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JournalISSN: 0957-9672

Current Opinion in Lipidology 

Lippincott Williams & Wilkins
About: Current Opinion in Lipidology is an academic journal published by Lippincott Williams & Wilkins. The journal publishes majorly in the area(s): Apolipoprotein B & Cholesterol. It has an ISSN identifier of 0957-9672. Over the lifetime, 2428 publications have been published receiving 116266 citations.


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Journal ArticleDOI
Frank B. Hu1
TL;DR: The rationale for studying dietary patterns is described, quantitative methods for analysing dietary patterns and their reproducibility and validity are discussed, and the available evidence regarding the relationship between major Dietary patterns and the risk of cardiovascular disease is discussed.
Abstract: Recently, dietary pattern analysis has emerged as an alternative and complementary approach to examining the relationship between diet and the risk of chronic diseases. Instead of looking at individual nutrients or foods, pattern analysis examines the effects of overall diet. Conceptually, dietary patterns represent a broader picture of food and nutrient consumption, and may thus be more predictive of disease risk than individual foods or nutrients. Several studies have suggested that dietary patterns derived from factor or cluster analysis predict disease risk or mortality. In addition, there is growing interest in using dietary quality indices to evaluate whether adherence to a certain dietary pattern (e.g. Mediterranean pattern) or current dietary guidelines lowers the risk of disease. In this review, we describe the rationale for studying dietary patterns, and discuss quantitative methods for analysing dietary patterns and their reproducibility and validity, and the available evidence regarding the relationship between major dietary patterns and the risk of cardiovascular disease.

3,383 citations

Journal ArticleDOI
TL;DR: 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.
Abstract: PURPOSE OF REVIEW: Peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC-1alpha) has been extensively described as a master regulator of mitochondrial biogenesis. However, PGC-1alpha activity is not constant and can be finely tuned in response to different metabolic situations. From this point of view, PGC-1alpha could be described as a mediator of the transcriptional outputs triggered by metabolic sensors, providing the idea that these sensors, together with PGC-1alpha, might be weaving a network controlling cellular energy expenditure. In this review, we will focus on how disorders such as type 2 diabetes and the metabolic syndrome might be related to an abnormal and improper function of this network. RECENT FINDINGS: Two metabolic sensors, AMP-activated protein kinase (AMPK) and SIRT1 have been described to directly affect PGC-1alpha activity through phosphorylation and deacetylation, respectively. Although the physiological relevance of these modifications and their molecular consequences are still largely unknown, recent insight from different in-vivo transgenic models clearly suggests that AMPK, SIRT1 and PGC-1alpha might act as an orchestrated network to improve metabolic fitness. SUMMARY: Metabolic sensors such as AMPK and SIRT1, gatekeepers of the activity of the master regulator of mitochondria, PGC-1alpha, are vital links in a regulatory network for metabolic homeostasis. Together, these players explain many of the beneficial effects of physical activity and dietary interventions in our battle against type 2 diabetes and related metabolic disorders. Hence, understanding the mechanisms by which they act could guide us to identify and improve preventive and therapeutic strategies for metabolic diseases.

1,275 citations

Journal ArticleDOI
TL;DR: Changes in cholesterol balance across the whole body may, in some way, cause alterations in sterol recycling and apolipoprotein E expression within the central nervous system, which, in turn, may affect neuron and myelin integrity.
Abstract: The central nervous system accounts for only 2% of the whole body mass but contains almost a quarter of the unesterified cholesterol present in the whole individual. This sterol is largely present in two pools comprised of the cholesterol in the plasma membranes of glial cells and neurons and the ch

870 citations

Journal ArticleDOI
TL;DR: This review will provide the reader with an update on the understanding of the adverse effects of fatty acid accumulation in non-adipose tissues, a phenomenon known as lipotoxicity.
Abstract: Purpose of reviewThis review will provide the reader with an update on our understanding of the adverse effects of fatty acid accumulation in non-adipose tissues, a phenomenon known as lipotoxicity Recent studies will be reviewed Cellular mechanisms involved in the lipotoxic response will be discu

813 citations

Journal ArticleDOI
TL;DR: Adiponectin is an endogenous biologically relevant modulator of vascular remodeling linking obesity and vascular disease, and acts as an anti-inflammatory and anti-atherogenic plasma protein.
Abstract: Purpose of review Obesity is the most common risk factor for cardiovascular diseases in industrial countries. It is now clear that adipose tissue secretes various bioactive substances, conceptualized as adipocytokines, and that dysregulation of adipocytokines directly contributes to obesity-related diseases. Chronic inflammatory processes contribute to the development of atherosclerosis. In this review, the authors focus on the relationship between adiponectin, a recently discovered anti-atherogenic adipocytokine, and vascular inflammation. Recent findings Plasma concentrations of adiponectin, an adipocyte-specific protein, are reduced in obese subjects and in patients with type 2 diabetes and coronary artery disease. Adiponectin inhibits the expression of tumor necrosis factor-alpha-induced endothelial adhesion molecules, macrophage-to-foam cell transformation, tumor necrosis factor-alpha expression in macrophages and adipose tissues, and smooth muscle cell proliferation. In addition, adenovirus-expressed adiponectin reduces atherosclerotic lesions in a mouse model of atherosclerosis, and adiponectin-deficient mice exhibit an excessive vascular remodeling response to injury. Clinically, hypoadiponectinemia is closely associated with increased levels of inflammatory markers such as C-reactive protein and interleukin-6. Summary Adiponectin acts as an anti-inflammatory and anti-atherogenic plasma protein. Adiponectin is an endogenous biologically relevant modulator of vascular remodeling linking obesity and vascular disease.

732 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202342
202289
202161
202055
201975
201879