Ontology highlight
ABSTRACT:
PROVIDER: PRJNA681427 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:From a long time ago, supplementation of fermented enzyme foods could have worked health effects on the body in the east nevertheless, only a few studies reported functions of them such as weight loss and metabolic syndrome. Thus, it is necessary to be verified whether supplementation of fermented enzyme foods can act in the body as a functional material. Therefore, we investigated the anti-obesity effects of fermented mixed grain with digestive enzymes (FMG) in high-fat diet induced mice. Sixty C57BL/6J mice were divided into six dietary groups and fed a normal diet (ND), a high-fat diet (HFD), Bacilus Coagulans group, steamed grain group, low-dose fermented mixed grain group(L-FMG), high-dose fermented mixed grain group (H-FMG) supplement for 12 weeks. After sacrificing, body weight and body fat mass in H-FMG group were significantly decreased compared to HFD group with a simultaneous decrease in plasma lipids. Also, H-FMG significantly decreased the blood glucose and improved the glucose tolerance compared to HFD group. Moreover high-dose FMG supplementation dramatically decreased the levels of inflammatory cytokines which secreted from adipocyte. Taken together, our findings suggest that H-FMG ameliorate high fat-diet induced obesity and its complication and could be used as a potential preventive agent for obesity.
2020-09-12 | GSE157822 | GEO
Project description:Developmental Origins of Health and Disease Hypothesis (DOHaD) all emphasized that maternal nutrition plays an important role on the growth and development of offspring. More and more attention has been paid on the effect of maternal high fat diet and overnutrition during pregnancy on the susceptibility of offspring metabolic diseases. So we aim to build the rat model of maternal high fat diet which may induce steatohepatitis and change of lipid metabolism in the early life of offspring, and explore their possible mechannisms.And then to investigate the influence of maternal high fat diet on the expression of hepatic metabolic genes in the early life of offspring. We used microarrays to detail the global program of gene expression underlying fatty acid liver and identified distinc distinct classes of up-regulated and down-regulated genes during this process.
2015-11-17 | GSE75079 | GEO
Project description:Exposure to a high fat (HF) diet in utero is associated with increased incidence of cardiovascular disease, diabetes and metabolic syndrome later in life. However, the molecular basis of this enhanced susceptibility for metabolic disease is poorly understood. We used gene expression microarray to examine mRNA expression patterns in liver of offspring exposed to a Control or HF maternal diet. WT mice were fed a Control (9.5% fat, 3.59 kcal/g) or HF (35.5% fat, 5.29 kcal/g) diet for 2 wk before mating, throughout pregnancy and lactation. Offspring were weaned to a low fat (5.6% fat, 3.4 kcal/g) diet and were sacrificed at 5wks of age. Exposure to a maternal HF milieu activated genes of immune response, inflammation, and hepatic dysfunction. Conversely genes of lipid metabolism and biogenesis were down regulated especially in the cholesterol biosynthesis pathway. In summary, exposure to a maternal HF diet significantly alters the gene expression patterns in the liver of exposed offspring and contributes to development of metabolic disease later in life.
2017-10-02 | GSE77431 | GEO
Project description:Exploration of new markers that define impaired metabolic flexibility using an acute postprandial challenge test. Healthy subjects underwent a 4-week high-fat high-calorie diet. High-fat challenges were performed in these subjects before and after the diet and in subjects with the metabolic syndrome.
2020-01-01 | GSE124534 | GEO
Project description:In obesity, misalignment of feeding time with the light/dark environment results in disruption of peripheral circadian clocks. Conversely, restricting feeding to the active period mitigates metabolic syndrome through mechanisms that remain unknown. Here we show that adipocyte thermogenesis is essential for the healthful metabolic response to time restricted feeding. Genetic enhancement of adipocyte thermogenesis through ablation of Zfp423 attenuates obesity caused by circadian mistimed high fat diet feeding through a mechanism involving creatine metabolism. Circadian control of adipocyte creatine metabolism underlies timing of diet-induced thermogenesis, and enhancement of adipocyte circadian rhythms through overexpression of the clock activator Bmal1 ameliorates metabolic complications during diet induced obesity. These findings establish creatine mediated diet-induced thermogenesis as a bioenergetic mechanism driving metabolic benefits during time-restricted feeding.
