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Jarkko Soronen

Researcher at National Institutes of Health

Publications -  17
Citations -  705

Jarkko Soronen is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Adipose tissue & Insulin. The author has an hindex of 12, co-authored 16 publications receiving 632 citations. Previous affiliations of Jarkko Soronen include Bayer & Minerva Foundation Institute for Medical Research.

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Vascular Endothelial Growth Factor-B Acts as a Coronary Growth Factor in Transgenic Rats Without Inducing Angiogenesis, Vascular Leak, or Inflammation

TL;DR: In rats, the heart-specific VEGF-B transgene induced impressive growth of the epicardial coronary vessels and their branches, with large arteries also seen deep inside the subendocardial myocardium, however, VEGf-B, unlike other V EGF family members, did not induce significant capillary angiogenesis, increased permeability, or inflammatory cell recruitment.
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Activated Forms of VEGF-C and VEGF-D Provide Improved Vascular Function in Skeletal Muscle

TL;DR: It is concluded that long-term expression of VEGF-C and V EGF-D in skeletal muscle results in the generation of new functional blood and lymphatic vessels.
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Adipose tissue gene expression analysis reveals changes in inflammatory, mitochondrial respiratory and lipid metabolic pathways in obese insulin-resistant subjects

TL;DR: In this article, the authors compared acute in vivo effects of insulin on adipose tissue transcriptional profiles between obese insulin-resistant and lean insulin-sensitive women and found that the most prominent difference in gene expression of the insulin resistant group during hyperinsulinemia was reduced transcription of nuclear genes involved in mitochondrial respiration (mitochondrial respiratory chain, GO:0001934).
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USF1 deficiency activates brown adipose tissue and improves cardiometabolic health

TL;DR: By inactivating USF1 in mice, protection against diet-induced dyslipidemia, obesity, insulin resistance, hepatic steatosis, and atherosclerosis is demonstrated and the potential of USf1 as a therapeutic target for cardiometabolic disease is pointed to.