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Special Issue "Dyslipidemia and Obesity"

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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (31 December 2012)

Special Issue Editor

Guest Editor
Prof. Dr. Gloria Lena Vega

Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9052, USA
Website | E-Mail
Phone: +1 214 648 2869
Fax: +1 214 648 4839
Interests: lipid and lipoprotein metabolism in atherosclerosis, diabetes mellitus, obesity

Special Issue Information

Dear Colleagues,

Excess body fat and/or abnormal body composition underlies “atherogenic dyslipidemia”, a risk burden for cardiovascular disease (CVD). Atherogenic dyslipidemia is characterized by reduced levels of high density lipoprotein (HDL), and increased levels of triglycerides and non-esterified fatty acids during the post-absorptive state. Unlike, isolated hypercholesterolemia, atherogenic dyslipidemia can be reversed by a ten percent weight reduction through persistent lifestyle modification. How do changes in body composition alter lipid metabolism and risk burden for cardiovascular disease? Some investigators find subcutaneous adipose tissue protective and dysfunctional subcutaneous adipose tissue a major risk burden for CVD. Others suggest that lower subcutaneous adipose tissue is most protective and still others find visceral adipose tissue to be a major risk burden. Still there are other cases of abnormal body composition, such as “sarcopenic obesity” that are associated with atherogenic dyslipidemia. In this special issue of Nutrients we shall examine emerging mechanisms of adipose tissue and/or muscle dysfunction that cause abnormalities in lipid metabolism and increase risk for cardiovascular disease.

Prof. Dr. Gloria Lena Vega
Guest Editor

Keywords

  • adipocity
  • sarcopenia
  • dyslipidemia
  • atherosclerosis
  • lypoatrophy
  • upper-body fat
  • lower-body fat
  • ectopic fat
  • visceral fat

Published Papers (8 papers)

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Research

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Open AccessArticle Hypertriglyceridemia
Nutrients 2013, 5(3), 981-1001; doi:10.3390/nu5030981
Received: 22 January 2013 / Revised: 14 March 2013 / Accepted: 15 March 2013 / Published: 22 March 2013
Cited by 27 | PDF Full-text (447 KB) | HTML Full-text | XML Full-text
Abstract
Hypertriglyceridemia (HTG) is commonly encountered in lipid and cardiology clinics. Severe HTG warrants treatment because of the associated increased risk of acute pancreatitis. However, the need to treat, and the correct treatment approach for patients with mild to moderate HTG are issues for
[...] Read more.
Hypertriglyceridemia (HTG) is commonly encountered in lipid and cardiology clinics. Severe HTG warrants treatment because of the associated increased risk of acute pancreatitis. However, the need to treat, and the correct treatment approach for patients with mild to moderate HTG are issues for ongoing evaluation. In the past, it was felt that triglyceride does not directly contribute to development of atherosclerotic plaques. However, this view is evolving, especially for triglyceride-related fractions and variables measured in the non-fasting state. Our understanding of the etiology, genetics and classification of HTG states is also evolving. Previously, HTG was considered to be a dominant disorder associated with variation within a single gene. The old nomenclature includes the term “familial” in the names of several hyperlipoproteinemia (HLP) phenotypes that included HTG as part of their profile, including combined hyperlipidemia (HLP type 2B), dysbetalipoproteinemia (HLP type 3), simple HTG (HLP type 4) and mixed hyperlipidemia (HLP type 5). This old thinking has given way to the idea that genetic susceptibility to HTG results from cumulative effects of multiple genetic variants acting in concert. HTG most is often a “polygenic” or “multigenic” trait. However, a few rare autosomal recessive forms of severe HTG have been defined. Treatment depends on the overall clinical context, including severity of HTG, concomitant presence of other lipid disturbances, and the patient's global risk of cardiovascular disease. Therapeutic strategies include dietary counselling, lifestyle management, control of secondary factors, use of omega-3 preparations and selective use of pharmaceutical agents. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)

