scholarly journals Correction to: A trans fatty acid substitute enhanced development of liver proliferative lesions induced in mice by feeding a cholinedeficient, methionine-lowered, L-amino acid-defined, high-fat diet.

2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Noriko Suzuki-Kemuriyama ◽  
Akari Abe ◽  
Kinuko Uno ◽  
Shuji Ogawa ◽  
Atsushi Watanabe ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Amino Acid ◽  
Trans Fatty Acid ◽  
High Fat Diet ◽  
High Fat

scholarly journals A Trans Fatty Acid Substitute Aggravates Nonalcoholic Steatohepatitis Induced in Mice by Feeding a Choline-Deficient, Methionine-Lowered, L-Amino Acid-Defined, High-Fat Diet

2020 ◽  
Author(s):  
Noriko Suzuki-Kemuriyama ◽  
Akari Abe ◽  
Kinuko Uno ◽  
Shuji Ogawa ◽  
Atsushi Watanabe ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Amino Acid ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Saturated Fatty Acids ◽  
Elevated Serum ◽  
High Fat ◽  
Hepatocellular Apoptosis ◽  
Liver Changes

Abstract Background: Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Trans fatty acid (TFA) is hazardous for human health and a risk factor of NASH; thus, efforts have focused on reducing its intake. However, the health benefits of reducing dietary TFA are not fully elucidated. We investigated effects of TFA and its substitute on NASH induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet (CDAA-HF). Methods: Mice were fed CDAA-HF containing shortening with TFA (CDAA-HF-T(+)), CDAA-HF containing shortening with a TFA substitute (CDAA-HF-T(−)), or a control chow for 13/26 weeks. Results: CDAA-HF-T(+) contained TFA, whereas CDAA-HF-T(−) contained no TFA and much saturated fatty acids. CDAA-HF-T(+) and CDAA-HF-T(−) induced NASH in mice, evidenced by elevated serum transaminase activity and liver changes, including steatosis, inflammation, and fibrosis. CDAA-HF-T(−) induced more hepatocellular apoptosis and proliferative (preneoplastic and non-neoplastic) nodular lesions than CDAA-HF-T(+). Conclusions: Thus, replacement of dietary TFA with its substitute does not prevent but aggravates nutritionally induced NASH in mice, at least under the present conditions. Attention should be paid regarding future TFA substitute use in humans, and a fatty acid balance is likely more important than the particular types of fatty acids.

scholarly journals Effect of a high fat diet on lipid absorption and fatty acid transport in a rat model of short bowel syndrome

2003 ◽  
Vol 19 (5) ◽  
pp. 385-390 ◽  
Author(s):  
Igor Sukhotnik ◽  
A. Semih Gork ◽  
Min Chen ◽  
Robert A. Drongowski ◽  
Arnold G. Coran ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Short Bowel Syndrome ◽  
Rat Model ◽  
High Fat Diet ◽  
Lipid Absorption ◽  
Fatty Acid Transport ◽  
Acid Transport ◽  
High Fat ◽  
Short Bowel

scholarly journals Molecular adaptation in adipose tissue in response to overfeeding with a high-fat diet under sedentary conditions in South Asian and Caucasian men

2019 ◽  
Vol 122 (03) ◽  
pp. 241-251
Author(s):  
Siti N. Wulan ◽  
Freek G. Bouwman ◽  
Klaas R. Westerterp ◽  
Edwin C. M. Mariman ◽  
Guy Plasqui
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
South Asian ◽  
High Fat Diet ◽  
South Asians ◽  
Molecular Adaptation ◽  
Body Fat Percentage ◽  
High Fat ◽  
Fat Percentage ◽  
Caucasian Men

AbstractFor the same BMI, South Asians have a higher body fat percentage than Caucasians. There might be differences in the fatty acid (FA) handling in adipose tissue when both ethnicities are exposed to high-fat overfeeding. The objective of the present study was to investigate the molecular adaptation in relation to FA metabolism in response to overfeeding with a high-fat diet (OHFD) in South Asian and Caucasian men. Ten South Asian men (BMI 18–29 kg/m2) and ten Caucasian men (BMI 22–33 kg/m2), matched for body fat percentage, aged 20–40 years were included. A weight-maintenance diet (30 % fat, 55 % carbohydrate and 15 % protein) was given for 3 d followed by 3 d of overfeeding (150 % energy requirement) with a high-fat diet (60 % fat, 25 % carbohydrate and 15 % protein) while staying in a respiration chamber. Before and after overfeeding, abdominal subcutaneous fat biopsies were taken. Proteins were isolated, analysed and quantified for short-chain 3-hydroxyacyl-CoA dehydrogenase (HADH), carnitine palmitoyl-transferase 1α (CPT1a), adipose TAG lipase, perilipin A (PLINA), perilipin B, lipoprotein lipase and fatty acid binding protein 4 using Western blotting. OHFD decreased the HADH level (P < 0·05) in Caucasians more than in Asians (P < 0·05), but the baseline and after intervention HADH level was relatively higher in Caucasians. The level of CPT1a decreased in South Asians and increased in Caucasians (P < 0·05). PLINA did not change with diet but the level was higher in South Asians (P < 0·05). The observed differences in HADH and PLINA levels as well as in CPT1a response may be important for differences in the long-term regulation of energy (fat) metabolism in these populations.

