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| Funder | Swedish Research Council |
|---|---|
| Recipient Organization | Karolinska Institutet |
| Country | Sweden |
| Start Date | Jan 01, 2025 |
| End Date | Dec 31, 2028 |
| Duration | 1,460 days |
| Number of Grantees | 1 |
| Roles | Principal Investigator |
| Data Source | Swedish Research Council |
| Grant ID | 2024-02432_VR |
Obesity remains the major risk factor for developing metabolic disease.
Numerous studies have shown that maintaining adipose tissue functionality is enough to prevent metabolic disease, but it remains unclear what tips the scales and causes healthy lipid storage to become disease-promoting weight gain in obesity.
Our lab studies the adipose tissue vasculature and proposes that metabolic cooperation between adipocytes and endothelial cells is crucial for the healthy function of the adipose tissue, but becomes disrupted during obesity.
In this project, we aim to map three aspects of adipocyte-endothelial crosstalk – fatty acid uptake, metabolite exchange and the vascular progenitor niche – and use our unique translational models of the vascularized human white adipose tissue to uncover how the microvasculature affects tissue function, metabolism, and expansion beyond its classical roles in delivering oxygen.
This will be combined with functional mouse experiments and transcriptional and metabolite omics analyses.
By uncovering novel aspects of adipocyte-EC crosstalk our results have the potential to highlight previously unrecognized disease mechanisms and identify ways to preserve adipose tissue functionality during obesity, which in the future could be harnessed to clinically prevent obesity-related diseases from emerging.
Karolinska Institutet
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