The Role of Lipids in the Pathogenesis of Metabolic Syndrome in Adolescents

2017 ◽  
Vol 126 (01) ◽  
pp. 14-22 ◽  
Author(s):  
Shahnaz Taghizadeh ◽  
Mohammad Alizadeh

AbstractThe increasing prevalence of childhood obesity is a driving force behind the increase in adolescent’s metabolic syndrome (MetS). Although there is no clear consensus about the pediatric definition for MetS, this syndrome is becoming very common among adolescents. It is characterized by insulin resistance (IR), dyslipidemia, abdominal obesity and hypertension, and is associated with a high risk of type 2 diabetes mellitus and CVD in adulthood. Due to the increasing prevalence of obesity, there is strong incentive to reduce the impact of the adverse health effects associated with MetS. We explored the etiological role of nutrient-derived metabolic stressors, especially fatty acids, in the development of obesity and MetS. We also reviewed the evidence that pro-inflammatory stressors may predispose to obesity-induced insulin resistance. This article presents the opinion that reducing the impact of metabolic and inflammatory stressors may reduce the adverse health effects of obesity, and slow the progression towards MetS and CVD in adolescents. Evidence so far is limited from pediatric dietary epidemiological and interventional studies investigating the potential preventive and therapeutic effects of dietary fatty acid modification. This review will further investigate our understanding of the interaction between fatty acids in the pathogenesis and progression of MetS in adolescents.

2005 ◽  
Vol 64 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Helen M. Roche

The metabolic syndrome is a very common condition, characterised by insulin resistance, dyslipidaemia, abdominal obesity and hypertension, that is associated with a high risk of type 2 diabetes mellitus (T2DM) and CVD. Obesity is a key aetiological factor in the development of the metabolic syndrome. In light of the increasing prevalence of obesity, there is a high requirement to reduce the impact of the adverse health effects associated with the metabolic syndrome. The aetiological role of nutrient-derived metabolic stressors, in particular fatty acids, in the development of obesity and the metabolic syndrome is explored. Also, the evidence that pro-inflammatory stressors may predispose to obesity-induced insulin resistance is reviewed. The present paper explores the concept that reducing the impact of metabolic and inflammatory stressors may reduce the adverse health effects of obesity and slow the progression towards the metabolic syndrome and T2DM. Evidence from human dietary intervention studies that have investigated the potential therapeutic effects of dietary fatty acid modification is explored. The present review highlights the requirement to take account of genetic background, within the context of nutrient regulation of gene expression and individual responsiveness to dietary therapy. This approach will further the understanding of the interaction between fatty acids in the pathogenesis and progression of the metabolic syndrome.


2019 ◽  
Vol 20 (19) ◽  
pp. 4901 ◽  
Author(s):  
Leonardo M. R. Ferreira ◽  
Teresa Cunha-Oliveira ◽  
Margarida C. Sobral ◽  
Patrícia L. Abreu ◽  
Maria Carmen Alpoim ◽  
...  

Worldwide, several million workers are employed in the various chromium (Cr) industries. These workers may suffer from a variety of adverse health effects produced by dusts, mists and fumes containing Cr in the hexavalent oxidation state, Cr(VI). Of major importance, occupational exposure to Cr(VI) compounds has been firmly associated with the development of lung cancer. Counterintuitively, Cr(VI) is mostly unreactive towards most biomolecules, including nucleic acids. However, its intracellular reduction produces several species that react extensively with biomolecules. The diversity and chemical versatility of these species add great complexity to the study of the molecular mechanisms underlying Cr(VI) toxicity and carcinogenicity. As a consequence, these mechanisms are still poorly understood, in spite of intensive research efforts. Here, we discuss the impact of Cr(VI) on the stress response—an intricate cellular system against proteotoxic stress which is increasingly viewed as playing a critical role in carcinogenesis. This discussion is preceded by information regarding applications, chemical properties and adverse health effects of Cr(VI). A summary of our current understanding of cancer initiation, promotion and progression is also provided, followed by a brief description of the stress response and its links to cancer and by an overview of potential molecular mechanisms of Cr(VI) carcinogenicity.


Foods ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2452
Author(s):  
Davit Pipoyan ◽  
Stella Stepanyan ◽  
Seda Stepanyan ◽  
Meline Beglaryan ◽  
Lara Costantini ◽  
...  

