A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice

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Standard

A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice. / Chen, Qiaoli; Xie, Bingxian; Zhu, Sangsang; Rong, Ping; Sheng, Yang; Ducommun, Serge; Chen, Liang; Quan, Chao; Li, Min; Sakamoto, Kei; MacKintosh, Carol; Chen, Shuai; Wang, Hong Yu.

I: Diabetologia, Bind 60, Nr. 2, 2017, s. 336-345.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Chen, Q, Xie, B, Zhu, S, Rong, P, Sheng, Y, Ducommun, S, Chen, L, Quan, C, Li, M, Sakamoto, K, MacKintosh, C, Chen, S & Wang, HY 2017, 'A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice', Diabetologia, bind 60, nr. 2, s. 336-345. https://doi.org/10.1007/s00125-016-4151-9

APA

Chen, Q., Xie, B., Zhu, S., Rong, P., Sheng, Y., Ducommun, S., Chen, L., Quan, C., Li, M., Sakamoto, K., MacKintosh, C., Chen, S., & Wang, H. Y. (2017). A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice. Diabetologia, 60(2), 336-345. https://doi.org/10.1007/s00125-016-4151-9

Vancouver

Chen Q, Xie B, Zhu S, Rong P, Sheng Y, Ducommun S o.a. A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice. Diabetologia. 2017;60(2):336-345. https://doi.org/10.1007/s00125-016-4151-9

Author

Chen, Qiaoli ; Xie, Bingxian ; Zhu, Sangsang ; Rong, Ping ; Sheng, Yang ; Ducommun, Serge ; Chen, Liang ; Quan, Chao ; Li, Min ; Sakamoto, Kei ; MacKintosh, Carol ; Chen, Shuai ; Wang, Hong Yu. / A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice. I: Diabetologia. 2017 ; Bind 60, Nr. 2. s. 336-345.

Bibtex

@article{3af3030851a54e65b9e7691191e172ab,
title = "A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice",
abstract = "Aims/hypothesis: TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab GTPase-activating protein (RabGAP) that has been implicated in regulating GLUT4 trafficking. TBC1D1 can be phosphorylated by the AMP-activated protein kinase (AMPK) on Ser231, which consequently interacts with 14-3-3 proteins. Given the key role for AMPK in regulating insulin-independent muscle glucose uptake, we hypothesised that TBC1D1-Ser231 phosphorylation and/or 14-3-3 binding may mediate AMPK-governed glucose homeostasis. Methods: Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR). Exercise-induced muscle glucose uptake and exercise capacity were also determined in the Tbc1d1Ser231Ala-knockin mice. Results: Skeletal muscle-specific deletion of Ampkα1/a2 in mice prevented AICAR-induced hypoglycaemia and muscle glucose uptake. The Tbc1d1Ser231Ala-knockin mutation also attenuated the glucose-lowering effect of AICAR in mice. Glucose uptake and cell surface GLUT4 content were significantly lower in muscle isolated from the Tbc1d1Ser231Ala-knockin mice upon stimulation with a submaximal dose of AICAR. However, this Tbc1d1Ser231Ala-knockin mutation neither impaired exercise-induced muscle glucose uptake nor affected exercise capacity in mice. Conclusions/interpretation: TBC1D1-Ser231 phosphorylation and/or 14-3-3 binding partially mediates AMPK-governed glucose homeostasis and muscle glucose uptake in a context-dependent manner.",
keywords = "14-3-3, AMPK, Glucose uptake, Phosphorylation, TBC1D1",
author = "Qiaoli Chen and Bingxian Xie and Sangsang Zhu and Ping Rong and Yang Sheng and Serge Ducommun and Liang Chen and Chao Quan and Min Li and Kei Sakamoto and Carol MacKintosh and Shuai Chen and Wang, {Hong Yu}",
year = "2017",
doi = "10.1007/s00125-016-4151-9",
language = "English",
volume = "60",
pages = "336--345",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "2",

}

RIS

TY - JOUR

T1 - A Tbc1d1 Ser231Ala-knockin mutation partially impairs AICAR- but not exercise-induced muscle glucose uptake in mice

