Sphingolipid species are not only increased in insulin-resistant humans with NASH but also correlate with hepatic oxidative stress and inflammation, suggesting that these lipids may play a role during progression of simple steatosis to NASH in humans.
Epidemiological studies reveal associations between obesity/metabolic syndrome and mood disorders. We assessed behavioural changes in rats fed diets enriched in fat and fructose in different proportions and correlated the observed alterations with biochemical changes induced by the diets. Three groups of rats were used as follows: control (C) animals fed regular rat chow, rats fed high-fat diet (HF) and rats fed high-fat and high-fructose diet (HFHF). HF and HFHF animals were also given a 10% fructose solution as drinking water. Behavioural and biochemical parameters were determined. Anxiety was measured by the open-field and the social interaction test. Depression-like behaviour was evaluated by the forced swimming test. The object recognition test was utilized to assess effects on memory. Diet-exposed animals displayed signs of anxiety in the open-field (HF rats had reduced central time; HFHF rats had reduced number of central entries) and in the social interaction test (decreased time of interaction in HF group). In the forced swimming test, the immobility time was prolonged in the HFHF group. While different measures of anxiety scores correlated with visceral adiposity and dyslipidemia, results from both social interaction and forced swimming tests were significantly associated with lipid peroxidation, which in turn also correlated with the metabolic parameters. The experimental diets did not affect the object recognition memory. Both experimental diets induced metabolic derangements in rats and provoked similar anxiety- and depression-like behaviours. Lipid peroxidation seems to play a role in translating diet-induced metabolic alterations into behavioural disorders.
Metabolic syndrome (MS) is a disorder comprising central obesity, dyslipidemia, raised blood pressure, insulin resistance. The aim of the present study was to develop a cheap, easy and reproducible rat model of MS. 36 male Wistar rats were divided in 3 groups: a control group (C) receiving regular rat chow diet, a high-fat (HF) group receiving lard enriched rat chow and a high-fat high-fructose (HFHF) group receiving lard and fructose enriched rat chow. HF and HFHF groups had also 10% fructose in their drinking water. The duration of the study was 8 weeks. Body weights were measured weekly. At the end of the study insulin tolerance test (ITT) was performed. Liver and fat weight index were measured after sacrifice. Lipid biochemical parameters and insulin concentration in serum were determined. Liver triglycerides (TG) were measured. The oxidative stress in serum was assessed by thiobarbituric reactive substances (TBARS). At the end of the study the animals did not differ in their body weights across the groups, but the fat index in both HF and HFHF groups was higher. Plasma TG and cholesterol were raised in both groups and the ratio cholesterol/ HDL-cholesterol was higher. Liver TG were elevated in HFHF rats. ITT revealed reduced insulin sensitivity in both experimental groups although serum insulin was elevated only in HFHF group. TBARS were increased in both HF and HFHF groups. Both models displayed most of the features of MS; the HFHF probably better reflects the 'cafeteria' diet and its unhealthy consequences.
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