Small LDL, Atherogenic Dyslipidemia, and the Metabolic Syndrome

Circulation ◽  
1997 ◽  
Vol 95 (1) ◽  
pp. 1-4 ◽  
Author(s):  
Scott M. Grundy
Keyword(s):  
Metabolic Syndrome ◽  
Atherogenic Dyslipidemia ◽  
The Metabolic Syndrome

scholarly journals Living in the Southern Hemisphere: Metabolic Syndrome and Its Components in Amazonian Riverine Populations

2021 ◽  
Vol 10 (16) ◽  
pp. 3630
Author(s):  
Gabriela P. Arrifano ◽  
Jacqueline I. Alvarez-Leite ◽  
Barbarella M. Macchi ◽  
Núbia F. S. S. Campos ◽  
Marcus Augusto-Oliveira ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Southern Hemisphere ◽  
Vulnerable Populations ◽  
Low Income ◽  
Hdl Cholesterol ◽  
Developed Countries ◽  
Atherogenic Dyslipidemia ◽  
Cross Sectional ◽  
The Metabolic Syndrome ◽  
Low Hdl

The metabolic syndrome (MetS) epidemic is a global challenge. Although developing countries (including Brazil, India, and South Africa) present a higher proportion of deaths by cardiovascular diseases than developed countries, most of our knowledge is from these developed countries. Amazonian riverine populations (ARP), as well as other vulnerable populations of the Southern Hemisphere, share low-income and traditional practices, among other features. This large cross-sectional study of ARP (n = 818) shows high prevalence of hypertension (51%) and obesity (23%). MetS was diagnosed in 38% of participants (especially in women and 60–69 years-old individuals) without the influence of ancestry. Only 7–8% of adults had no cardio-metabolic abnormalities related to MetS. Atherogenic dyslipidemia (low HDL-cholesterol) was generally observed, including in individuals without MetS. Still, slight differences were detected between settings with a clear predominance of hypertension in Tucuruí. Hypotheses on possible genetic influence and factors (nutrition transition and environmental pollutants -mercury) are proposed for future studies. Moreover, a roadmap to MetS progression based on the most prevalent components is provided for the development of tailored interventions in the Amazon (initially, individuals would present low HDL-cholesterol levels, later progressing to increased blood pressure characterizing hypertension, and ultimately reaching MetS with obesity). Our alarming results support the need to improve our knowledge on these vulnerable populations.

Effects of rosuvastatin, atorvastatin, simvastatin, and pravastatin on atherogenic dyslipidemia in patients with characteristics of the metabolic syndrome

2005 ◽  
Vol 95 (3) ◽  
pp. 360-366 ◽  
Author(s):  
Prakash C. Deedwania ◽  
Donald B. Hunninghake ◽  
Harold E. Bays ◽  
Peter H. Jones ◽  
Valerie A. Cain ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Atherogenic Dyslipidemia ◽  
The Metabolic Syndrome

Redox-inflammatory synergy in the metabolic syndrome

2013 ◽  
Vol 91 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Sean Bryan ◽  
Boran Baregzay ◽  
Drew Spicer ◽  
Pawan K. Singal ◽  
Neelam Khaper
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Atherogenic Dyslipidemia ◽  
Disease States ◽  
The Metabolic Syndrome ◽  
Anthropometric Features ◽  
Inflammatory Processes ◽  
Inflammatory Milieu

Metabolic syndrome (MetS) comprises interrelated disease states including obesity, insulin resistance and type 2 diabetes (T2DM), dyslipidemia, and hypertension. Essential to normal physiological function, and yet massively damaging in excess, oxidative stress and inflammation are pivotal common threads among the pathologies of MetS. Increasing evidence indicates that redox and inflammatory dysregulation parallels the syndrome's physiological, biochemical, and anthropometric features, leading many to consider the pro-oxidative, pro-inflammatory milieu an unofficial criterion in itself. Left unchecked, cross-promotion of oxidative stress and inflammation creates a feed-forward cycle that can initiate and advance disease progression. Such redox-inflammatory integration is evident in the pathogenesis of obesity, insulin resistance and T2DM, atherogenic dyslipidemia, and hypertension, and is thus hypothesized to be the “common soil” from which they develop. The present review highlights the synergistic contributions of redox-inflammatory processes to each of the components of the MetS.

scholarly journals Abnormal lipid metabolism in metabolic syndrome: an epigenetic perspective

2016 ◽  
Vol 24 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Ioana Brudașcă ◽  
Mircea Cucuianu
Keyword(s):  
Metabolic Syndrome ◽  
Dna Methylation ◽  
Life Span ◽  
Maternal Obesity ◽  
Maternal Nutrition ◽  
Hdl Cholesterol ◽  
Atherogenic Dyslipidemia ◽  
Epigenetic Changes ◽  
The Metabolic Syndrome ◽  
Increased Risk

