Short-term caloric restriction promotes resolution, while weight regain accelerates atherosclerosis in mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA933691 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23408310_1.fastq.gz | Fastqsanger.gz | |||
| SRR23408310_2.fastq.gz | Fastqsanger.gz | |||
| SRR23408311_1.fastq.gz | Fastqsanger.gz | |||
| SRR23408311_2.fastq.gz | Fastqsanger.gz | |||
| SRR23408312_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:While weight loss is highly recommended for obesity, promoting inflammation resolution, >80% of those who lose weight will regain it back, resulting in worsening of disease outcomes (including cardiovascular disease), relative to never having lost weight. However, how weight loss and regain directly influence atherosclerotic inflammation was unknown and investigated in this stud. Using short-term caloric restriction (stCR) in obese mice, we found that weight loss promotes atherosclerosis resolution, independently of plasma cholesterol. Mechanistically, we found that this is partly attributed to a unique subset of macrophage, distinguished by high expression of the antibody receptor Fcgr4, that accumulated in epididymal adipose tissue and plaques with stCR and help to clear necrotic cores. Interestingly, our data suggest that eWAT-derived Fcgr4 macrophages contribute to the clearance of plaque necrotic cores. On the other hand, weight regain achieved by ab libitum feeding following the stCR phase resulted in acceleration of atherosclerosis progression and disappearance of Fcgr4 macrophages from both adipose and plaques. Furthermore, weight regain caused inflammatory reprogramming of bone marrow immune progenitors, retaining hyper-inflammatory capabilities for long periods thereafter.
2024-02-09 | GSE225077 | GEO
Project description:The present study was designed to identify determinants that foreshadow successful weight maintenance. More specifically, we examined whether subcutaneous adipose tissue (scAT) gene expression of participants who experience successful weight maintenance following caloric restriction differed from that of participants who regain weight. Forty women followed a dietary protocol consisting of an 8-week low calorie diet (LCD) and a 6-month weight maintenance phase. At the end of the protocol, participants were classified as weight maintainers (WM; 0-10% weight regain) and weight regainers (WR; 50-100% weight regain). Anthropometric measurements, plasma parameters, and scAT biopsies were taken before and after the LCD. Adipose tissue gene expression profiles were studied in all individuals before and after the LCD.
2011-09-29 | E-GEOD-24432 | biostudies-arrayexpress
Project description:The present study was designed to identify determinants that foreshadow successful weight maintenance. More specifically, we examined whether subcutaneous adipose tissue (scAT) gene expression of participants who experience successful weight maintenance following caloric restriction differed from that of participants who regain weight.
2011-09-30 | GSE24432 | GEO
Project description:We recruited ten normal-weight healthy men using inclusion criteria as previously described (Collet et al 2017). All males were healthy and not obese or overweight (average age: 23.8 years, average BMI (kg/m2): 23.3). Participants at baseline consumed a balanced diet (50% carbohydrate, 30% fat, and 20% protein). During caloric restriction, volunteers consumed 10% of normal energy requirement (226 kcal/d) for two days, again balanced (50% carbohydrate, 30% fat, and 20% protein), with the same macronutrient composition. After caloric restriction, volunteers were offered three substantial ad libitum buffet meals per day (20 MJ = 4,777 kcal) and additional snacks (16 MJ = 3,821 kcal) between meals for 2 days. They were invited to eat freely until comfortably full; food consumption was covertly measured. We collected fasting plasma samples at 0800 AM at baseline, after CR and refeeding (RF).
2022-12-12 | PXD038526 | Pride
Project description:We investigated the effect of weight loss maintenance (WLM) and weight regain on skeletal muscle in rodents. In skeletal muscle of obesity prone rats, WLM reduced fat oxidative capacity and down-regulated genes involved in fat metabolism. After weight was regained in rats, the genes involved in fat metabolism were still reduced. Mice with skeletal muscle lipoprotein lipase overexpression (mCK-hLPL), which augments fat metabolism, were subjected to our WLM and weight regain paradigm. We found that mCK-hLPL attenuated weight regain by potentiating energy expenditure.Irrespective of genotype, weight regain suppressed dietary fat oxidation and down-regulated genes involved in fat metabolism in skeletal muscle. However, mCK-hLPL mice oxidized more fat throughout weight regain and had greater expression of genes involved in fat metabolism and lower expression of genes involved in carbohydrate metabolism during WLM and regain.
2021-03-24 | GSE154943 | GEO
Project description:Most individuals do not maintain weight loss, and weight regain increases cardio-metabolic risk beyond that of obesity. Adipose inflammation directly contributes to insulin resistance; however, immune-related changes that occur with weight loss and weight regain are not well understood. Single cell RNA-sequencing was completed with CITE-sequencing and biological replicates to profile changes in murine immune subpopulations following obesity, weight loss, and weight cycling. Weight loss normalized glucose tolerance, however, type 2 immune cells did not repopulate adipose following weight loss. Many inflammatory populations persisted with weight loss and increased further following weight regain. Obesity drove T cell exhaustion and broad increases in antigen presentation, lipid handing, and inflammation that persisted with weight loss and weight cycling. This work provides critical groundwork for understanding the immunological causes of weight cycling-accelerated metabolic disease.
2022-03-04 | GSE182233 | GEO
Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1 and PPARto wild type levels; CR paradoxically further suppressed cardiac PPAR. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction. 6 month aged ob/ob mice were either leptin repleted with osmotic mini-pumps, calorie restricted to match the caloric intake of the leptin repleted mice, or fed ad lib for one month. 6-8 month C57Bl/6J mice were aged to serve as controls.
2011-04-29 | E-GEOD-16790 | biostudies-arrayexpress
Project description:Patients with heart failure with preserved ejection fraction (HFpEF) often have an unfavorable cardiometabolic profile, and obesity-related HFpEF has become a well-recognized HFpEF sub-phenotype. Targeting this unfavorable cardiometabolic profile may therefore represent a rational treatment strategy. The glucagon-like peptide-1 receptor agonist (GLP1-RA) semaglutide has been shown to induce significant weight loss and to improve cardiovascular outcomes. In this study, we investigated the cardiometabolic effects of semaglutide in a representative mouse model of HFpEF and compared it to the effects of weight loss by caloric restriction.
2024-01-26 | PXD034625 | Pride
Project description:Characterization of the fecal metaproteome in rats fed ad libitum or following a caloric restriction diet
2018-10-08 | PXD007252 | Pride