OcrV1, PascalFrancis, Corpus, bibRecord, 000050

Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function

Identifieur interne : 000050 ( PascalFrancis/Corpus ); précédent : 000049; suivant : 000051

Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function

Auteurs : CHEN WANG ; XIAOWEN LI ; KAIDA MU ; LING LI ; SHIHONG WANG ; YUNXIA ZHU ; MINGLIANG ZHANG ; JIYOON RYU ; ZHIFANG XIE ; DONGYUN SHI ; Weiping J. Zhang ; Lily Q. Dong ; WEIPING JIA

Source :

Diabetologia : (Berlin) [ 0012-186X ] ; 2013.

RBID : Pascal:13-0281139

Descripteurs français

Pascal (Inist)
- Déficit, Glucose, Insuline, Sécrétion, Animal, Inhibition, Cellule β, Diabète, Mitochondrie, Adiponectine, Souris.

English descriptors

KwdEn :
- Adiponectin, Animal, Deficiency, Diabetes mellitus, Glucose, Inhibition, Insulin, Mitochondria, Mouse, Secretion, β Cell.

Abstract

Aims/hypothesis Adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1) is an adapter protein that positively mediates adiponectin signalling. Deficiency of APPL1 in the target tissues of insulin induces insulin resistance. We therefore aimed, in the present study, to determine its role in regulating pancreatic beta cell function. Methods A hyperglycaemic clamp test was performed to determine insulin secretion in APPL1 knockout (KO) mice. Glucose- and adiponectin-induced insulin release was measured in islets from APPL1 KO mice or INS-1(832/13) cells with either APPL1 knockdown or overproduction. RT-PCR and western blotting were conducted to analyse gene expression and protein abundance. Oxygen consumption rate (OCR), ATP production and mitochondrial membrane potential were assayed to evaluate mitochondrial function. Results APPL1 is highly expressed in pancreatic islets, but its levels are decreased in mice fed a high-fat diet and db/db mice compared with controls. Deletion of the Appl1 gene leads to impairment of both the first and second phases of insulin secretion during hyperglycaemic clamp tests. In addition, glucose-stimulated insulin secretion (GSIS) is significantly decreased in islets from APPL1 KO mice. Conversely, overproduction of APPL1 leads to an increase in GSIS in beta cells. In addition, expression levels of several genes involved in insulin production, mitochondrial biogenesis and mitochondrial OCR, ATP production and mitochondrial membrane potential are reduced significantly in APPL1-knockdown beta cells. Moreover, suppression or overexproduction of APPL1 inhibits or stimulates adiponectin-potentiated GSIS in beta cells, respectively. Conclusions/interpretation Our study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03		`1`		`@0 Diabetologia : (Berl.)`
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A08	`01`	`1`	`ENG`	`@1 Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function`
A11	`01`	`1`		`@1 CHEN WANG`
A11	`02`	`1`		`@1 XIAOWEN LI`
A11	`03`	`1`		`@1 KAIDA MU`
A11	`04`	`1`		`@1 LING LI`
A11	`05`	`1`		`@1 SHIHONG WANG`
A11	`06`	`1`		`@1 YUNXIA ZHU`
A11	`07`	`1`		`@1 MINGLIANG ZHANG`
A11	`08`	`1`		`@1 JIYOON RYU`
A11	`09`	`1`		`@1 ZHIFANG XIE`
A11	`10`	`1`		`@1 DONGYUN SHI`
A11	`11`	`1`		`@1 ZHANG (Weiping J.)`
A11	`12`	`1`		`@1 DONG (Lily Q.)`
A11	`13`	`1`		`@1 WEIPING JIA`
A14	`01`			`@1 Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road @2 Shanghai 200233 @3 CHN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut.`
A14	`02`			`@1 Diabetes Institute, Shanghai Jiao Tong University @2 Shanghai @3 CHN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut. @Z 13 aut.`
A14	`03`			`@1 Shanghai Key Laboratory of Diabetes Mellitus @2 Shanghai @3 CHN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut. @Z 13 aut.`
A14	`04`			`@1 Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive @2 San Antonio, TX 78229-3900 @3 USA @Z 8 aut. @Z 12 aut.`
