Specific macronutrients exert unique influences on the adipose-liver axis to promote hepatic steatosis in mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE93800 | GEO | 2017/09/01
SECONDARY ACCESSION(S): PRJNA362374
REPOSITORIES: GEO
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Project description:Background & aimsThe factors that distinguish metabolically healthy obesity from metabolically unhealthy obesity are not well understood. Diet has been implicated as a determinant of the unhealthy obesity phenotype, but which aspects of the diet induce dysmetabolism are unknown. The goal of this study was to investigate whether specific macronutrients or macronutrient combinations provoke dysmetabolism in the context of isocaloric, high-energy diets.MethodsMice were fed 4 high-energy diets identical in calorie and nutrient content but different in nutrient composition for 3 weeks to 6 months. The test diets contained 42% carbohydrate (sucrose or starch) and 42% fat (oleate or palmitate). Weight and glucose tolerance were monitored; blood and tissues were collected for histology, gene expression, and immunophenotyping.ResultsMice gained weight on all 4 test diets but differed significantly in other metabolic outcomes. Animals fed the starch-oleate diet developed more severe hepatic steatosis than those on other formulas. Stable isotope incorporation showed that the excess hepatic steatosis in starch-oleate-fed mice derived from exaggerated adipose tissue lipolysis. In these mice, adipose tissue lipolysis coincided with adipocyte necrosis and inflammation. Notably, the liver and adipose tissue abnormalities provoked by starch-oleate feeding were reproduced when mice were fed a mixed-nutrient Western diet with 42% carbohydrate and 42% fat.ConclusionsThe macronutrient composition of the diet exerts a significant influence on metabolic outcome, independent of calories and nutrient proportions. Starch-oleate appears to cause hepatic steatosis by inducing progressive adipose tissue injury. Starch-oleate phenocopies the effect of a Western diet; consequently, it may provide clues to the mechanism whereby specific nutrients cause metabolically unhealthy obesity.
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2022-12-12 | PXD038526 | Pride
Project description:Two months-old Shp flox/flox male mice were injected with either AAV8 expressing Cre recombinase driven by the thyroxine-binding globulin (Tbg) promoter (AAV8-Tbg-Cre) or control AAV8 (AAV8-Tbg-null) and fed chow or a diet enriched in high fat, cholesterol, and fructose (Research diet D09100301: 40 kcal% fat, 2% cholesterol, 20 kcal% fructose, hereafter referred to as HFCF diet) for 3 months. Liver RNA was isolated and submitted to RNA-seq.
2019-12-10 | GSE133566 | GEO
Project description:The specific role of nutritional status during gestation in exacerbating or mitigating fetal toxicity of ethanol (EtOH) remains unclear. We used an intragastric infusion model (Total enteral nutrition, TEN) to appropriately control for dietary EtOH consumption and caloric intake. Time impregnated female Sprague Dawley rats (250-300 g) were surgically cannulated with intragastric cannulae (on gestation day 4) and infused either control or EtOH-containing diets. Rats were fed 220 kcal/ kg3/4/d (NRC recommended caloric intake for gestation) or 160 kcal/ kg3/4/d (undernourished to 72% of control) diets containing either 12 g/kg/d EtOH or an isocaloric amount of carbohydrates from gestation days 6-15. Maternal hepatic gene expression profiles were assessed on GD15. The present data dissect specific effects of nutritional status during gestation and EtOH intake and the interaction thereof. The data reveal a highly significant interaction between undernutrition and EtOH consumption. Experiment Overall Design: Four groups of time impregnated female Sprague Dawley rats were utilized. Experiment Overall Design: Group 1: Control, TEN-220, control group fed normal (non-EtOH containing) diets at 220 kcal/ kg3/4/d. Experiment Overall Design: Group 2: Ethanol-220, EtOH-220 (EtOH group fed EtOH containing diets) at 12 g EtOH/kg/d diets at 220 kcal/ kg3/4/d. Experiment Overall Design: Group 3: Control-160, TEN-160, (undernourished control group fed normal (non-EtOH containing) diets at 160 kcal/ kg3/4/d. Experiment Overall Design: Group 4: Ethanol-160, EtOH-160, (undernourished rats fed EtOH containing diets) at 12 g EtOH/kg/d diets at 160 kcal/ kg3/4/d
2008-06-12 | E-GEOD-3740 | biostudies-arrayexpress
Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in the liver Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Liver samples were harvested at the end of the experiment and analyzed by microarray.
2016-02-29 | E-GEOD-73195 | biostudies-arrayexpress
Project description:Dietary lipids and gut microbiota may both influence adipose tissue physiology. By feeding conventional and germ-free mice high fat diets with different lipid compositon we aimed to investigate how dietary lipids and the gut microbiota interact to influence inflammation and metabolism in epididymal adipiose tissue (EWAT) Wild-type C57Bl/6 male mice 11 weeks of age were fed isocaloric diets (45% kcal fat) with either menhaden fish oil (Research Diets, D05122102) or lard (Research Diets, D10011202) for 11 weeks. Epididymal WAT samples were harvested at the end of the experiment and analyzed by microarray.