The effects of fish oil consumption on cardiovascular remodeling in ApoE deficient mice

2013 ◽  
Vol 91 (11) ◽  
pp. 960-965 ◽  
Author(s):  
Kelby Cleverley ◽  
Xiaozhou Du ◽  
Sheena Premecz ◽  
Khuong Le ◽  
Matthew Zeglinski ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acid ◽  
Fish Oil ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Omega 3 ◽  
High Fat ◽  
Omega 3 Fatty Acid ◽  
Deficient Mice

Owing to their spontaneous development of atherosclerosis, apolipoprotein E knockout mice (ApoEKO) are one of the best studied animal models for this disease. Little is known about the utility of various omega-3 fatty acid regimens, in particular fish oils, in preventing cardiac disease in ApoEKO mice. The purpose of this study was to determine the cardiovascular effects of omega-3 fatty acid supplementation with either safflower oil (control), fish oil, flaxseed oil, or designed oil in ApoEKO mice fed a high-fat diet for a total of 16 weeks. In-vivo cardiac function was assessed weekly using murine echocardiography. Blood pressure, plasma lipid levels, and brain natriuretic peptide (BNP) were serially measured. The results show that ApoEKO mice fed fish oil demonstrated an increase in left ventricular wall thickness as a result of increased afterload. Despite chronic treatment with fish oil over 16 weeks, blood pressure increased in ApoEKO mice by 20% compared with the baseline. Both echocardiographic evidence of left ventricular hypertrophy and biochemical increase in BNP levels confirmed diastolic dysfunction in ApoEKO mice fed fish oil. This suggests that high-fat diet supplemented with fish oil may lead to adverse cardiovascular effects in ApoE deficient mice.

Ezetimibe prevents hepatic steatosis induced by a high-fat but not a high-fructose diet

2013 ◽  
Vol 305 (2) ◽  
pp. E293-E304 ◽  
Author(s):  
Masateru Ushio ◽  
Yoshihiko Nishio ◽  
Osamu Sekine ◽  
Yoshio Nagai ◽  
Yasuhiro Maeno ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Fatty Acid Synthase ◽  
Binding Protein ◽  
High Fat ◽  
High Fructose Diet ◽  
High Fructose ◽  
Element Binding Protein

Nonalcoholic fatty liver disease is the most frequent liver disease. Ezetimibe, an inhibitor of intestinal cholesterol absorption, has been reported to ameliorate hepatic steatosis in human and animal models. To explore how ezetimibe reduces hepatic steatosis, we investigated the effects of ezetimibe on the expression of lipogenic enzymes and intestinal lipid metabolism in mice fed a high-fat or a high-fructose diet. CBA/JN mice were fed a high-fat diet or a high-fructose diet for 8 wk with or without ezetimibe. High-fat diet induced hepatic steatosis accompanied by hyperinsulinemia. Treatment with ezetimibe reduced hepatic steatosis, insulin levels, and glucose production from pyruvate in mice fed the high-fat diet, suggesting a reduction of insulin resistance in the liver. In the intestinal analysis, ezetimibe reduced the expression of fatty acid transfer protein-4 and apoB-48 in mice fed the high-fat diet. However, treatment with ezetimibe did not prevent hepatic steatosis, hyperinsulinemia, and intestinal apoB-48 expression in mice fed the high-fructose diet. Ezetimibe decreased liver X receptor-α binding to the sterol regulatory element-binding protein-1c promoter but not expression of carbohydrate response element-binding protein and fatty acid synthase in mice fed the high-fructose diet, suggesting that ezetimibe did not reduce hepatic lipogenesis induced by the high-fructose diet. Elevation of hepatic and intestinal lipogenesis in mice fed a high-fructose diet may partly explain the differences in the effect of ezetimibe.

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