A14	`05`			`@1 Department of Pathophysiology, Second Military Medical University @2 Shanghai @3 CHN @Z 9 aut. @Z 11 aut.`
A14	`06`			`@1 Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University @2 Shanghai @3 CHN @Z 10 aut.`
A20				`@1 1999-2009`
A21				`@1 2013`
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A43	`01`			`@1 INIST @2 13012 @5 354000503689440190`
A44				`@0 0000 @1 © 2013 INIST-CNRS. All rights reserved.`
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C01	`01`		`ENG`	@0 Aims/hypothesis Adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1) is an adapter protein that positively mediates adiponectin signalling. Deficiency of APPL1 in the target tissues of insulin induces insulin resistance. We therefore aimed, in the present study, to determine its role in regulating pancreatic beta cell function. Methods A hyperglycaemic clamp test was performed to determine insulin secretion in APPL1 knockout (KO) mice. Glucose- and adiponectin-induced insulin release was measured in islets from APPL1 KO mice or INS-1(832/13) cells with either APPL1 knockdown or overproduction. RT-PCR and western blotting were conducted to analyse gene expression and protein abundance. Oxygen consumption rate (OCR), ATP production and mitochondrial membrane potential were assayed to evaluate mitochondrial function. Results APPL1 is highly expressed in pancreatic islets, but its levels are decreased in mice fed a high-fat diet and db/db mice compared with controls. Deletion of the Appl1 gene leads to impairment of both the first and second phases of insulin secretion during hyperglycaemic clamp tests. In addition, glucose-stimulated insulin secretion (GSIS) is significantly decreased in islets from APPL1 KO mice. Conversely, overproduction of APPL1 leads to an increase in GSIS in beta cells. In addition, expression levels of several genes involved in insulin production, mitochondrial biogenesis and mitochondrial OCR, ATP production and mitochondrial membrane potential are reduced significantly in APPL1-knockdown beta cells. Moreover, suppression or overexproduction of APPL1 inhibits or stimulates adiponectin-potentiated GSIS in beta cells, respectively. Conclusions/interpretation Our study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.
C02	`01`	`X`		`@0 002B21E01A`
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C03	`01`	`X`	`ENG`	`@0 Deficiency @5 01`
C03	`01`	`X`	`SPA`	`@0 Déficiencia @5 01`
C03	`02`	`X`	`FRE`	`@0 Glucose @2 NK @5 02`
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C03	`03`	`X`	`FRE`	`@0 Insuline @5 03`
C03	`03`	`X`	`ENG`	`@0 Insulin @5 03`
C03	`03`	`X`	`SPA`	`@0 Insulina @5 03`
C03	`04`	`X`	`FRE`	`@0 Sécrétion @5 04`
C03	`04`	`X`	`ENG`	`@0 Secretion @5 04`
C03	`04`	`X`	`SPA`	`@0 Secreción @5 04`
C03	`05`	`X`	`FRE`	`@0 Animal @5 05`
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C03	`06`	`X`	`FRE`	`@0 Inhibition @5 07`
C03	`06`	`X`	`ENG`	`@0 Inhibition @5 07`
C03	`06`	`X`	`SPA`	`@0 Inhibición @5 07`
C03	`07`	`X`	`FRE`	`@0 Cellule β @5 08`
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C03	`07`	`X`	`SPA`	`@0 Célula β @5 08`
C03	`08`	`X`	`FRE`	`@0 Diabète @2 NM @5 09`
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C03	`10`	`X`	`FRE`	`@0 Adiponectine @5 14`
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C07	`01`	`X`	`SPA`	`@0 Páncreas endocrino @5 20`
C07	`02`	`X`	`FRE`	`@0 Hormone pancréatique @5 21`
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C07	`02`	`X`	`SPA`	`@0 Hormona pancreática @5 21`
C07	`03`	`X`	`FRE`	`@0 Ilot Langerhans @5 22`
C07	`03`	`X`	`ENG`	`@0 Langerhans islet @5 22`
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N21				`@1 266`
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Format Inist (serveur)

