Gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA752174 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15356600.fastq.gz | Fastqsanger.gz | |||
| SRR15356601.fastq.gz | Fastqsanger.gz | |||
| SRR15356602.fastq.gz | Fastqsanger.gz | |||
| SRR15356603.fastq.gz | Fastqsanger.gz | |||
| SRR15356604.fastq.gz | Fastqsanger.gz |
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Project description:DNA methylation analysis using HumanMethylation850K BeadChips (Illumina) in human blood samples before and after an 18 months weight-loss intervention: the CENTRAL study [randomized controlled trial; NCT01530724]. All subjects underwent either Mediterranean/low-carbohydrate or low-fat diet with or without physical activity.
2020-04-14 | E-MTAB-8956 | biostudies-arrayexpress
Project description:OBJECTIVE Diet intervention in obese adults is the first strategy to induce weight loss and to improve insulin sensitivity. We hypothesized that improvements in insulin sensitivity after weight loss from a short-term dietary intervention tracks with alterations in expression of metabolic genes and abundance of specific lipid species. RESEARCH DESIGN AND METHODS Eight obese, insulin resistant, non-diabetic adults were recruited to participate in a three-week low calorie diet intervention study (1000 kcal/day). Fasting blood samples and vastus lateralis skeletal muscle biopsies were obtained before and after the dietary intervention. Clinical chemistry and measures of insulin sensitivity were determined. Unbiased microarray gene expression and targeted lipidomic analysis of skeletal muscle was performed. RESULTS Body weight was reduced, insulin sensitivity (HOMA-IR) was enhanced, and serum insulin concentration and blood lipid (triglyceride, cholesterol, LDL and HDL) levels were improved after dietary intervention. Gene set enrichment analysis of skeletal muscle revealed that oxidative phosphorylation and inflammatory processes were among the most enriched KEGG-pathways identified after dietary intervention. mRNA expression of PDK4 and MLYCD increased, while SCD decreased in skeletal muscle after dietary intervention. Dietary intervention altered the intramuscular lipid profile of skeletal muscle, with changes in content of phosphatidylcholine and triglyceride species among the pronounced. CONCLUSIONS Short-term diet intervention and weight loss in obese adults alters metabolic gene expression and reduces specific phosphatidylcholine and triglyceride species in skeletal muscle, concomitant with improvements in clinical outcomes and enhanced insulin sensitivity.
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Project description:A ketogenic diet (KD) is a very low-carbohydrate, very high-fat diet recently proposed to treat obesity and type 2 diabetes. While KD grows in popularity, its effects on metabolic health are understudied. (here) We show that, while KD protects against weight gain and induces weight loss, over long-term, mice develop hyperlipidemia, hepatic steatosis, and severe glucose intolerance. Unlike HFD-fed mice, KD mice are not insulin resistant and have low levels of insulin. Hyperglycemic clamp and ex vivo GSIS revealed cell-autonomous and whole-body impairments in insulin secretion. Major ER/Golgi stress and disrupted ER-Golgi protein trafficking was indicated by transcriptomic profiling of KD islets and confirmed by electron micrographs showing a dilated and fragmented Golgi network compatible with defects in insulin granule biogenesis and secretion. Overall, our results suggest long-term KD leads to multiple aberrations of metabolic parameters that caution its systematic use as a health promoting dietary intervention.
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Project description:A ketogenic diet (KD) is a very low-carbohydrate, very high-fat diet recently proposed to treat obesity and type 2 diabetes. While KD grows in popularity, its effects on metabolic health are understudied. (here) We show that, while KD protects against weight gain and induces weight loss, over long-term, mice develop hyperlipidemia, hepatic steatosis, and severe glucose intolerance. Unlike HFD-fed mice, KD mice are not insulin resistant and have low levels of insulin. Hyperglycemic clamp and ex vivo GSIS revealed cell-autonomous and whole-body impairments in insulin secretion. Major ER/Golgi stress and disrupted ER-Golgi protein trafficking was indicated by transcriptomic profiling of KD islets and confirmed by electron micrographs showing a dilated and fragmented Golgi network compatible with defects in insulin granule biogenesis and secretion. Overall, our results suggest long-term KD leads to multiple aberrations of metabolic parameters that caution its systematic use as a health promoting dietary intervention
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Project description:Despite the largely beneficial impact of bariatric surgery on obesity and metabolic disease, many patients continue to suffer from obesity after surgery and weight recurrence is common. The success of bariatric surgery may be impacted by diet. While bariatric surgery guidelines recommend a high-protein diet following surgery based on the theory that this will preserve lean mass, emerging evidence suggests that both humans and mice are metabolically healthier when consuming low protein diets. Here, we assess the effect of varying dietary protein levels on post-surgical weight loss and weight regain in a mouse model of bariatric surgery, sleeve gastrectomy. We find that a low protein diet optimally drives post-surgical weight loss, boosting energy expenditure and improving blood glucose regulation. Using a multi-omics approach, we identified clusters of differentially expressed genes and metabolites that correlated with these phenotypes and find that diet heavily influences the molecular response of the liver to sleeve gastrectomy. These results suggest that current post-surgical dietary guidelines recommending a high protein diet may limit both the short and long-term benefits of surgery and lead us to conclude that a low protein diet may improve patient outcomes.
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Project description:Background: Despite the established relation between energy restriction and metabolic health, the most beneficial nutrient composition of a weight-loss diet is still subject of debate. Objectives: The aim of the study was to examine the additional effects of nutrient quality on top of energy restriction(ER). Methods: A parallel-designed 12-week 25%ER dietary intervention study was conducted. Participants aged 40-70 years with abdominal obesity were randomized over three groups: a 25%ER high nutrient quality diet (n = 40); a 25%ER low nutrient quality diet (n = 40); or a habitual diet (n = 30). Both ER diets were nutritionally adequate, the high nutrient quality ER diet was enriched in monounsaturated and n-3 polyunsaturated fatty acids, fiber, and plant protein and reduced in fructose. Before and after the intervention intra-hepatic lipids, body fat distribution, fasting and postprandial responses to a mixed meal shake challenge test of cardio-metabolic risk factors, lipoproteins, vascular measurements, and adipose tissue transcriptome were assessed. Results: The high quality ER diet (-8.4 ± 3.2) induced 2.1 kg more weight loss (P = 0.007) than the low quality ER diet (-6.3 ± 3.9), reduced fasting serum total cholesterol (P = 0.014) and plasma triglycerides (P < 0.001), promoted an anti-atherogenic lipoprotein profile and induced a more pronounced decrease in adipose tissue gene expression of energy metabolism pathways than the low quality ER diet. Explorative analyses showed that the difference in weight loss between both ER diets were specifically present in insulin sensitive subjects (HOMA-IR ≤ 2.5), in whom the high nutrient quality diet induced 3.9 kg more weight loss than the low nutrient quality diet. Conclusion: A high nutrient quality 25%ER diet is more beneficial for cardiometabolic health than a low nutrient quality 25%ER diet. Overweight insulin sensitive subjects may benefit more from a high than a low nutrient quality ER diet with respect to weight loss, due to potential attenuation of glucose-induced lipid synthesis in adipose tissue. Trial registration: ClinicalTrials.gov NCT02194504.
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