2015-07-14 | E-GEOD-70922 | biostudies-arrayexpress
Project description:Intertemporal choices involve trade-offs between the value of rewards and the delay before those rewards are experienced. Canonical intertemporal choice models such as hyperbolic discounting assume that reward amount and time until delivery are integrated within each option prior to comparison1,2. An alternative view posits that intertemporal choice reflects attribute-wise processes in which amount and time attributes are compared separately3-6. Here, we use multi-attribute drift diffusion modelling (DDM) to show that attribute-wise comparison represents the choice process better than option-wise comparison for intertemporal choice in a young adult population. We find that, while accumulation rates for amount and time information are uncorrelated, the difference between those rates predicts individual differences in patience. Moreover, patient individuals incorporate amount earlier than time into the decision process. Using eye tracking, we link these modelling results to attention, showing that patience results from a rapid, attribute-wise process that prioritizes amount over time information. Thus, we find converging evidence that distinct evaluation processes for amount and time determine intertemporal financial choices. Because intertemporal decisions in the lab have been linked to failures of patience ranging from insufficient saving to addiction7-13, understanding individual differences in the choice process is important for developing more effective interventions.
| S-EPMC8020819 | biostudies-literature
Project description:The specific role of nutritional status during gestation in exacerbating or mitigating fetal toxicity of ethanol (EtOH) remains unclear. We used an intragastric infusion model (Total enteral nutrition, TEN) to appropriately control for dietary EtOH consumption and caloric intake. Time impregnated female Sprague Dawley rats (250-300 g) were surgically cannulated with intragastric cannulae (on gestation day 4) and infused either control or EtOH-containing diets. Rats were fed 220 kcal/ kg3/4/d (NRC recommended caloric intake for gestation) or 160 kcal/ kg3/4/d (undernourished to 72% of control) diets containing either 12 g/kg/d EtOH or an isocaloric amount of carbohydrates from gestation days 6-15. Maternal hepatic gene expression profiles were assessed on GD15. The present data dissect specific effects of nutritional status during gestation and EtOH intake and the interaction thereof. The data reveal a highly significant interaction between undernutrition and EtOH consumption. Keywords: Nutrition-gene interactions
2006-12-03 | GSE3740 | GEO
Project description:The specific genes influencing the quantitative variation in macronutrient preference and food intake are virtually unknown. We refined a previously identified mouse chromosome 17 (MMU17) region harboring quantitative trait loci (QTL) with large effects on preferential macronutrient intake-carbohydrate (Mnic1), total kilcalories (Kcal2), and total food volume (Tfv1) using interval-specific congenic strains. These loci were isolated in the [C57BL/6J.CAST/EiJ-17.1-(D17Mit19-D17Mit50); B6.CAST-17.1] strain, developed by introgressing a ~40.1 Mb CAST MMU17 region into recipient B6 genome. In a diet selection paradigm (carbohydrate/protein vs. fat/protein), these B6.CAST-17.1 sub-congenic mice eat 30% more calories from the carbohydrate-rich diet, ~10% more total calories, and ~9% more total food volume per body weight. In the current study, this carbohydrate-preferring B6.CAST-17.1 subcongenic strain was crossed with the fat-preferring inbred B6 strain to generate a subcongenic-derived F2 mapping population; genotypes were determined using a high-density, custom SNP panel. The main outcome of this study is that genetic linkage analysis greatly reduced the 95% confidence interval (CI) for Mnic1 (encompassing Kcal2 and Tfv1) from 40.1 to 29.5 Mb and more precisely established the QTL boundaries. Specifically, the genetic architecture for Mnic1 (preferential carbohydrate intake) does not follow the same pattern as that for co-localized Kcal2/Tfv1 (total kcal and food volume, respectively), suggesting the presence of separate quantitative trait genes for these food intake traits. No genetic linkage for self-selected fat intake was detected, underscoring the carbohydrate-specific effects of this MMU17 locus. The Mnic1/Kcal2/Tfv1 QTL was further de-limited to a ~19.1 Mb interval, based on the absence of macronutrient diet selection phenotypes in subcongenic HQ17IIa mice that possess CAST MMU17 donor segment on a C57BL/6Jhg/hg background. A second key finding is the separation of two energy balance QTLs: Mnic1/Kcal2/Tfv1 for food intake and a newly discovered locus regulating short term body weight gain. The genes Decr2, Ppard and Agapt1 in the critical QTL interval were identified and prioritized using a combination of genome sequence analysis, and tag-based transcriptome sequencing to measure hypothalamic gene expression in non-recombinant F2 controls, possessing cast/cast and b6/b6 genotypes across the sub-congenic segment. Global gene expression profiles in the hypothalamus were compared between non-recombinant subcongenic-derived F2 mice, possessing a genotype of cast/cast (n=12) or b6/b6 (n=12) across the Chr 17 subcongenic segment and b6/b6 across the rest of the genome. RNA was isolated from individual mice of each genotype that were selected for study. Specifically, twelve mice of each genotype that displayed the most divergent phenotypic values for self-selected carbohydrate and total kcal intake were chosen for gene expression analysis, i.e., cast/cast mice with the highest and b6/b6 mice with the lowest kcal intake from carbohydrate, or the 25% tails of the distribution. Tissues were harvested ~48 h after re-initiation of the carbohydrate/protein vs. fat/protein diets, following an extended wash-out period on chow diet after completion of the 10 d macronutrient selection test.
2015-05-15 | E-GEOD-60756 | biostudies-arrayexpress
Project description:To assess whether changes in islet gene expression contribute to differences in phenotypes in response to high fat diet or tretament with pioglitazone, Agilent Whole Mouse Genome Oligo Microarrays were performed on RNA isolated from islets of 4 mice per each treatment group for discovery analysis of gene expression. Male 8 week-old BL6 and BLKS mice were fed normal chow (18% kcal from fat), HFD (42% kcal from fat), or HFD supplemented with the PPAR-γ agonist pioglitazone (PIO) (140 mg PIO/kg diet) for 16 weeks.
2013-09-21 | E-GEOD-51055 | biostudies-arrayexpress