Serum Is Not Necessary for Prior Pharmacological Activation of AMPK to Increase Insulin Sensitivity of Mouse Skeletal Muscle.

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Serum Is Not Necessary for Prior Pharmacological Activation of AMPK to Increase Insulin Sensitivity of Mouse Skeletal Muscle.

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2018 nî lūn-bûn

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2018年の論文

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

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Serum Is Not Necessary for Pri ...... vity of Mouse Skeletal Muscle.

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Serum Is Not Necessary for Pri ...... vity of Mouse Skeletal Muscle.

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Serum Is Not Necessary for Pri ...... vity of Mouse Skeletal Muscle.

@en

Serum Is Not Necessary for Pri ...... vity of Mouse Skeletal Muscle.

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Serum Is Not Necessary for Pri ...... vity of Mouse Skeletal Muscle.

@en

Serum Is Not Necessary for Pri ...... vity of Mouse Skeletal Muscle.

@nl

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Serum Is Not Necessary for Pri ...... ivity of Mouse Skeletal Muscle

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P2093

Rasmus Kjøbsted

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Identification of a novel phosphorylation site on TBC1D4 regulated by AMP-activated protein kinase in skeletal muscle

Postexercise improvement in insulin-stimulated glucose uptake occurs concomitant with greater AS160 phosphorylation in muscle from normal and insulin-resistant rats.

In vivo exercise followed by in vitro contraction additively elevates subsequent insulin-stimulated glucose transport by rat skeletal muscle.

Mice with AS160/TBC1D4-Thr649Ala knockin mutation are glucose intolerant with reduced insulin sensitivity and altered GLUT4 trafficking.

Exercise alleviates lipid-induced insulin resistance in human skeletal muscle-signaling interaction at the level of TBC1 domain family member 4.

The B2 receptor of bradykinin is not essential for the post-exercise increase in glucose uptake by insulin-stimulated mouse skeletal muscle

Postexercise skeletal muscle glucose transport is normal in kininogen-deficient rats.

Role of Akt substrate of 160 kDa in insulin-stimulated and contraction-stimulated glucose transport.

Increased AS160 phosphorylation, but not TBC1D1 phosphorylation, with increased postexercise insulin sensitivity in rat skeletal muscle.

Skeletal muscle insulin resistance is the primary defect in type 2 diabetes.

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scholarly article

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10.3390/IJMS19041201

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English

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Jørgen Wojtaszewski

Nicolas O Jørgensen

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2018-04-15T00:00:00Z

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29662023

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5979416

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