The toxicity of dietary trans fats

Ganguly, Riya; Pierce, Grant N.

doi:10.1016/j.fct.2015.02.004

Cited by 67 publications

(37 citation statements)

References 56 publications

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“…Specifically, they found that trans fatty acids raise plasma low density lipoprotein (LDL) cholesterol and reduce plasma high density lipoprotein (HDL) cholesterol levels. Following this important finding, multiple epidemiological studies found strong positive associations between consumption of industrial trans fatty acids and the onset and progression of coronary heart disease . A recent meta‐analysis convincingly established that intake of trans fatty acids is positively associated with all‐cause mortality, total coronary heart disease, and coronary heart disease mortality …”

Section: Introductionmentioning

confidence: 91%

Industrial Trans Fatty Acids Stimulate SREBP2‐Mediated Cholesterogenesis and Promote Non‐Alcoholic Fatty Liver Disease

Oteng

Loregger

Weeghel

et al. 2019

Molecular Nutrition Food Res

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Scope The mechanisms underlying the deleterious effects of trans fatty acids on plasma cholesterol and non‐alcoholic fatty liver disease (NAFLD) are unclear. Here, the aim is to investigate the molecular mechanisms of action of industrial trans fatty acids. Methods and results Hepa1‐6 hepatoma cells were incubated with elaidate, oleate, or palmitate. C57Bl/6 mice were fed diets rich in trans‐unsaturated, cis‐unsaturated, or saturated fatty acids. Transcriptomics analysis of Hepa1‐6 cells shows that elaidate but not oleate or palmitate induces expression of genes involved in cholesterol biosynthesis. Induction of cholesterogenesis by elaidate is mediated by increased sterol regulatory element‐binding protein 2 (SREBP2) activity and is dependent on SREBP cleavage–activating protein (SCAP), yet independent of liver‐X receptor and ubiquitin regulatory X domain‐containing protein 8. Elaidate decreases intracellular free cholesterol levels and represses the anticholesterogenic effect of exogenous cholesterol. In mice, the trans‐unsaturated diet increases the ratio of liver to gonadal fat mass, steatosis, hepatic cholesterol levels, alanine aminotransferase activity, and fibrosis markers, suggesting enhanced NAFLD, compared to the cis‐unsaturated and saturated diets. Conclusion Elaidate induces cholesterogenesis in vitro by activating the SCAP–SREBP2 axis, likely by lowering intracellular free cholesterol and attenuating cholesterol‐dependent repression of SCAP. This pathway potentially underlies the increase in liver cholesterol and NAFLD by industrial trans fatty acids.

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Section: Introductionmentioning

confidence: 91%

Industrial Trans Fatty Acids Stimulate SREBP2‐Mediated Cholesterogenesis and Promote Non‐Alcoholic Fatty Liver Disease

Oteng

Loregger

Weeghel

et al. 2019

Molecular Nutrition Food Res

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“…Mind in vivo, mind in vitro kísérleti rendszerekben kimutatták azonban, hogy a telített zsír-savak (például palmitát és sztearát) lényegesen toxikusabbak a telítetleneknél (például oleát, linoleát és linolenát), sőt a telítetlenek -elsősorban a többszörösen telítetlenek -gyakran csökkentik a telítettek káros hatá-sait [5][6][7]. Sok tanulmány utal a transz konfigurációjú kettős kötés(eke)t tartalmazó zsírsavak által okozott ár-talmakra, elsősorban a cardiovascularis betegségek megnövekedett kockázata vonatkozásában [8]. Bár az észlelt egészségkárosító hatások mechanizmusa még tisztázat-lan, máris sok országban korlátozzák e -főként kérődző állatokból, illetve mesterségesen hidrogénezett olajokból/zsírokból származó -lipidkomponensek mennyisé-gét az élelmiszerekben.…”

