Trans fatty acids: effects on metabolic syndrome, heart disease and diabetes.Micha R,
Mozaffarian D.
Nat Rev Endocrinol. 2009 Jun;5(6):335-44.
Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.
Abstract
The major dietary sources of trans fatty acids (TFAs) in most countries are partially hydrogenated vegetable oils. TFA consumption is a modifiable dietary risk factor for metabolic syndrome, diabetes mellitus, and coronary heart disease. Here, we review the available data on various effects of TFAs, including metabolic and signaling pathways that mediate these effects, affected tissues, and relationships with clinical end points. TFA consumption causes metabolic dysfunction: it adversely affects circulating lipid levels, triggers systemic inflammation, induces endothelial dysfunction, and, according to some studies, increases visceral adiposity, body weight, and insulin resistance. Dietary TFAs influence the function of multiple cell types, including hepatocytes, adipocytes, macrophages and endothelial cells. Among dietary fats and nutrients, TFAs seem to have a unique cardiometabolic imprint that is linked to insulin-resistance and metabolic-syndrome pathways. Consistent with these adverse physiological effects, consumption of even small amounts of TFAs (2% of total energy intake) is consistently associated with a markedly increased incidence of coronary heart disease. Relationships between TFA consumption and diabetes mellitus have been less consistent, possibly owing to differences in study designs. Nevertheless, the documented adverse effects of TFAs underscore their potential to cause harm and the importance of policy measures to minimize consumption of industrially produced TFAs.
Trans-fatty acids and cancer: a mini-review.Smith BK,
Robinson LE,
Nam R,
Ma DW.
Br J Nutr. 2009 Nov;102(9):1254-66.
Department of Human Health and Nutritional Sciences, College of Biological Science, University of Guelph, Ontario, Canada.
Abstract
The association between trans-fatty acids (TFA) and cancer risk is poorly understood and remains controversial. It is recognised that unique biological effects are associated with specific isoforms within families of fatty acids such as those belonging to the n-3 fatty acids. Furthermore, the interactions between diet and genetic polymorphisms are increasingly recognised for their potential risk-modifying effects on human health and disease. Therefore, the aim of the present review is to evaluate whether specific TFA isomers and genetic polymorphisms differentially modify cancer risk in prostate, colon and breast cancers in animal and human models. Potential mechanisms of action by which TFA may affect cancer development are also reviewed. Overall, across a number of experimental models and human studies, there is insufficient and inconsistent evidence linking specific TFA isomers to cancers of the prostate, colon and breast. A number of methodological limitations and experimental considerations were identified which may explain the inconsistencies observed across these studies. Therefore, further research is warranted to accurately assess the relationship between TFA and cancer risk.
Trans fatty acids and weight gain.Thompson AK,
Minihane AM,
Williams CM.
Int J Obes (Lond). 2011 Mar;35(3):315-24. Epub 2010 Jul 20.
Hugh Sinclair Unit of Human Nutrition, Department of Food and Nutritional Sciences, University of Reading, Reading, UK.
a.k.thompson@reading.ac.ukAbstract
Increasing rates of obesity have stimulated research into possible contributing factors, including specific dietary components such as trans fatty acids (TFAs). This review considers the evidence for an association between TFA intake and weight gain. It concludes that there is limited but consistent evidence from epidemiological studies, and from a primate model, that increased TFA consumption may result in a small additional weight gain. Data from a long-term study in a primate model suggest that TFA may have a greater adipogenic effect than cis monounsaturated fatty acids; however, there are currently inadequate mechanistic data to provide a comprehensive and plausible explanation for any such metabolic differences between the types of fatty acids.
Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis.
Tilg H,
Moschen AR.
Hepatology. 2010 Nov;52(5):1836-46.
Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Innsbruck, Austria.
herbert.tilg@i-med.ac.atAbstract
Whereas in most cases a fatty liver remains free of inflammation, 10%-20% of patients who have fatty liver develop inflammation and fibrosis (nonalcoholic steatohepatitis [NASH]). Inflammation may precede steatosis in certain instances. Therefore, NASH could reflect a disease where inflammation is followed by steatosis. In contrast, NASH subsequent to simple steatosis may be the consequence of a failure of antilipotoxic protection. In both situations, many parallel hits derived from the gut and/or the adipose tissue may promote liver inflammation. Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.