Review

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Open AccessReview Obesity and Lifespan Health—Importance of the Fetal Environment
Nutrients 2014, 6(4), 1725-1736; doi:10.3390/nu6041725
Received: 7 January 2014 / Revised: 9 April 2014 / Accepted: 15 April 2014 / Published: 24 April 2014
Cited by 12 | PDF Full-text (728 KB) | HTML Full-text | XML Full-text
Abstract
A marked increase in the frequency of obesity at the population level has resulted in an increasing number of obese women entering pregnancy. The increasing realization of the importance of the fetal environment in relation to chronic disease across the lifespan has focused
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A marked increase in the frequency of obesity at the population level has resulted in an increasing number of obese women entering pregnancy. The increasing realization of the importance of the fetal environment in relation to chronic disease across the lifespan has focused attention on the role of maternal obesity in fetal development. Previous studies have demonstrated that obesity during adolescence and adulthood can be traced back to fetal and early childhood exposures. This review focuses on factors that contribute to early developmental events, such as epigenetic modifications, the potential for an increase in inflammatory burden, early developmental programming changes such as the variable development of white versus brown adipose tissue, and alterations in organ ontogeny. We hypothesize that these mechanisms promote an unfavorable fetal environment and can have a long-standing impact, with early manifestations of chronic disease that can result in an increased demand for future health care. In order to identify appropriate preventive measures, attention needs to be placed both on reducing maternal obesity as well as understanding the molecular, cellular, and epigenetic mechanisms that may be responsible for the prenatal onset of chronic disease. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
Open AccessReview Obesity and Dyslipidemia in South Asians
Nutrients 2013, 5(7), 2708-2733; doi:10.3390/nu5072708
Received: 1 May 2013 / Revised: 22 May 2013 / Accepted: 28 May 2013 / Published: 16 July 2013
Cited by 48 | PDF Full-text (774 KB) | HTML Full-text | XML Full-text
Abstract
Obesity and dyslipidemia are emerging as major public health challenges in South Asian countries. The prevalence of obesity is more in urban areas than rural, and women are more affected than men. Further, obesity in childhood and adolescents is rising rapidly. Obesity in
[...] Read more.
Obesity and dyslipidemia are emerging as major public health challenges in South Asian countries. The prevalence of obesity is more in urban areas than rural, and women are more affected than men. Further, obesity in childhood and adolescents is rising rapidly. Obesity in South Asians has characteristic features: high prevalence of abdominal obesity, with more intra-abdominal and truncal subcutaneous adiposity than white Caucasians. In addition, there is greater accumulation of fat at “ectopic” sites, namely the liver and skeletal muscles. All these features lead to higher magnitude of insulin resistance, and its concomitant metabolic disorders (the metabolic syndrome) including atherogenic dyslipidemia. Because of the occurrence of type 2 diabetes, dyslipidemia and other cardiovascular morbidities at a lower range of body mass index (BMI) and waist circumference (WC), it is proposed that cut-offs for both measures of obesity should be lower (BMI 23–24.9 kg/m2 for overweight and ≥25 kg/m2 for obesity, WC ≥80 cm for women and ≥90 cm for men for abdominal obesity) for South Asians, and a consensus guideline for these revised measures has been developed for Asian Indians. Increasing obesity and dyslipidemia in South Asians is primarily driven by nutrition, lifestyle and demographic transitions, increasingly faulty diets and physical inactivity, in the background of genetic predisposition. Dietary guidelines for prevention of obesity and diabetes, and physical activity guidelines for Asian Indians are now available. Intervention programs with emphasis on improving knowledge, attitude and practices regarding healthy nutrition, physical activity and stress management need to be implemented. Evidence for successful intervention program for prevention of childhood obesity and for prevention of diabetes is available for Asian Indians, and could be applied to all South Asian countries with similar cultural and lifestyle profiles. Finally, more research on pathophysiology, guidelines for cut-offs, and culturally-specific lifestyle management of obesity, dyslipidemia and the metabolic syndrome are needed for South Asians. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