Abstract Metabolic syndrome is a complex pathology including central obesity, impaired glucose tolerance/diabetes, an atherogenic dyslipidemia and a prothrombotic state. A new perspective on understanding the mechanisms underlying metabolic syndrome is provided by the epigenetic changes (mainly DNA methylation and histone covalent modifications), which influence gene expression without changing of the DNA sequence. DNA methylation (mainly in carnitine palmitoyltransferase 1A gene) and histone modifications were shown to be associated with VLDL and LDL phenotypes, with hyperglycemia and reduced level of HDL cholesterol, with hypertriglyceridemic waist phenotype and with progression of atherosclerotic occlusion in peripheral arteries. The epigenetic changes can occur in the prenatal period, throughout the life span, and can be transmitted to the offspring. Both poor maternal nutrition and maternal obesity, diabetes and overfeeding can result in epigenetic alterations that amplify the risk of metabolic syndrome for the offspring. Throughout life span, environmental factors, such as nutrition and exercise can induce epigenetic changes influencing the evolution of the metabolic syndrome (through adipocyte metabolism and insulin signaling pathway). The epigenetic modifications are not completely erased during gametogenesis and embryogensis, resulting in a transgenerational transmission of an epigenetic state up to the fifth generation. Epigenetic mechanisms are an interface between environmental stimuli and resulting phenotype by inducing a certain transcriptional state, which may be also transmitted to the next generation(s) and which may predispose to an increased risk for developing metabolic syndrome in the context of a mismatched environment. Elucidating epigenetic modulation might provide additional information about risk evaluation and more targeted therapeutical intervention.

Generation and characterization of two novel mouse models exhibiting the phenotypes of the metabolic syndrome: Apob48−/−Lepob/ob mice devoid of ApoE or Ldlr

2008 ◽  
Vol 294 (3) ◽  
pp. E496-E505 ◽  
Author(s):  
David J. Lloyd ◽  
Jocelyn McCormick ◽  
Joan Helmering ◽  
Ki Won Kim ◽  
Minghan Wang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Food Intake ◽  
Apolipoprotein B ◽  
Plasma Cholesterol ◽  
Density Lipoprotein ◽  
Suppressive Effect ◽  
Human Condition ◽  
Atherogenic Dyslipidemia ◽  
Direct Role ◽  
The Metabolic Syndrome

The metabolic syndrome is a group of disorders including obesity, insulin resistance, atherogenic dyslipidemia, hyperglycemia, and hypertension. To date, few animal models have been described to recapitulate the phenotypes of the syndrome. In this study, we generated and characterized two lines of triple-knockout mice that are deficient in either apolipoprotein E (Apoe−/−) or low-density lipoprotein receptor (Ldlr−/−) and express no leptin (Lepob/ob) or apolipoprotein B-48 but exclusively apolipoprotein B-100 (Apob100/100). These two lines are referred to as Apoe triple-knockout-Apoe 3KO (Apoe−/−Apob100/100Lepob/ob) and Ldlr triple-knockout-Ldlr 3KO (Ldlr−/−Apob100/100Lepob/ob) mice. Both lines develop obesity, hyperinsulinemia, hyperlipidemia, hypertension, and atherosclerosis. However, only Apoe 3KO mice are hyperglycemic and glucose intolerant and are more obese than Ldlr 3KO mice. To evaluate the utility of these lines as pharmacological models, we treated both with leptin and found that leptin therapy ameliorated most metabolic derangements. Leptin was more effective in improving glucose tolerance in Ldlr 3KO than Apoe 3KO animals. The reduction of plasma cholesterol by leptin in Ldlr 3KO mice can be accounted for by its suppressive effect on food intake. However, in Apoe 3KO mice, leptin further reduced plasma cholesterol independently of its effect on food intake, and this improvement correlated with a smaller plaque lesion area. These effects suggest a direct role of leptin in modulating VLDL levels and, likewise, the lesion areas in VLDL-enriched animals. These two lines of mice represent new models with features of the metabolic syndrome and will be useful in testing therapies targeted for combating the human condition.

scholarly journals Overnutrition, ectopic lipid and the metabolic syndrome

2016 ◽  
Vol 64 (6) ◽  
pp. 1082-1086 ◽  
Author(s):  
Scott M Grundy
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Elevated Serum ◽  
Density Lipoprotein ◽  
Metabolic Risk Factors ◽  
Atherogenic Dyslipidemia ◽  
Current View ◽  
Metabolic Risk ◽  
Serum Triglycerides ◽  
The Metabolic Syndrome

The metabolic syndrome is a constellation of metabolic risk factors including atherogenic dyslipidemia (elevated serum triglycerides, reduced high-density lipoprotein (HDL) cholesterol), elevated blood pressure, dysglycemia (insulin resistance and elevated serum glucose), a pro-inflammatory state, and a prothrombotic state. Most persons with metabolic syndrome are obese, and usually have abdominal obesity. Generally, obesity is a reflection of overnutrition. A current view is that when adipose tissue fails to store all excess nutrients as triglyceride, lipid begins to accumulate in various tissues (eg, muscle, liver, pancreas, and heart). This accumulation is called ectopic lipid. Various mechanisms have been proposed whereby ectopic lipid is detrimental in different tissues; these derangements induce metabolic risk factors. The foundation of the metabolic syndrome thus appears to be overnutrition, that is, more nutrient intake than can be safely disposed by lipid oxidation. Excess dietary carbohydrate also induces ectopic lipid. Of interest, less than half of obese individuals develop metabolic syndrome. Through various mechanisms they adapt to overnutrition so as to minimize lipid overload in tissues, and consequently, prevent the syndrome.

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