Health effects of trans fatty acids (TFAs) on human organisms can vary according to their type, structure, composition, and origin. Even though the adverse health effects of industrial TFAs (iTFAs) have been widely discussed, the health effects of natural TFAs (nTFAs) are still questionable. Hence, it is important to review the literature and provide an overall picture on the health effects of different TFAs coming from industrial and ruminant sources, underlining those types that have adverse health effects as well as suggesting methods for reducing their harmful effects. Multiple databases (PubMed, Medline, Cochrane Library, etc.) were searched with the key words “trans fatty acid sources”, “ruminant”, “industrial”, “conjugated trans linoleic acid”, “human”, “coronary heart disease”, “cancer”, etc. Reference lists of the studies were scanned discussing the health effects of iTFAs and nTFAs. The review of the literature showed that iTFAs are found to be more harmful than ruminant-produced nTFAs. Although several beneficial effects (such as reduced risk of diabetes) for nTFAs have been observed, they should be used with caution. Since during labeling it is usually not mentioned whether the TFAs contained in food are of industrial or natural origin, the general suggestion is to reduce their consumption.


2015 ◽  
Vol 15 (3) ◽  
pp. 139-146 ◽  
Author(s):  
Deepak Kumar Semwal ◽  
Satyendra Prasad Mishra ◽  
Ashutosh Chauhan ◽  
Ruchi Badoni Semwal

Author(s):  
Zhiming Yang ◽  
Qianhao Song ◽  
Jing Li ◽  
Yunquan Zhang

Chinese air pollution is obviously increasing, and the government makes efforts to strengthen air pollution treatment. Although adverse health effects gradually emerge, research determining individual vulnerability is limited. This study estimated the relationship between air pollution and obesity. Individual information of 13,414 respondents from 125 cities is used in the analysis. This study employs ordinary least squares (OLS) and multinomial logit model (m-logit) to estimate the impact of air pollution on obesity. We choose different air pollution and Body Mass Index (BMI) indicators for estimation. Empirical results show Air Quality Index (AQI) is significantly positively associated with the BMI score. As AQI adds one unit, the BMI score increases 0.031 (SE = 0.002; p < 0.001). The influence coefficients of particle size smaller than 2.5 μm (PM2.5), particle size smaller than 10 μm (PM10), carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), and sulfur dioxide (SO2) to the BMI score are 0.034 (SE = 0.002; p < 0.001), 0.023 (SE = 0.001; p < 0.001), 0.52 (SE = 0.095; p < 0.001), 0.045 (SE = 0.004; p < 0.001), 0.021 (SE = 0.002; p < 0.001), 0.008 (SE = 0.003; p = 0.015), respectively. Generally, air pollution has an adverse effect on body weight. CO is the most influential pollutant, and female, middle-aged, and low-education populations are more severely affected. The results confirm that the adverse health effects of air pollution should be considered when making the air pollution policies. Findings also provide justification for health interventions, especially for people with obesity.


Author(s):  
Maria-Viola Martikainen ◽  
Päivi Aakko-Saksa ◽  
Lenie van den Broek ◽  
Flemming R. Cassee ◽  
Roxana O. Carare ◽  
...  

The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.


2008 ◽  
Vol 54 (6) ◽  
pp. 945-955 ◽  
Author(s):  
Sarah de Ferranti ◽  
Dariush Mozaffarian

Abstract Background: As the prevalence of adiposity soars in both developed and developing nations, appreciation of the close links between obesity and disease increases. The strong relationships between excess adipose tissue and poor health outcomes, including cardiovascular disease, diabetes, and cancer, mandate elucidation of the complex cellular, hormonal, and molecular pathophysiology whereby adiposity initiates and maintains adverse health effects. Content: In this report we review adipocyte metabolism and function in the context of energy imbalance and postprandial nutrient excess, including adipocyte hypertrophy and hyperplasia, adipocyte dysfunction, and other systemic consequences. We also discuss implications for laboratory evaluation and clinical care, including the role of lifestyle modifications. Chronic energy imbalance produces adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These processes lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic β-cells, and skeletal muscle as well as the heart and vascular beds. Several specialized laboratory tests can quantify these processes and predict clinical risk, but translation to the clinical setting is premature. Current and future pharmacologic interventions may target these pathways; modest changes in diet, physical activity, weight, and smoking are likely to have the greatest impact. Summary: Adipocyte endoplasmic reticulum and mitochondrial stress, and associated changes in circulating adipokines, free fatty acids, and inflammatory mediators, are central to adverse health effects of adiposity. Future investigation should focus on these pathways and on reversing the adverse lifestyle behaviors that are the fundamental causes of adiposity.


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