Open AccessReview Body Fat Distribution and Insulin Resistance
Nutrients 2013, 5(6), 2019-2027; doi:10.3390/nu5062019
Received: 8 April 2013 / Revised: 23 May 2013 / Accepted: 24 May 2013 / Published: 5 June 2013
Cited by 37 | PDF Full-text (275 KB) | HTML Full-text | XML Full-text
Abstract
The burden of obesity has increased globally over the last few decades and its association with insulin resistance and related cardio-metabolic problems have adversely affected our ability to reduce population morbidity and mortality. Traditionally, adipose tissue in the visceral fat depot has been
[...] Read more.
The burden of obesity has increased globally over the last few decades and its association with insulin resistance and related cardio-metabolic problems have adversely affected our ability to reduce population morbidity and mortality. Traditionally, adipose tissue in the visceral fat depot has been considered a major culprit in the development of insulin resistance. However, there is a growing body of evidence supporting the role of subcutaneous truncal/abdominal adipose tissue in the development of insulin resistance. There are significant differences in the functional characteristics of subcutaneous abdominal/truncal vs. intraabdominal vs. gluteo-femoral fat depots. More recently, mounting evidence has been supporting the role of adipose tissue function in the development of metabolic complications independent of adipose tissue volume or distribution. Decreased capacity for adipocyte differentiation and angiogenesis along with adipocyte hypertrophy can trigger a vicious cycle of inflammation leading to subcutaneous adipose tissue dysfunction and ectopic fat deposition. Therapeutic lifestyle change continues to be the most important intervention in clinical practice to improve adipose tissue function and avoid development of insulin resistance and related cardio-metabolic complications. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
Open AccessReview Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease
Nutrients 2013, 5(5), 1544-1560; doi:10.3390/nu5051544
Received: 25 February 2013 / Revised: 12 April 2013 / Accepted: 16 April 2013 / Published: 10 May 2013
Cited by 118 | PDF Full-text (1170 KB) | HTML Full-text | XML Full-text
Abstract
Non-alcoholic fatty liver disease is marked by hepatic fat accumulation not due to alcohol abuse. Several studies have demonstrated that NAFLD is associated with insulin resistance leading to a resistance in the antilipolytic effect of insulin in the adipose tissue with an increase
[...] Read more.
Non-alcoholic fatty liver disease is marked by hepatic fat accumulation not due to alcohol abuse. Several studies have demonstrated that NAFLD is associated with insulin resistance leading to a resistance in the antilipolytic effect of insulin in the adipose tissue with an increase of free fatty acids (FFAs). The increase of FFAs induces mitochondrial dysfunction and development of lipotoxicity. Moreover, in subjects with NAFLD, ectopic fat also accumulates as cardiac and pancreatic fat. In this review we analyzed the mechanisms that relate NAFLD with metabolic syndrome and dyslipidemia and its association with the development and progression of cardiovascular disease. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
Open AccessReview Dyslipidemia in Obesity: Mechanisms and Potential Targets
Nutrients 2013, 5(4), 1218-1240; doi:10.3390/nu5041218
Received: 21 December 2012 / Revised: 14 February 2013 / Accepted: 27 March 2013 / Published: 12 April 2013
Cited by 134 | PDF Full-text (793 KB) | HTML Full-text | XML Full-text
Abstract
Obesity has become a major worldwide health problem. In every single country in the world, the incidence of obesity is rising continuously and therefore, the associated morbidity, mortality and both medical and economical costs are expected to increase as well. The majority of
[...] Read more.
