinical Update: Cardiovascular Disease in Diabetes Mellitus: Atherosclerotic Cardiovascular Disease and Heart Failure in Type 2 Diabetes Mellitus – Mechanisms, Management, and Clinical Considerations
TL;DR: This review considers the mechanisms, history, controversies, new pharmacological agents, and recent evidence for current guidelines for cardiovascular management in the patient with diabetes mellitus to support evidence-based care outside of the acute care setting.
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PCSK9: a convertase that coordinates LDL catabolism.
TL;DR: Individuals with loss-of-function mutations in PCSK9 have reduced plasma levels of LDL cholesterol and are protected from CHD; these observations have validatedPCSK9 as a therapeutic target and suggested new approaches for the treatment and prevention of CHD.
655
PCSK9: A Key Modulator of Cardiovascular Health
TL;DR: This review will address the biochemical, genetic, and clinical aspects associated with PCSK9’s biology and pathophysiology in cells, rodent and human, with emphasis on the clinical benefits of silencing the expression/activity ofPCSK9 as a new modality in the treatment of hypercholesterolemia and associated pathologies.
569
Genetic and metabolic determinants of plasma PCSK9 levels
TL;DR: Although levels of PCSK9 correlate with plasma levels of LDL-C, they account for only a small proportion of the variation in the levels of this lipoprotein.
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References
Monogenic hypercholesterolemia: new insights in pathogenesis and treatment
TL;DR: A subset of patients with very high plasma LDL-C levels have monogenic forms of hyper-cholesterolemia, which are associated with the deposition of cholesterol in tissues, producing xanthomas and coronary atherosclerosis, and how insights gleaned from the study of these disorders may be extended to the treatment of hypercholesterine in the general population is discussed.
Cooperation by Sterol Regulatory Element-binding Protein and Sp1 in Sterol Regulation of Low Density Lipoprotein Receptor Gene
TL;DR: The experiments reported here demonstrate that Sp1 participates in sterol regulation of the LDL receptor in an orientation-specific fashion and suggest that sterol regulatory element-binding protein (SREBP) increases the binding of Sp1 to the adjacent repeat 3 sequence.
Sterol Regulatory Element-binding Protein-1 as a Key Transcription Factor for Nutritional Induction of Lipogenic Enzyme Genes
Hitoshi Shimano,Naoya Yahagi,Michiyo Amemiya-Kudo,Alyssa H. Hasty,Jun-ichi Osuga,Yoshiaki Tamura,Futoshi Shionoiri,Yoko Iizuka,Ken Ohashi,Kenji Harada,Takanari Gotoda,Shun Ishibashi,Nobuhiro Yamada +12 more
TL;DR: It is demonstrated that SREBP-1 plays a crucial role in the induction of lipogenesis but not cholesterol biosynthesis in liver when excess energy by carbohydrates is consumed.
Inhibitors of Cholesterol Biosynthesis Increase Hepatic Low-Density Lipoprotein Receptor Protein Degradation
TL;DR: It appears that increased potential for LDL receptorprotein synthesis, reflected in increased mRNA levels, is offset by a corresponding increase in the rate of receptor protein degradation resulting in constant steady-state levels of hepatic LDL receptor protein.
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