The effects of weight cycling on the metabolic homeostasis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE134336 | GEO | 2021/09/30
REPOSITORIES: GEO
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Project description:Dietary interventions are effective ways to extend or shorten lifespan. By examining midlife hepatic gene expressions in mice under different dietary conditions, which resulted in different lifespans and aging-related phenotypes, we were able to identify genes and pathways that modulate the aging process. We found that pathways transcriptionally correlated with diet-modulated lifespan and physiological changes were enriched for lifespan-modifying genes. Male C57BL/6J mice at 4 weeks of age were purchased from Shanghai Animal Co, Ltd. Mice were maintained under a 12-hour dark/light cycle (lights on at 6:30 am) at a temperature of 22 ± 3 °C in accredited animal facilities. Prior to the start of experiment, mice were maintained on a low-fat diet (Research Diets Inc., New Brunswick, NJ) for one week. At the age of 5 weeks, animals were randomly assigned to one of the 6 intervention groups (n = 30 for each group): feeding of a low-fat diet (10% fat, D12450B, Research Diets) ad libitum (LF) or with 30% calorie restriction (LF+CR) or with voluntary running exercise (LF+Ex), feeding of a high-fat diet (60% fat, D12492, Research Diets) ad libitum (HF) or with 30% calorie restriction (HF+CR) or with voluntary running exercise (HF+Ex). All mice were housed individually during the study. The daily consumption of food in LF and HF groups was recorded over a week and averaged to determine the amount of food for the following week for the LF+CR and HF+CR groups, respectively. After 1 week acclimation in cage with the locked running wheels, mice in the LF+Ex and HF+Ex groups were allowed free access to a running wheel, and the running distance and time were recorded automatically by the equipment. The hepatic transcriptional level for 3 mice from each intervention group at 62 weeks of age was analyzed using Affymetrix Mouse Genome 430 2.0 Arrays.
2012-03-27 | E-GEOD-36838 | biostudies-arrayexpress
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Project description:We studied the effect of dietary fat type, varying in polyunsaturated/saturated fatty acid ratio's (P/S) on development of metabolic syndrome. C57Bl/6J mice were fed purified high-fat diets (45E% fat) containing palm oil (HF-PO; P/S 0.4), olive oil (HF-OO; P/S 1.1) or safflower oil (HF-SO; P/S 7.8) for 8 weeks. A low-fat palm oil diet (LF-PO; 10E% fat) was used as a reference. Additionally, we analyzed diet-induced changes in gut microbiota composition and mucosal gene expression. The HF-PO diet induced a higher body weight gain and liver triglyceride content compared to the HF-OO, HF-SO or LF-PO diet. In the intestine, the HF-PO diet reduced microbial diversity and increased the Firmicutes/Bacteroidetes ratio. Although this fits a typical obesity profile, our data clearly indicate that an overflow of the HF-PO diet to the distal intestine, rather than obesity itself, is the main trigger for these gut microbiota changes. A HF-PO diet-induced elevation of lipid metabolism-related genes in the distal small intestine confirmed the overflow of palm oil to the distal intestine. Some of these lipid metabolism-related genes were previously already associated with the metabolic syndrome. In conclusion, our data indicate that saturated fat (HF-PO) has a more stimulatory effect on weight gain and hepatic lipid accumulation than unsaturated fat (HF-OO and HF-SO). The overflow of fat to the distal intestine on the HF-PO diet induced changes in gut microbiota composition and mucosal gene expression. We speculate that both are directly or indirectly contributive to the saturated fat-induced development of obesity and hepatic steatosis. Keywords: Diet intervention study Nine-week-old C57Bl/6J mice were fed a low-fat diet (LF-PO) and three different types of high-fat diet, based on palm oil (HF-PO; P/S1.0), olive oil (HF-OO; P/S4.6) and safflower oil (HF-SO; P/S10.1) for 8 weeks. Body weight was recorded weekly and after 7 weeks of diet intervention an oral glucose tolerance test was performed. After 2 weeks of diet intervention, 6 mice per high-fat 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 mucosal scrapings.
2012-06-17 | E-GEOD-18586 | biostudies-arrayexpress
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2007-11-30 | E-GEOD-8524 | 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 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.
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Project description:The impact of high fat diet on secreted milk small RNA transcriptome was studied by isolating total RNA from milk fat fraction collected on lactation day 10 from control diet fed (C; n=5; 10% fat; 7% sucrose; Research Diets #D12450J, Brunswick, NJ) and high fat diet fed (HF; n=4; Research Diets #D12492, 60% of total kcal energy is fat and match 7% of total kcal is sucrose; Brunswick, NJ) mice.
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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.
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Project description:How signals from fatty acid metabolism are translated into changes in food intake remains unclear. Previously we reported that mice with a genetic inactivation of Acads (short-chain acyl-CoA dehydrogenase), encoding the enzyme responsible for mitochondrial beta-oxidation of C4-C6 short-chain fatty acids (SCFAs), shift consumption away from fat and toward carbohydrate when offered a choice. This finding demonstrated that the loss of a specific enzyme in fatty acid oxidation alters the choice of diet intake. To our knowledge, there are no reports of studies on the effects of dietary fat on the brain transcriptome in genetic models of fatty acid oxidation deficiency. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. The current study aimed to identify molecular mediators underlying the effects of SCFA oxidation deficiency on food intake. We performed a transcriptional screen for gene expression in brain tissue of Acads-/- and Acads+/+ mice fed either high-fat (HF) or low-fat (LF) diet for 2 d. Ingenuity Pathway Analysis revealed three top-scoring pathways significantly modified by genotype or diet: oxidative phosphorylation, mitochondrial dysfunction, and CREB signaling in neurons. A comparison of statistically significant responses in HF Acads-/- vs. HF Acads+/+ (3917) and Acads+/+ HF vs. LF Acads+/+ (3879) revealed 2551 genes or approximately 65% in common between the two experimental comparisons. All but one of these genes were expressed in opposite direction with similar magnitude, demonstrating that Acads-deficient mice fed HF diet display transcriptional responses that mimic those of wildtype Acads+/+ mice fed LF diet. Intriguingly, genes involved in energy sensing and metabolism followed this pattern. Quantitative RT-PCR in hypothalamus confirmed the dysregulation of several genes in these pathways. Western blotting showed that the combination of Acads deficiency and HF diet increased hypothalamic AMP-kinase, a key protein in an energy-sensing cascade that responds to depletion of ATP. Our results suggest that the decreased beta oxidation of short-chain fatty acids in Acads-deficient mice fed HF diet produces a state of energy deficiency in the brain and that AMP-kinase is the cellular energy-sensing mechanism linking fatty acid oxidation to feeding behavior in this model. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from whole brain tissue was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in brain was compared between strains and between diets. Twelve-week old male BALB/cByJ (Acads-/-) and BALB/cByKZ (Acads+/+) mice were fed a high-fat (D12331; Research Diets) and low-fat (D12329) diet for two days. Total RNA from liver was obtained from three mutant (Acads-/-) and three wild-type (Acads+/+) mice of each diet group. All mice had similar body weights before diets were initiated. Gene expression in liver was compared between strains and diets.
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