Lipogenesis and lipid peroxidation in high- fructose and cafeteria diet rodent models
Tomislav MašekPetra RoškarićMaja MaurićJosip BarišićMarcela ŠperandaKrešimir SeverinKristina Starčević
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Cafeteria
Lipogenesis
Rodent model
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Lipogenesis
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Nowadays, diseases associated with lipid accumulation in the human body such as obesity are becoming very important health issues. The aim of this study is to evaluate the impact of cafeteria diet feeding by Wistar rats, used as an experimental model of nutritional obesity, during 8 weeks, on lipid metabolism. Thus, we determined the levels of total cholesterol (TC) and triglycerides (TG) in plasma, lipoproteins and organs (liver, adipose tissue, muscle), and the activities of lipoprotein lipase (LPL) in organs, and hormone-sensitive lipase (HSL). The results show that cafeteria diet causes increased accumulation of lipids in adipose tissue leads to obesity with ectopic accumulation of lipids in other organs as liver, and induce lipoproteins metabolic disorders. Our results also show a disruption in the pathway of lipid storage enzyme (LPL) and lipid mobilization enzyme (HSL). Cafeteria diet is not only a primary risk for obesity, but also acts indirectly by adversely affecting other primary risk factors to serious chronic disease.
Cafeteria
Lipid Profile
Hepatic lipase
Hormone-sensitive lipase
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In recent years, several studies focused their attention on the role of dietary fats in the pathogenesis of hepatic steatosis. It has been demonstrated that a high-fat diet is able to induce hyperglycemia, hyperinsulinemia, obesity, and nonalcoholic fatty liver disease. On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis. In this study we have investigated the effects of krill oil on mitochondrial energetic metabolism in animals fed a high-fat diet. To this end, male Sprague-Dawley rats were divided into three groups and fed for 4 weeks with a standard diet (control group), a diet with 35% fat (HF group), or a high-fat diet supplemented with 2.5% krill oil (HF+KO group). The obtained results suggest that krill oil promotes the burning of fat excess introduced by the high-fat diet. This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity. Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed. Overall, krill oil counteracts the negative effects of a high-fat diet on mitochondrial energetic metabolism.
Steatosis
Hyperinsulinemia
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Aims The recovery of body weight after a period of caloric restriction is accompanied by an enhanced efficiency of fat deposition and hyperinsulinemia – which are exacerbated by isocaloric refeeding on a high fat diet rich in saturated and monounsaturated fatty acids (SFA-MUFA), and poor in polyunsaturated fatty acids (PUFA), and associated with a blunting of de novo lipogenesis in adipose tissue and liver. As high fat diets rich in PUFA have been shown to limit the excess fat deposition and improve glucose homeostasis, we investigated here the extent to which de novo lipogenesis in liver and adipose tissues (white and brown), as well as hepatic oxidative stress, are influenced by refeeding on diets rich in PUFA. Design In rats calorically restricted for 14 days and refed for 14 days on isocaloric amounts of a high fat diet rich in lard (i.e. high SFA-MUFA) or in safflower and linseed oils (rich in PUFA), we investigated energy balance, body composition, glycemic profile and the regulation of fatty acid synthase (rate-limiting enzyme of de novo lipogenesis) in liver, white and brown adipose tissue. We also evaluated oxidative stress in liver and skeletal muscle and markers of hepatic inflammation. Results Rats refed the PUFA diet gained less lipids and more proteins compared to rats refed SFA-MUFA diet and showed lower amount of visceral and epididymal white adipose tissue, but increased depots of interscapular brown adipose tissue, with higher expression of the uncoupling protein 1. A significant increase in non-protein respiratory quotient and carbohydrate utilisation was found in rats refed PUFA diet, with. Rats refed PUFA diet showed improved glucose homeostasis, as well as lower triglycerides and cholesterol levels. Fatty acid synthase activity was significantly higher in liver, white and brown adipose tissue, while lipid peroxidation and the degree of inflammation in the liver were significantly lower, in rats refed PUFA diet. Conclusions When considering the composition of high fat diets for nutritional rehabilitation, the inclusion of PUFA could be useful for improving protein deposition and maintaining glucose homeostasis, while limiting lipid storage in adipose tissue and oxidative stress and inflammation in the liver.
Lipogenesis
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Fatty acid synthesis
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Previously, we reported that 4-week enzymatically synthesized glycogen (ESG) supplementation reduced lipid accumulation in diet-induced obese rats. The aim of this study was to investigate the effects of long-term dietary ESG supplementation on lipid metabolism of diet-induced obese mice. Male C57BL/6NCr mice were fed a control or a high-fat diet containing 0%, 10%, or 20% ESG for 15 weeks. In the high-fat diet groups, ESG showed significant suppressive effect on adipose tissue weight. Supplementation of ESG decreased plasma cholesterol and liver lipid levels. Although, ESG substantially increased fecal lipid, ESG did not affect lipid metabolism related gene expression. In control groups ESG increased body temperature and plasma NO, although the effects were not observed in high-fat groups. In the test of single administration, ESG significantly suppressed lipid absorption. In this study, we confirmed the anti-obese effect of ESG. It is mainly due to inhibition of lipid absorption by ESG.
Lipid Profile
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