Section: Különféle Zsírsavak Toxicitásaunclassified

Zsírsavtúltengés – inzulinrezisztencia és β-sejt-halál

Csala

2016

Orvosi Hetilap

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A 2-es típusú diabetes terjedése összefügg az elhízás gyakoriságának és mértékének növekedésével. A tápanyagfelesleg raktározása megviseli a zsírsejteket, ami lokális gyulladás révén felgyorsítja a triglicerid-anyagcsere körforgását és megemeli a szabad zsírsavak plazmaszintjét. A tartós zsírsavtúltengés károsítja a sejtek működését (lipotoxicitás), sőt akár programozott sejthalált is okozhat. Az aktiválódó stresszkinázok akadályozzák az inzulin-jelátvitelt, és gyakran elősegítik az apoptózist. A zsírsavtúltengés tehát az inzulinrezisztencia és a β-sejt-károsodás révén összekapcsolja az elhízást a cukorbetegséggel. A lipotoxicitással kapcsolatos kutatások -és ezen belül a telített, telítetlen, illetve transzzsírsavak hatásainak összehasonlítása -magyarázattal szolgálnak számos korábban is ismert jelenségre. Az e téren bővülő ismeretek pedig a metabolikus szindróma és a diabetes megelőzésének, illetve gyógyításának új stratégiáit kínálják. Orv. Hetil., 2016, 157(19), 733-739. Kulcsszavak: elhízás, szabad zsírsav, lipotoxicitás, lipoapoptózis, inzulinrezisztencia Hyper-free fatty acidemia -insulin resistance and β-cell deathThe increasing prevalence of type 2 diabetes correlates with the rapid spread of obesity worldwide. Adipocytes are strained by the demand of excessive storage, and the local inflammation accelerates triglyceride turnover, which elevates the plasma levels of free fatty acids. Sustained hyper-free fatty acidemia leads to disturbances in cellular functions (lipotoxicity) or even to programmed cell death. Activated stress kinases interfere with insulin signaling, and often facilitate apoptosis. Hyper-free fatty acidemia, therefore, links obesity to diabetes through insulin resistance and β-cell damage. Lipotoxicity research -including the comparison of the effects exerted by saturated, unsaturated and trans fatty acids -provides explanations for long-known phenomena. Our widening knowledge in the field offers new strategies for prevention and treatment of the metabolic syndrome and diabetes.Keywords: obesity, free fatty acid, lipotoxicity, lipoapoptosis, insulin resistance Csala, M. [Hyper-free fatty acidemia -insulin resistance and β-cell death]. Orv. Hetil., 2016, 157(19), 733-739. Rövidítések ATF-6 = aktiváló transzkripciós faktor-6; ER = endoplazmás reticulum; FAT/CD-36 = zsírsav/transzlokáz receptor; FFA = szabad zsírsav; FFAR-1/GPR-40 = szabadzsírsav-receptor-1 -más néven G-fehérjéhez kapcsolt receptor-40; IGF-1 = inzulinszerű növekedési faktor-1; IKK = inhibitor-κB-kináz; IL-1β = interleukin-1β; IL-1R = interleukin-1-receptor; IL-6 = interleukin-6; IRE-1α = inozitolfüggő enzim-1α; IRS = inzulinreceptor-szubsztrát; JNK = c-Jun aminoterminális kináz; KoA = koenzim-A; MCP-1 = monocyta kemotaktikus fehérje-1; NEFA = szabad (nem észteresített) zsírsav; NF-κB = nukleáris faktor-κB; p38 MAPK = p38 mitogénaktivált proteinkináz; PERK = PKR-szerű ER-beli kináz; PKC = proteinkináz C; PLC = foszfolipáz C; PPAR = peroxiszómaproliferátor-aktivált receptor; ROS = reaktív oxigénszármazék(ok); SFA = telített...

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“…There are many factors that affect formation of trans fatty acid including partial hydrogenation, refining process, baking, and frying [3,10]. These factors may change a double bond from a cis position to a trans position (geometric isomerization) or move to another position in the carbon chain (positional isomerization) and both types of isomerization may occur in the same molecule [11].…”

Section: Introductionmentioning

confidence: 99%

“…The human lipase enzyme digest, transport, and process dietary lipids such as triglycerides, fats, and oils and works only on the cis configuration and cannot metabolize trans fatty acids [1,4]. Consumption of diets high in hydrogenated fat and/or trans fatty acids has been shown to have an adverse effect on lipoprotein profiles with respect to cardiovascular disease risk [3,5,6,7].…”

Section: Introductionmentioning

confidence: 99%

“…Trans fatty acid has been a matter for debate in last years, especially after the studies which showed that industrial trans acids such as elaidic acid occurs in hydrogenation of vegetable oils, margarine, fat spread, shortening vegetable oils and food containing hydrogenation of plant oils and margarine, such as bakery, sweets, cakes, donuts, and frying foods, made with partially-hydrogenated fats [1,2,3]. The human lipase enzyme digest, transport, and process dietary lipids such as triglycerides, fats, and oils and works only on the cis configuration and cannot metabolize trans fatty acids [1,4].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Frying Temperature and duration on the Formation of Trans Fatty Acids in Selected Fats and Oils

Afaneh¹,

Abbadi²,

Al‐Rimawi³

et al. 2017

AJFST

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Trans fatty acids occur in food either naturally or produced during heat processing of food containing unsaturated fats. Naturally occurring trans fatty acids have different physiological and biological functions as compared to those formed in heat processed food which increase the risk of coronary heart disease. The aim of this study was to investigate the effect of heat treatments [heating temperature: 120, 150, 190 and 250°C and heating period: 10, 30, 60 and 180 minutes] on the amount of trans fatty acids (as elaidic acid) of fat and oil samples [two solid-state (margarine and ghee) and two liquids-state (olive oil and corn oil)]. Results showed that elaidic acid content in margarine was not affected by heat at 120°C at all studied heating durations. At 150, 190 and 250°C, there is a cubic significant relationship between elaidic acid content and time of heating. Elaidic acid content in ghee was not affected by heat treatment at 120°C, while at 150°C, there was a cubic significant relationship between elaidic acid content and heating time. At 190°C, there was a negative linear relationship between elaidic acid content and time of frying, while at 250°C, there was oscillatory relationship in the amounts of elaidic acid with time of heating. As a conclusion, all margarine and ghee samples analyzed in this study had elaidic acid before and after heat treatment used in the study. However, corn oil and olive oil were free from elaidic acid before and after studied heat treatments. Therefore, it is recommended to cook and bake with vegetable oils (such as corn oil) instead of solid fats, and to keep margarine and ghee consumption as low as possible in nutrition.

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The toxicity of dietary trans fats

Cited by 67 publications

References 56 publications

Industrial Trans Fatty Acids Stimulate SREBP2‐Mediated Cholesterogenesis and Promote Non‐Alcoholic Fatty Liver Disease

Industrial Trans Fatty Acids Stimulate SREBP2‐Mediated Cholesterogenesis and Promote Non‐Alcoholic Fatty Liver Disease

Zsírsavtúltengés – inzulinrezisztencia és β-sejt-halál

Effect of Frying Temperature and duration on the Formation of Trans Fatty Acids in Selected Fats and Oils

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