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Daniel J. Fazakerley

Researcher at University of Sydney

Publications -  74
Citations -  3089

Daniel J. Fazakerley is an academic researcher from University of Sydney. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 25, co-authored 63 publications receiving 2232 citations. Previous affiliations of Daniel J. Fazakerley include University of Cambridge & National Institutes of Health.

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Mitochondrial oxidative stress causes insulin resistance without disrupting oxidative phosphorylation.

TL;DR: It is concluded that elevated mitochondrial oxidants rapidly impair insulin-regulated GLUT4 translocation and significantly contribute to insulin resistance and that MitoPQ is an ideal tool for studying the link between mitochondrial oxidative stress and regulatedGLUT4 trafficking.
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Selective insulin resistance in adipocytes.

TL;DR: It is concluded that insulin resistance in adipose tissue is highly selective for glucose metabolism and likely involves a defect in one of the components regulating GLUT4 translocation to the cell surface in response to insulin.
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Identification of fatty acid binding protein 4 as an adipokine that regulates insulin secretion during obesity.

TL;DR: It is shown that fatty acid binding protein 4 (FABP4/aP2) is an adipokine released from adipocytes under obesogenic conditions, such as hypoxia, to augment insulin secretion, and that FABP 4 and insulin form an endocrine loop coordinating the β-cell response to obesity.
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Opening of the mitochondrial permeability transition pore links mitochondrial dysfunction to insulin resistance in skeletal muscle.

TL;DR: Insulin resistance is associated with mitochondrial dysfunction, but the mechanism by which mitochondria inhibit insulin-stimulated glucose uptake into the cytoplasm is unclear and the mPTP is placed at a critical intersection between alterations in mitochondrial function and insulin resistance in skeletal muscle.
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mTORC1 Is a Major Regulatory Node in the FGF21 Signaling Network in Adipocytes

TL;DR: It is suggested that mTORC1 may act to facilitate FGF21-mediated health benefits in vivo, including UCP1 and F GF21 induction, increased adiponectin secretion, and enhanced glucose uptake without any adverse effects on insulin action.