NO :	PASCAL 13-0281139 INIST
ET :	Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function
AU :	CHEN WANG; XIAOWEN LI; KAIDA MU; LING LI; SHIHONG WANG; YUNXIA ZHU; MINGLIANG ZHANG; JIYOON RYU; ZHIFANG XIE; DONGYUN SHI; ZHANG (Weiping J.); DONG (Lily Q.); WEIPING JIA
AF :	Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road/Shanghai 200233/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.); Diabetes Institute, Shanghai Jiao Tong University/Shanghai/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 13 aut.); Shanghai Key Laboratory of Diabetes Mellitus/Shanghai/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 13 aut.); Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive/San Antonio, TX 78229-3900/Etats-Unis (8 aut., 12 aut.); Department of Pathophysiology, Second Military Medical University/Shanghai/Chine (9 aut., 11 aut.); Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University/Shanghai/Chine (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	Diabetologia : (Berlin); ISSN 0012-186X; Allemagne; Da. 2013; Vol. 56; No. 9; Pp. 1999-2009; Bibl. 48 ref.
LA :	Anglais
EA :	Aims/hypothesis Adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1) is an adapter protein that positively mediates adiponectin signalling. Deficiency of APPL1 in the target tissues of insulin induces insulin resistance. We therefore aimed, in the present study, to determine its role in regulating pancreatic beta cell function. Methods A hyperglycaemic clamp test was performed to determine insulin secretion in APPL1 knockout (KO) mice. Glucose- and adiponectin-induced insulin release was measured in islets from APPL1 KO mice or INS-1(832/13) cells with either APPL1 knockdown or overproduction. RT-PCR and western blotting were conducted to analyse gene expression and protein abundance. Oxygen consumption rate (OCR), ATP production and mitochondrial membrane potential were assayed to evaluate mitochondrial function. Results APPL1 is highly expressed in pancreatic islets, but its levels are decreased in mice fed a high-fat diet and db/db mice compared with controls. Deletion of the Appl1 gene leads to impairment of both the first and second phases of insulin secretion during hyperglycaemic clamp tests. In addition, glucose-stimulated insulin secretion (GSIS) is significantly decreased in islets from APPL1 KO mice. Conversely, overproduction of APPL1 leads to an increase in GSIS in beta cells. In addition, expression levels of several genes involved in insulin production, mitochondrial biogenesis and mitochondrial OCR, ATP production and mitochondrial membrane potential are reduced significantly in APPL1-knockdown beta cells. Moreover, suppression or overexproduction of APPL1 inhibits or stimulates adiponectin-potentiated GSIS in beta cells, respectively. Conclusions/interpretation Our study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.
CC :	002B21E01A
FD :	Déficit; Glucose; Insuline; Sécrétion; Animal; Inhibition; Cellule β; Diabète; Mitochondrie; Adiponectine; Souris
FG :	Pancréas endocrine; Hormone pancréatique; Ilot Langerhans; Adipokine; Endocrinopathie; Rodentia; Mammalia; Vertebrata
ED :	Deficiency; Glucose; Insulin; Secretion; Animal; Inhibition; β Cell; Diabetes mellitus; Mitochondria; Adiponectin; Mouse
EG :	Endocrine pancreas; Pancreatic hormone; Langerhans islet; Adipokine; Endocrinopathy; Rodentia; Mammalia; Vertebrata
SD :	Déficiencia; Glucosa; Insulina; Secreción; Animal; Inhibición; Célula β; Diabetes; Mitocondria; Adiponectina; Ratón
LO :	INIST-13012.354000503689440190
ID :	13-0281139