Obesity has become a major worldwide health problem. In every single country in the world, the incidence of obesity is rising continuously and therefore, the associated morbidity, mortality and both medical and economical costs are expected to increase as well. The majority of these complications are related to co-morbid conditions that include coronary artery disease, hypertension, type 2 diabetes mellitus, respiratory disorders and dyslipidemia. Obesity increases cardiovascular risk through risk factors such as increased fasting plasma triglycerides, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels and high blood pressure. Novel lipid dependent, metabolic risk factors associated to obesity are the presence of the small dense LDL phenotype, postprandial hyperlipidemia with accumulation of atherogenic remnants and hepatic overproduction of apoB containing lipoproteins. All these lipid abnormalities are typical features of the metabolic syndrome and may be associated to a pro-inflammatory gradient which in part may originate in the adipose tissue itself and directly affect the endothelium. An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin. The current review will focus on these aspects of lipid metabolism in obesity and potential interventions to treat the obesity related dyslipidemia. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
Open AccessReview Lipoprotein Subfractions in Metabolic Syndrome and Obesity: Clinical Significance and Therapeutic Approaches
Nutrients 2013, 5(3), 928-948; doi:10.3390/nu5030928
Received: 28 January 2013 / Revised: 6 March 2013 / Accepted: 6 March 2013 / Published: 18 March 2013
Cited by 50 | PDF Full-text (420 KB) | HTML Full-text | XML Full-text
Abstract
Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to
[...] Read more.
Small, dense low density lipoprotein (sdLDL) represents an emerging cardiovascular risk factor, since these particles can be associated with cardiovascular disease (CVD) independently of established risk factors, including plasma lipids. Obese subjects frequently have atherogenic dyslipidaemia, including elevated sdLDL levels, in addition to elevated triglycerides (TG), very low density lipoprotein (VLDL) and apolipoprotein-B, as well as decreased high density lipoprotein cholesterol (HDL-C) levels. Obesity-related co-morbidities, such as metabolic syndrome (MetS) are also characterized by dyslipidaemia. Therefore, agents that favourably modulate LDL subclasses may be of clinical value in these subjects. Statins are the lipid-lowering drug of choice. Also, anti-obesity and lipid lowering drugs other than statins could be useful in these patients. However, the effects of anti-obesity drugs on CVD risk factors remain unclear. We review the clinical significance of sdLDL in being overweight and obesity, as well as the efficacy of anti-obesity drugs on LDL subfractions in these individuals; a short comment on HDL subclasses is also included. Our literature search was based on PubMed and Scopus listings. Further research is required to fully explore both the significance of sdLDL and the efficacy of anti-obesity drugs on LDL subfractions in being overweight, obesity and MetS. Improving the lipoprotein profile in these patients may represent an efficient approach for reducing cardiovascular risk. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
Open AccessReview Fat Depots, Free Fatty Acids, and Dyslipidemia
Nutrients 2013, 5(2), 498-508; doi:10.3390/nu5020498
Received: 31 December 2012 / Revised: 31 January 2013 / Accepted: 4 February 2013 / Published: 7 February 2013
Cited by 50 | PDF Full-text (411 KB) | HTML Full-text | XML Full-text
Abstract
Body fat deposition and excess free fatty acid (FFA) metabolism contribute to dyslipidemia and the adverse health consequences of obesity. Individuals with upper body obesity have impaired functioning of adipocytes, the primary fatty acid storage site. Excess visceral fat is strongly associated with
[...] Read more.
Body fat deposition and excess free fatty acid (FFA) metabolism contribute to dyslipidemia and the adverse health consequences of obesity. Individuals with upper body obesity have impaired functioning of adipocytes, the primary fatty acid storage site. Excess visceral fat is strongly associated with impaired suppression of FFA release in response to insulin, as well as with hypertriglyceridemia and low concentrations of high density lipoprotein (HDL) cholesterol. High FFA concentrations can induce insulin resistance in muscle and liver. Furthermore, failure of hyperinsulinemia to normally suppress FFA is associated with impaired carbohydrate oxidation and muscle glucose storage, reduced hepatic insulin clearance and elevated triglycerides. Understanding the impact of body fat distribution on FFA metabolism and dyslipidemia is critical for determining the link between overweight and obesity and cardiovascular disease risk. In the current review, we will explore the relationship between adipose tissue, body fat depots, and FFA metabolism. Full article
(This article belongs to the Special Issue Dyslipidemia and Obesity)
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