scholarly journals Fatty acids and the metabolic syndrome

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.

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.


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.


Toxics ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 105
Author(s):  
Ilona Górna ◽  
Marta Napierala ◽  
Ewa Florek

The metabolic syndrome is a combination of several metabolic disorders, such as cardiovascular disease, atherosclerosis, and type 2 diabetes. Lifestyle modifications, including quitting smoking, are recommended to reduce the risk of metabolic syndrome and its associated complications. Not much research has been conducted in the field of e-cigarettes and the risk of metabolic syndrome. Furthermore, taking into account the influence of e-cigarettes vaping on the individual components of metabolic syndrome, i.e, abdominal obesity, insulin resistance, dyslipidemia and elevated arterial blood pressure, the results are also ambiguous. This article is a review and summary of existing reports on the impact of e-cigarettes on the development of metabolic syndrome as well as its individual components. A critical review for English language articles published until 30 June 2020 was made, using a PubMed (including MEDLINE), Cochrane, CINAHL Plus, and Web of Science data. The current research indicated that e-cigarettes use does not affect the development of insulin resistance, but could influence the level of glucose and pre-diabetic state development. The lipid of profile an increase in the TG level was reported, while the influence on the level of concentration of total cholesterol, LDL fraction, and HDL fraction differed. In most cases, e-cigarettes use increased the risk of developing abdominal obesity or higher arterial blood pressure. Further research is required to provide more evidence on this topic.


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.


2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Eduardo Spinedi ◽  
Daniel P. Cardinali

Polycystic ovary syndrome is a highly frequent reproductive-endocrine disorder affecting up to 8–10% of women worldwide at reproductive age. Although its etiology is not fully understood, evidence suggests that insulin resistance, with or without compensatory hyperinsulinemia, and hyperandrogenism are very common features of the polycystic ovary syndrome phenotype. Dysfunctional white adipose tissue has been identified as a major contributing factor for insulin resistance in polycystic ovary syndrome. Environmental (e.g., chronodisruption) and genetic/epigenetic factors may also play relevant roles in syndrome development. Overweight and/or obesity are very common in women with polycystic ovary syndrome, thus suggesting that some polycystic ovary syndrome and metabolic syndrome female phenotypes share common characteristics. Sleep disturbances have been reported to double in women with PCOS and obstructive sleep apnea is a common feature in polycystic ovary syndrome patients. Maturation of the luteinizing hormone-releasing hormone secretion pattern in girls in puberty is closely related to changes in the sleep-wake cycle and could have relevance in the pathogenesis of polycystic ovary syndrome. This review article focuses on two main issues in the polycystic ovary syndrome-metabolic syndrome phenotype development: (a) the impact of androgen excess on white adipose tissue function and (b) the possible efficacy of adjuvant melatonin therapy to improve the chronobiologic profile in polycystic ovary syndrome-metabolic syndrome individuals. Genetic variants in melatonin receptor have been linked to increased risk of developing polycystic ovary syndrome, to impairments in insulin secretion, and to increased fasting glucose levels. Melatonin therapy may protect against several metabolic syndrome comorbidities in polycystic ovary syndrome and could be applied from the initial phases of patients’ treatment.


2021 ◽  
Author(s):  
Ranyao Yang ◽  
Yue Hu ◽  
Chi Ho Lee ◽  
Yan Liu ◽  
Candela Diaz-Canestro ◽  
...  

Objective: Peptidase M20 domain containing 1 (PM20D1), a secreted enzyme catalysing condensation of fatty acids and amino acids into the bioactive lipids N-acyl amino acids (NAAA), induces uncoupling protein 1 (UCP1)-independent adaptive thermogenesis in brown/beige adipocytes in mice. This study aimed to explore the associations of the circulating levels of PM20D1 and major NAAA with obesity-related metabolic complications in humans. Design and Methods: Serum concentrations of PM20D1 and NAAA (C18:1-Leu and C18:1-Phe) in 256 Chinese subjects, including 78 lean and 178 overweight/obese individuals with or without diabetes, were measured with immunoassays and liquid chromatography-mass spectrometry respectively. The impact of sulfonylurea and rosiglitazone on their circulating levels was examined in 62 patients with type 2 diabetes. Results: Serum PM20D1 level was significantly elevated in overweight/obese individuals, and was closely associated with circulating levels of C18:1-Leu and C18:1-Phe. Furthermore, serum PM20D1, C18:1-Leu and C18:1-Phe concentrations correlated positively with several parameters of adiposity as well as fasting and 2-h postprandial glucose, HbA1c, fasting insulin, and HOMA-IR independent of BMI and age. Moreover, a significant elevation in PM20D1, C18:1-Leu and C18:1-Phe concentrations corresponding with increases in the number of components of the metabolic syndrome (MetS) was observed. Treatment with sulfonylurea significantly decreased circulating PM20D1, C18:1-Leu and C18:1-Phe in patients with type 2 diabetes. Conclusions: Increased serum levels of PM20D1 and its catalytic products NAAA are closely associated with obesity-related glucose dysregulation, insulin resistance and MetS, and can be potentially used as clinical biomarkers for diagnosing and monitoring these disorders.


2021 ◽  
Vol 74 (10) ◽  
pp. 2510-2515
Author(s):  
Inna Diemieszczyk ◽  
Paulina Głuszyńska ◽  
Pawel Andrzej Wojciak ◽  
Jerzy Robert Ładny ◽  
Hady Razak Hady

The aim of the study was to assess the impact of individual components of the metabolic syndrome on the human body, taking into account their etiology and pathogenesis. This article is analytical analysis of scientific and medical literature basing on aspects of the etiology and pathogenesis of the metabolic syndrome. The key role in the pathogenesis of the metabolic syndrome is played by insulin resistance, which may be a result of lifestyle conditions (low physical activity, overweight or obesity) or genetic background. A certain role in the pathogenesis of the metabolic syndrome is also attributed to disorders of the hypothalamic-pituitary-adrenal axis in the form of increased cortisol control, which may initiate the development of abdominal obesity, insulin resistance, hypertension and dyslipidemia. Aforementioned factors (environmental, hormonal and genetic) lead to excessive fat tissue gathering. The excess of abdominal fat tissue – abdominal obesity – leads to insulin resistance, the concentration of which causes body mass gain. Such mechanism is dangerous for our health and may lead to the occurrence of type 2 diabetes and premature development of atherosclerosis with all its consequences such as atherosclerotic cardiovascular diseases including coronary artery disease.


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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