Project description:High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver. Adult male Wistar rats were fed diets with varying amounts of protein, carbohydrates and fat for 5 weeks. At the end of the experiment, rats were killed and tanscriptome analysis was performed on pooled liver samples.
Project description:Miniature pigs are useful model animal for gene expression studies on dietary-induced hyperlipidemia, because they have similar digestive physiology to human. Two typical dietary components were used for dietary-induced hyperlipidemia miniature pig models. One is a high-fat and high-cholesterol diet (HFCD) containing 15% lard and 2% cholesterol, the other is a high-fat, high-cholesterol and high-sucrose diet (HFCSD) containing 15% lard, 2% cholesterol and 37% sucrose.
Project description:High-protein diets are known to reduce adiposity in the context of high carbohydrate and Western diets. However, few studies have investigated the specific high-protein effect on lipogenesis induced by a high-sucrose (HS) diet or fat deposition induced by high-fat feeding. We aimed to determine the effects of high protein intake on the development of fat deposition and partitioning in response to high-fat and/or HS feeding. A total of thirty adult male Wistar rats were assigned to one of the six dietary regimens with low and high protein, sucrose and fat contents for 5 weeks. Body weight (BW) and food intake were measured weekly. Oral glucose tolerance tests and meal tolerance tests were performed after 4th and 5th weeks of the regimen, respectively. At the end of the study, the rats were killed 2 h after ingestion of a calibrated meal. Blood, tissues and organs were collected for analysis of circulating metabolites and hormones, body composition and mRNA expression in the liver and adipose tissues. No changes were observed in cumulative energy intake and BW gain after 5 weeks of dietary treatment. However, high-protein diets reduced by 20 % the adiposity gain induced by HS and high-sucrose high-fat (HS-HF) diets. Gene expression and transcriptomic analysis suggested that high protein intake reduced liver capacity for lipogenesis by reducing mRNA expressions of fatty acid synthase (fasn), acetyl-CoA carboxylase a and b (Acaca and Acacb) and sterol regulatory element binding transcription factor 1c (Srebf-1c). Moreover, ketogenesis, as indicated by plasma β-hydroxybutyrate levels, was higher in HS-HF-fed mice that were also fed high protein levels. Taken together, these results suggest that high-protein diets may reduce adiposity by inhibiting lipogenesis and stimulating ketogenesis in the liver.
Project description:Miniature pigs are useful model animal for gene expression studies on dietary-induced hyperlipidemia, because they have similar digestive physiology to human. Two typical dietary components were used for dietary-induced hyperlipidemia miniature pig models. One is a high-fat and high-cholesterol diet (HFCD) containing 15% lard and 2% cholesterol, the other is a high-fat, high-cholesterol and high-sucrose diet (HFCSD) containing 15% lard, 2% cholesterol and 37% sucrose. Whole blood gene expression in HFCD, HFCSD and control male miniature pigs was measured at 10, 19 and 27 weeks of feeding periods.M-cM-^@M-^@White blood cell gene expression in HFCD, HFCSD and control male miniature pigs was measured at 27 weeks of feeding period.
Project description:Cardiovascular (CV) disease is a leading cause of morbidity and mortality in Western societies. Even after accounting for traditional CV risk factors (e.g. obesity, smoking and hypertension), the inflammation-driven thickening and stiffening of central arteries is a strong predictor of adverse outcomes. Arterial wall changes are universally associated with advancing age and show unparalleled worsening in metabolic syndrome. In mice, resveratrol ameliorates a high-fat diet induced arterial wall inflammation and slows age-associated physiologic deteriorations within the arterial wall. Here we tested resveratrol in adult male rhesus monkeys, an experimental model relevant to humans. A diet rich in fat and sucrose (HFS) led to an increase in body weight as well as thickening and stiffening of the aortic wall, marked by diffuse inflammation, fibrosis and fat infiltration. Dietary resveratrol supplementation prevented diet-induced structural and functional alterations within the aortic wall, and abrogated the deleterious vascular endothelial and smooth muscle responses. Integrative genomic and proteomic analyses of aortic tissues revealed molecular signatures consistent with improved vascular functions. Thus, resveratrol conferred protection against the initiation of diet-induced inflammatory events that progress to pathological thickening and stiffening of large arteries. Dietary resveratrol may therefore hold promise as a novel therapy to ameliorate metabolic stress-induced CV disease. After baseline assessment, four male rhesus monkeys remained on the healthy standard diet (SD), 10 male rhesus monkeys were begun on a high fat/high sucrose (HFS) diet and 10 male rhesus monkeys were begun on a high fat/high sucrose (HFS) diet plus Resveratrol, 80mg/day. After one year of dietary intervention, the amount of resveratrol was increased to 240mg/day for one additional year. Tissues were then harvested for the array experiments.