Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Incretin triple agonist retatrutide (LY3437943) alleviates obesity-associated cancer progression

ABSTRACT: Medical weight loss is becoming increasingly prevalent, but impacts on cancer remain unclear. We report that in mice with significant retatrutide (RETA, LY3437943)-induced weight loss, reduced food intake, and improved glucose tolerance and other metabolic parameters, subsequent obesity-associated pancreatic cancer engraftment was reduced, and tumor onset was delayed, with blunted progression resulting in a 14-fold reduction in tumor volume compared to only 4-fold reduction in single agonist semaglutide-treated mice. Interestingly, when RETA was withdrawn before tumor implantation, the anti-tumor benefits of RETA persisted with reduced tumor burden despite weight regain. RETA induced durable anti-tumor immunity evidenced by activation of pro-inflammatory pathways in the tumor microenvironment. These findings suggest that patients with RETA-mediated weight loss may benefit from reduced cancer risk and improved outcomes.

ORGANISM(S): Mus musculus

PROVIDER: GSE288998 | GEO | 2025/03/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bariatric surgery reduces obesity associated breast cancer and enhances response to immunotherapy [Mammary Fat Pad RNA-seq]

Project description:Patients undergoing bariatric surgery are protected from subsequent breast cancer risk. It is unknown whether weight loss alone or surgery-specific alterations mediate risk reduction. We examined breast cancer in a pre-clinical model of diet induced obesity (DIO) followed by vertical sleeve gastrectomy (VSG) or dietary weight loss. DIO exacerbated tumor progression compared to lean controls, while VSG-induced weight loss reversed this exacerbation. However, dietary interventions were more effective than VSG despite similar reductions in weight and adiposity, potentially due to elevated immunosuppression after VSG. In tumor bearing mice, anti-PD-L1 immunotherapy after VSG improved anti-tumor immunity and potently impaired tumor progression. Thus, weight loss before tumor onset was protective regardless of intervention. Importantly, immunotherapy specifically improved outcomes in VSG.

2021-05-21 | GSE174760 | GEO

Bariatric surgery reduces obesity associated breast cancer and enhances response to immunotherapy [Tumor - breast cancer RNA-seq]

2021-05-21 | GSE174761 | GEO

Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure

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

CagriSema drives weight loss in rats by reducing energy intake and preserving energy expenditure

Project description:CagriSema is a combination of amylin (cagrilintide) and glucagon-like peptide-1 (semaglutide) analogues being developed for weight management. We quantified CagriSema’s action on energy intake and expenditure in rats. CagriSema caused 12% weight loss and a 39% reduction in food intake. In contrast, pair-feeding caused less weight loss while weight-matching required a 51% decrease in food intake. Approximately 1/3 of CagriSema’s weight loss efficacy was from an energy expenditure effect, blunting of metabolic adaptation, which is likely a hallmark of successful treatment of obesity.

2025-04-23 | GSE295272 | GEO

Multiomics reveals persistence of obesity-associated immune cell phenotypes in adipose tissue during weight loss and subsequent weight regain

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

Semaglutide exerts stronger cardioprotective effects than caloric restriction in mice with HFpEF

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

Semaglutide in the treatment of MOSH alter the methylation pattern of genes related to glycolipid metabolism

Project description:Secondary hypogonadism related to male obesity (MOSH) is a common disease among male patients with severe obesity. Semaglutide has a remarkable effect in weight loss treatment. To explore the epigenetic change mechanism of Semaglutide in the treatment of MOSH, this study, through DNA methylation and miRNA sequencing, discovered the significant epigenetic changes that occurred during the treatment of MOSH with Semaglutide.

2025-07-17 | GSE302472 | GEO

Short-term caloric restriction promotes resolution, while weight regain accelerates atherosclerosis in mice

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

CDA HFD mice analysed for hepatic gene expression after treatment with semaglutide

Project description:Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic liver disease strongly associated with cardiometabolic risk factors. Semaglutide, a glucagon-like peptide-1 receptor agonist, improves liver histology in MASH, but the underlying signals and pathways driving semaglutide-induced MASH resolution are not well understood. We show that, in two preclinical MASH models, semaglutide improved histological markers of fibrosis and inflammation, and reduced hepatic expression of fibrosis- and inflammation-related gene pathways.

2025-04-25 | GSE294630 | GEO

DIO-MASH mice analysed for hepatic gene expression after treatment with semaglutide

Project description:Modulation of metabolic, inflammatory, and fibrotic pathways by semaglutide in metabolic dysfunction-associated steatohepatitis Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic liver disease strongly associated with cardiometabolic risk factors. Semaglutide, a glucagon-like peptide-1 receptor agonist, improves liver histology in MASH, but the underlying signals and pathways driving semaglutide-induced MASH resolution are not well understood. We show that, in two preclinical MASH models, semaglutide improved histological markers of fibrosis and inflammation, and reduced hepatic expression of fibrosis- and inflammation-related gene pathways.

2025-04-25 | GSE294629 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data