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      Oxidative stress and fatty acid profile in Wistar rats subjected to acute food restriction and refeeding with high-fat diets

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          Abstract

          PURPOSE: To assess oxidative stress and the profile of fatty acids incorporated into the hepatic tissue of animals refed with high-fat (HF) diets after acute food restriction.METHODS: Fifty male Wistar rats were divided into five groups and fasting for 48 hours. One group was sacrificed without refeeding (NR), a control group (C) was refed with the standard AIN-93 diet and the remaining groups with HF diets respectively consisting of hydrogenated vegetable oil (PHVO), trans-free (TF) margarine and trans-free margarine enriched with ω-3 and ω-6 (O). After this period the animals were sacrificed for malondialdehyde (MDA), catalase and hepatic fatty acid determination.RESULTS: The groups refed with HF diets showed elevation of MDA levels compared to the C group (p<0.001 for GVH and p<0.01 for TF and O). Hepatic catalase activity was higher in the TF and O groups compared to group C (p<0.05 for both). The amount of saturated fatty acids was lower in the PHVO and O groups compared to the remaining ones (p<0.001).CONCLUSION: The consumption of high-fat diets after prolonged fasting favors oxidative imbalance in hepatic tissue.

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          Review: The role of insulin resistance in nonalcoholic fatty liver disease.

          Insulin resistance is an almost universal finding in nonalcoholic fatty liver disease (NAFLD). This review outlines the evidence linking insulin resistance and NAFLD, explores whether liver fat is a cause or consequence of insulin resistance, and reviews the current evidence for treatment of NAFLD. Evidence from epidemiological, experimental, and clinical research studies investigating NAFLD and insulin resistance was reviewed. Insulin resistance in NAFLD is characterized by reductions in whole-body, hepatic, and adipose tissue insulin sensitivity. The mechanisms underlying the accumulation of fat in the liver may include excess dietary fat, increased delivery of free fatty acids to the liver, inadequate fatty acid oxidation, and increased de novo lipogenesis. Insulin resistance may enhance hepatic fat accumulation by increasing free fatty acid delivery and by the effect of hyperinsulinemia to stimulate anabolic processes. The impact of weight loss, metformin, and thiazolidinediones, all treatments aimed at improving insulin sensitivity, as well as other agents such as vitamin E, have been evaluated in patients with NAFLD and have shown some benefit. However, most intervention studies have been small and uncontrolled. Insulin resistance is a major feature of NAFLD that, in some patients, can progress to steatohepatitis. Treatments aimed at reducing insulin resistance have had some success, but larger placebo-controlled studies are needed to fully establish the efficacy of these interventions and possibly others in reducing the deleterious effects of fat accumulation in the liver.
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            Clinical Review: Nonalcoholic fatty liver disease: a novel cardiometabolic risk factor for type 2 diabetes and its complications.

            Nonalcoholic fatty liver disease (NAFLD) is increasingly diagnosed worldwide and is the most common chronic liver disease in Western countries. In this review, we discuss the role of NAFLD as a novel cardiometabolic risk factor for the development of type 2 diabetes (T2DM) and for the development of major chronic complications and poor glycemic control in people with established T2DM. This is a clinical, narrative review and not a systematic review and meta-analysis. PubMed was extensively searched for articles using the keywords "nonalcoholic fatty liver disease" or "fatty liver" combined with "diabetes risk," "cardiovascular risk," "cardiovascular mortality," "chronic kidney disease," or "diabetic nephropathy" between 1990 and 2012. Articles published in languages other than English were excluded from the analysis. NAFLD exacerbates hepatic insulin resistance and increases the risk of developing T2DM. Growing evidence also indicates that NAFLD may worsen glycemic control in people with T2DM and may contribute to the development and progression of the most important chronic complications of diabetes, such as cardiovascular disease and chronic kidney disease. The adverse impact of NAFLD on risk for T2DM and its major chronic vascular complications deserves particular attention among endocrinologists/cardiologists/hepatologists, in view of the implications for screening and surveillance strategies in the growing number of patients with NAFLD. Clinicians who manage patients with NAFLD should not only focus on liver disease, but should also recognize the increased risk of developing T2DM and its chronic vascular complications and undertake early, aggressive risk factor modification.
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              The comparative physiology of food deprivation: from feast to famine.

              The ability of animals to survive food deprivation is clearly of considerable survival value. Unsurprisingly, therefore, all animals exhibit adaptive biochemical and physiological responses to the lack of food. Many animals inhabit environments in which food availability fluctuates or encounters with appropriate food items are rare and unpredictable; these species offer interesting opportunities to study physiological adaptations to fasting and starvation. When deprived of food, animals employ various behavioral, physiological, and structural responses to reduce metabolism, which prolongs the period in which energy reserves can cover metabolism. Such behavioral responses can include a reduction in spontaneous activity and a lowering in body temperature, although in later stages of food deprivation in which starvation commences, activity may increase as food-searching is activated. In most animals, the gastrointestinal tract undergoes marked atrophy when digestive processes are curtailed; this structural response and others seem particularly pronounced in species that normally feed at intermittent intervals. Such animals, however, must be able to restore digestive functions soon after feeding, and these transitions appear to occur at low metabolic costs.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                acb
                Acta Cirurgica Brasileira
                Acta Cir. Bras.
                Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (São Paulo )
                1678-2674
                March 2014
                : 29
                : 3
                : 178-185
                Affiliations
                [1 ] Universidade de São Paulo Brazil
                [2 ] Universidade de São Paulo Brazil
                [3 ] Universidade de São Paulo Brazil
                [4 ] Universidade de São Paulo Brazil
                Article
                S0102-86502014000300178
                10.1590/S0102-86502014000300006
                24626730
                6b947747-8844-4e01-ac53-dcf41df2c614

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0102-8650&lng=en
                Categories
                SURGERY

                Surgery
                Fasting,Diet, High-Fat, Oxidative Stress,Fatty Acids,Rats
                Surgery
                Fasting, Diet, High-Fat, Oxidative Stress, Fatty Acids, Rats

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