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Agnieszka Dobrzyn

Researcher at Nencki Institute of Experimental Biology

Publications -  97
Citations -  4650

Agnieszka Dobrzyn is an academic researcher from Nencki Institute of Experimental Biology. The author has contributed to research in topics: Stearoyl-CoA Desaturase & Insulin resistance. The author has an hindex of 33, co-authored 88 publications receiving 4000 citations. Previous affiliations of Agnieszka Dobrzyn include Medical University of Białystok & University of Wisconsin-Madison.

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Stearoyl-CoA desaturase 1 deficiency increases fatty acid oxidation by activating AMP-activated protein kinase in liver

TL;DR: The phosphorylation and activity of AMP-activated protein kinase (AMPK), a metabolic sensor that regulates lipid metabolism during increased energy expenditure is significantly increased and identified as a mediator of increased fatty acid oxidation in liver of SCD1-deficient mice.
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Stearoyl-CoA desaturase 1 gene expression is necessary for fructose-mediated induction of lipogenic gene expression by sterol regulatory element-binding protein-1c-dependent and -independent mechanisms.

TL;DR: It is demonstrated that oleate produced by SCD is necessary for fructose-mediated induction of lipogenic gene expression through SREBP-1c-dependent and -independent mechanisms and suggested that SCD1 gene expression is important in lipid and carbohydrate homeostasis.
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Islet β-cell failure in type 2 diabetes – Within the network of toxic lipids

TL;DR: Various types of toxic lipid metabolites that may play a significant role in pancreatic islet failure are reviewed and various aspects of lipid action in β-cells are discussed, including effects on metabolic pathways, stress responses, and gene expression.
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Stearoyl-CoA Desaturase-1 Mediates the Pro-lipogenic Effects of Dietary Saturated Fat

TL;DR: It is shown that a diet high in the saturated fat stearate induces lipogenic genes in wild-type mice, with the induction of the Scd1 (stearoyl-CoA desaturase-1) gene preceding that of otherlipogenic genes, indicating that SCD1 serves as a molecular switch in the promotion or prevention of lipid-induced disorders brought on by consumption of excess saturated fat.
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Stearoyl-CoA desaturase 1 deficiency elevates insulin-signaling components and down-regulates protein-tyrosine phosphatase 1B in muscle.

TL;DR: It is hypothesized that loss of SCD1 function induces increased insulin signaling at least in part by a reduction in the expression of protein-tyrosine phosphatase 1B, which could be a therapeutic target in the treatment of diabetes.