Fructose in combination with TFA caused NASH with fibrosis by inducing oxidative stress and inflammation, whereas, fructose in combination with SFA caused simple steatosis, suggesting that the type of fatty acid is more important for the progression of NAFLD.
Background. Increased fructose consumption is linked to the development of metabolic syndrome (MS). Here we investigated the time course of development of MS features in high-fructose-fed Sprague Dawley rats along with circulatory testosterone and homocysteine levels. Methods. Rats were divided into control and experimental groups and fed with diets containing 54.5% starch and fructose, respectively, for 4, 12, and 24 weeks. Plasma testosterone and homocysteine levels were measured along with insulin, glucose, and lipids. Body composition, insulin resistance, and hepatic lipids were measured. Results. Increase in hepatic triglyceride content was first observed in metabolic disturbance followed by hypertriglyceridemia and systemic insulin resistance in fructose-fed rats. Hepatic lipids were increased in time-dependent manner by fructose-feeding starting from 4 weeks, but circulatory triglyceride levels were increased after 12 weeks. Fasting insulin and Homeostatis Model Assessment of Insulin Resistance (HOMA-IR) were increased after 12 weeks of fructose-feeding. Decreased visceral adiposity, circulatory testosterone, and homocysteine levels were observed after 4 weeks of fructose-feeding, which were normalized at 12 and 24 weeks. Conclusions. We conclude that transient decrease in circulatory testosterone and homocysteine levels and increased hepatic triglyceride content are the earliest metabolic disturbances that preceded hypertriglyceridemia and insulin resistance in fructose-fed SD rats.
Effect of dietary n‐6/n‐3 polyunsaturated fatty acids (PUFA) ratio on the fructose‐induced adipose tissue oxidative and endoplasmic reticulum (ER) stress was not explored previously. Here, we studied the effect of diets containing n‐6 PUFA & α‐linolenic acid (ALA, 18:3 n‐3 PUFA) and n‐6 PUFA & long chain n‐3 PUFA (docosahexanoic acid and eicosapentaenoic acid, DHA and EPA) in the ratio of 2:1 and 5:1 respectively on fructose‐induced oxidative and ER stress in adipose tissue.Weanling Wistar rats were divided in to four groups and fed with diets containing starch (n‐6/n‐3 PUFA ratio 215:1), fructose (n‐6/n‐3 PUFA ratio 215:1) and fructose‐with n‐6/n‐3 PUFA ratio 2:1 (18:3 n‐3 PUFA) and 5:1 (long chain n‐3 PUFA) diets for twenty‐four weeks. Activities of glucose‐6‐phosphate dehydrogenase (G6PDH), glutathione peroxidase (GPx), and catalase and superoxide dismutase (SOD) were measured in visceral adipose tissue along with glutathione levels and lipid peroxidation. Expression of p22 phox gene related oxidative stress was quantified along with ER stress marker gene, GRP78.ALA and long chain (LC) n‐3 PUFA feeding significantly reduced fructose‐induced G6PDH activity to similar extent by 28% (p≤0.01). Both ALA and LC n‐3 PUFA significantly reduced the fructose‐induced SOD activity by 15% and 12% respectively (p≤0.01), whereas they reduced fructose‐induced catalase activity to similar extent by 23.5% (p≤0.05). ALA and long chain (LC) n‐3 PUFA feeding significantly elevated the GPx activity that is reduced by high fructose‐ diet feeding by 14.6% and 12% respectively (p≤0.05) without altering the tissue glutathione levels. Lipid peroxidation, an important determinant of tissue oxidative stress is significantly reduced by both ALA‐ and LC n‐3 PUFA‐enriched diets by 12% and 35% respectively (p≤0.01). p22 phox gene expression is significantly reduced by both ALA and LC n‐3 PUFA by 12% and 33% respectively (p≤0.05) along with ER stress marker, GRP78 by 40% and 30% respectively (p≤0.05).We conclude that replacement of dietary n‐6 PUFA with ALA and LC n‐3 PUFA ameliorates fructose‐induced oxidative and ER stress in visceral adipose tissue. Though both ALA and LC n‐ 3 PUFA significantly reduced fructose‐induced oxidative stress, considering beneficial effects LC n‐3 PUFA on lipid peroxidation and LC n‐3 PUFA exhibited protective nature at less quantity than ALA, we propose that diets rich in LC n‐3 PUFA may protect against fructose‐induced oxidative and ER stress in adipose tissue.Support or Funding InformationThe present study was carried out with the financial support of Department of Biotechnology (DBT), Ministry of Science and Technology, Government of India, and Indian Council of Medical Research (ICMR), Government of India. AS was supported by Council of Scientific and Industrial Research (CSIR).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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