AU - Chen, Qiaoli

AU - Xie, Bingxian

AU - Zhu, Sangsang

AU - Rong, Ping

AU - Sheng, Yang

AU - Ducommun, Serge

AU - Chen, Liang

AU - Quan, Chao

AU - Li, Min

AU - Sakamoto, Kei

AU - MacKintosh, Carol

AU - Chen, Shuai

AU - Wang, Hong Yu

PY - 2017

Y1 - 2017

N2 - Aims/hypothesis: TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab GTPase-activating protein (RabGAP) that has been implicated in regulating GLUT4 trafficking. TBC1D1 can be phosphorylated by the AMP-activated protein kinase (AMPK) on Ser231, which consequently interacts with 14-3-3 proteins. Given the key role for AMPK in regulating insulin-independent muscle glucose uptake, we hypothesised that TBC1D1-Ser231 phosphorylation and/or 14-3-3 binding may mediate AMPK-governed glucose homeostasis. Methods: Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR). Exercise-induced muscle glucose uptake and exercise capacity were also determined in the Tbc1d1Ser231Ala-knockin mice. Results: Skeletal muscle-specific deletion of Ampkα1/a2 in mice prevented AICAR-induced hypoglycaemia and muscle glucose uptake. The Tbc1d1Ser231Ala-knockin mutation also attenuated the glucose-lowering effect of AICAR in mice. Glucose uptake and cell surface GLUT4 content were significantly lower in muscle isolated from the Tbc1d1Ser231Ala-knockin mice upon stimulation with a submaximal dose of AICAR. However, this Tbc1d1Ser231Ala-knockin mutation neither impaired exercise-induced muscle glucose uptake nor affected exercise capacity in mice. Conclusions/interpretation: TBC1D1-Ser231 phosphorylation and/or 14-3-3 binding partially mediates AMPK-governed glucose homeostasis and muscle glucose uptake in a context-dependent manner.

AB - Aims/hypothesis: TBC1D1 (tre-2/USP6, BUB2, cdc16 domain family member 1) is a Rab GTPase-activating protein (RabGAP) that has been implicated in regulating GLUT4 trafficking. TBC1D1 can be phosphorylated by the AMP-activated protein kinase (AMPK) on Ser231, which consequently interacts with 14-3-3 proteins. Given the key role for AMPK in regulating insulin-independent muscle glucose uptake, we hypothesised that TBC1D1-Ser231 phosphorylation and/or 14-3-3 binding may mediate AMPK-governed glucose homeostasis. Methods: Whole-body glucose homeostasis and muscle glucose uptake were assayed in mice bearing a Tbc1d1Ser231Ala-knockin mutation or harbouring skeletal muscle-specific Ampkα1/α2 (also known as Prkaa1/2) double-knockout mutations in response to an AMPK-activating agent, 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR). Exercise-induced muscle glucose uptake and exercise capacity were also determined in the Tbc1d1Ser231Ala-knockin mice. Results: Skeletal muscle-specific deletion of Ampkα1/a2 in mice prevented AICAR-induced hypoglycaemia and muscle glucose uptake. The Tbc1d1Ser231Ala-knockin mutation also attenuated the glucose-lowering effect of AICAR in mice. Glucose uptake and cell surface GLUT4 content were significantly lower in muscle isolated from the Tbc1d1Ser231Ala-knockin mice upon stimulation with a submaximal dose of AICAR. However, this Tbc1d1Ser231Ala-knockin mutation neither impaired exercise-induced muscle glucose uptake nor affected exercise capacity in mice. Conclusions/interpretation: TBC1D1-Ser231 phosphorylation and/or 14-3-3 binding partially mediates AMPK-governed glucose homeostasis and muscle glucose uptake in a context-dependent manner.

KW - 14-3-3

KW - AMPK

KW - Glucose uptake

KW - Phosphorylation

KW - TBC1D1

U2 - 10.1007/s00125-016-4151-9

DO - 10.1007/s00125-016-4151-9

M3 - Journal article

C2 - 27826658

AN - SCOPUS:84994462147

VL - 60

SP - 336

EP - 345

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 2

ER -

ID: 238739930