2022-10-24 | GSE181443 | GEO
Project description:Studies have reported opposing effects of high-fat diet and mechanical stimulation on lineage commitment of the bone marrow stem cells. Yet, how the bone marrow modulates its gene expression in response to the combined effects of mechanical loading and a high-fat diet has not yet been addressed. We investigated whether early-life voluntary physical activity can modulate the effects of a high-fat diet on body composition, bone phenotype and bone marrow gene expression in male Sprague Dawley rats. We show that early-life high-fat diet positively affected body weight, total fat percentage and bone mass indices. In the bone marrow, early-life high-fat diet resulted in adipocyte hypertrophy and a pro-inflammatory and pro-adipogenic gene expression profile. Crucially, the bone marrow of the rats that undertook wheel exercise while on a high-fat diet retained a memory of the early-life exercise. This memory lasted at least 60 days after the cessation of the voluntary exercise and was manifest by: 1) the bone marrow adipocyte size of the exercised rats not exhibiting hypertrophy; and 2) genes associated with mature adipocyte function being down-regulated. Our results are consistent with the marrow adipose tissue having a unique and long-lasting response to high-fat feeding in the presence or absence of exercise.
2017-08-30 | GSE97376 | GEO
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.
2014-07-21 | E-GEOD-45927 | biostudies-arrayexpress
Project description:Exposure to a high fat (HF) diet in utero is associated with increased incidence of cardiovascular disease, diabetes and metabolic syndrome later in life. However, the molecular basis of this enhanced susceptibility for metabolic disease is poorly understood. We performed genome-wide DNA methylation analysis to examine DNA methylation patterns in liver of offspring exposed to a Control or HF maternal diet. WT mice were fed a C (9.5% fat, 3.59 kcal/g) or HF (35.5% fat, 5.29 kcal/g) diet for 2 wk before mating, throughout pregnancy and lactation. Offspring were weaned to a low fat (5.6% fat, 3.4 kcal/g) diet and were sacrificed at 5wks of age. DNA methylation analysis revealed the majority of differentially methylated regions were hypermethylated in HF liver. Chromosomal distribution analysis showed hypermethylation hot spots on chromosomes 4 (atherosclerosis susceptibility QTL1) and 18 (insulin dependent susceptibility 21). Most of the hypermethylated genes in these hot spots are associated with cardiovascular system development and function. In summary, exposure to a maternal HF diet significantly alters the DNA methylation patterns in the liver of exposed offspring and contributes to programmed development of metabolic disease later in life.
2017-10-02 | GSE77430 | GEO
Project description:There is increased interest in the potential protective role of dietary Ca in the development of metabolic disorders related to the metabolic syndrome. Ca-induced intestinal precipitation of fatty acids and bile acids as well as systemic metabolic effects of Ca on adipose tissue is proposed to play a causal role. In this experiment, we have studied all these aspects to validate the suggested protective effect of Ca supplementation, independent of other dietary changes, on the development of diet-induced obesity and insulin resistance. In our diet intervention study, C57BL/6J mice were fed high-fat diets differing in Ca concentrations (50 v. 150 mmol/kg). Faecal excretion analyses showed an elevated precipitation of intestinal fatty acids (2·3-fold; P < 0·01) and bile acids (2-fold; P < 0·01) on the high-Ca diet. However, this only led to a slight reduction in fat absorption (from 98 to 95 %; P < 0·01), mainly in the distal small intestine as indicated by gene expression changes. We found no effect on body-weight gain. Lipolysis and lipogenesis-related parameters in adipose tissue also showed no significant changes on the high-Ca diet, indicating no systemic effects of dietary Ca on adiposity. Furthermore, early gene expression changes of intestinal signaling molecules predicted no protective effect of dietary Ca on the development of insulin resistance, which was confirmed by equal values for insulin sensitivity on both diets. Taken together, our data do not support the proposed protective effect of dietary Ca on the development of obesity and/or insulin resistance, despite a significant increase in fecal excretion of fatty acids and bile acids. Keywords: Diet intervention study Nine-week-old mice were fed a high fat purified diet with a low calcium concentration of 50mmol/kg (LCa diet) or a high calcium concentration of 150mmol/kg (HCa diet) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. For microarray analysis, after 2 weeks of diet intervention, 6 mice per diet group were anaesthetized with a mixture of isofluorane (1.5%), nitrous oxide (70%) and oxygen (30%) and the small intestines were excised. Adhering fat and pancreatic tissue were carefully removed. The small intestines were divided in three equal parts along the proximal to distal axis (SI 1, SI 2 and SI 3) and microarray analysis was performed on pooled mucosal scrapings.
2011-03-03 | E-GEOD-18581 | biostudies-arrayexpress