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Pascal:13-0281139

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<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
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<author><name sortKey="Jiyoon Ryu" sort="Jiyoon Ryu" uniqKey="Jiyoon Ryu" last="Jiyoon Ryu">JIYOON RYU</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive</s1>
<s2>San Antonio, TX 78229-3900</s2>
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<author><name sortKey="Zhifang Xie" sort="Zhifang Xie" uniqKey="Zhifang Xie" last="Zhifang Xie">ZHIFANG XIE</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Pathophysiology, Second Military Medical University</s1>
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<affiliation><inist:fA14 i1="06"><s1>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University</s1>
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<s3>CHN</s3>
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</author>
<author><name sortKey="Zhang, Weiping J" sort="Zhang, Weiping J" uniqKey="Zhang W" first="Weiping J." last="Zhang">Weiping J. Zhang</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Pathophysiology, Second Military Medical University</s1>
<s2>Shanghai</s2>
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<author><name sortKey="Dong, Lily Q" sort="Dong, Lily Q" uniqKey="Dong L" first="Lily Q." last="Dong">Lily Q. Dong</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive</s1>
<s2>San Antonio, TX 78229-3900</s2>
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<author><name sortKey="Weiping Jia" sort="Weiping Jia" uniqKey="Weiping Jia" last="Weiping Jia">WEIPING JIA</name>
<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
<s2>Shanghai</s2>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">13-0281139</idno>
<date when="2013">2013</date>
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<idno type="wicri:Area/PascalFrancis/Corpus">000050</idno>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function</title>
<author><name sortKey="Chen Wang" sort="Chen Wang" uniqKey="Chen Wang" last="Chen Wang">CHEN WANG</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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<author><name sortKey="Xiaowen Li" sort="Xiaowen Li" uniqKey="Xiaowen Li" last="Xiaowen Li">XIAOWEN LI</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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</author>
<author><name sortKey="Kaida Mu" sort="Kaida Mu" uniqKey="Kaida Mu" last="Kaida Mu">KAIDA MU</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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</author>
<author><name sortKey="Ling Li" sort="Ling Li" uniqKey="Ling Li" last="Ling Li">LING LI</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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<author><name sortKey="Shihong Wang" sort="Shihong Wang" uniqKey="Shihong Wang" last="Shihong Wang">SHIHONG WANG</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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<author><name sortKey="Yunxia Zhu" sort="Yunxia Zhu" uniqKey="Yunxia Zhu" last="Yunxia Zhu">YUNXIA ZHU</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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<author><name sortKey="Mingliang Zhang" sort="Mingliang Zhang" uniqKey="Mingliang Zhang" last="Mingliang Zhang">MINGLIANG ZHANG</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
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<sZ>1 aut.</sZ>
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<affiliation><inist:fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
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<author><name sortKey="Jiyoon Ryu" sort="Jiyoon Ryu" uniqKey="Jiyoon Ryu" last="Jiyoon Ryu">JIYOON RYU</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive</s1>
<s2>San Antonio, TX 78229-3900</s2>
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<author><name sortKey="Zhifang Xie" sort="Zhifang Xie" uniqKey="Zhifang Xie" last="Zhifang Xie">ZHIFANG XIE</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Pathophysiology, Second Military Medical University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>9 aut.</sZ>
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<author><name sortKey="Dongyun Shi" sort="Dongyun Shi" uniqKey="Dongyun Shi" last="Dongyun Shi">DONGYUN SHI</name>
<affiliation><inist:fA14 i1="06"><s1>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>10 aut.</sZ>
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<author><name sortKey="Zhang, Weiping J" sort="Zhang, Weiping J" uniqKey="Zhang W" first="Weiping J." last="Zhang">Weiping J. Zhang</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Pathophysiology, Second Military Medical University</s1>
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<sZ>9 aut.</sZ>
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<author><name sortKey="Dong, Lily Q" sort="Dong, Lily Q" uniqKey="Dong L" first="Lily Q." last="Dong">Lily Q. Dong</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive</s1>
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<affiliation><inist:fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
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<series><title level="j" type="main">Diabetologia : (Berlin)</title>
<title level="j" type="abbreviated">Diabetologia : (Berl.)</title>
<idno type="ISSN">0012-186X</idno>
<imprint><date when="2013">2013</date>
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<term>Animal</term>
<term>Deficiency</term>
<term>Diabetes mellitus</term>
<term>Glucose</term>
<term>Inhibition</term>
<term>Insulin</term>
<term>Mitochondria</term>
<term>Mouse</term>
<term>Secretion</term>
<term>β Cell</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Déficit</term>
<term>Glucose</term>
<term>Insuline</term>
<term>Sécrétion</term>
<term>Animal</term>
<term>Inhibition</term>
<term>Cellule β</term>
<term>Diabète</term>
<term>Mitochondrie</term>
<term>Adiponectine</term>
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<front><div type="abstract" xml:lang="en">Aims/hypothesis Adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1) is an adapter protein that positively mediates adiponectin signalling. Deficiency of APPL1 in the target tissues of insulin induces insulin resistance. We therefore aimed, in the present study, to determine its role in regulating pancreatic beta cell function. Methods A hyperglycaemic clamp test was performed to determine insulin secretion in APPL1 knockout (KO) mice. Glucose- and adiponectin-induced insulin release was measured in islets from APPL1 KO mice or INS-1(832/13) cells with either APPL1 knockdown or overproduction. RT-PCR and western blotting were conducted to analyse gene expression and protein abundance. Oxygen consumption rate (OCR), ATP production and mitochondrial membrane potential were assayed to evaluate mitochondrial function. Results APPL1 is highly expressed in pancreatic islets, but its levels are decreased in mice fed a high-fat diet and db/db mice compared with controls. Deletion of the Appl1 gene leads to impairment of both the first and second phases of insulin secretion during hyperglycaemic clamp tests. In addition, glucose-stimulated insulin secretion (GSIS) is significantly decreased in islets from APPL1 KO mice. Conversely, overproduction of APPL1 leads to an increase in GSIS in beta cells. In addition, expression levels of several genes involved in insulin production, mitochondrial biogenesis and mitochondrial OCR, ATP production and mitochondrial membrane potential are reduced significantly in APPL1-knockdown beta cells. Moreover, suppression or overexproduction of APPL1 inhibits or stimulates adiponectin-potentiated GSIS in beta cells, respectively. Conclusions/interpretation Our study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.</div>
</front>
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<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0012-186X</s0>
</fA01>
<fA03 i2="1"><s0>Diabetologia : (Berl.)</s0>
</fA03>
<fA05><s2>56</s2>
</fA05>
<fA06><s2>9</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>CHEN WANG</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>XIAOWEN LI</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>KAIDA MU</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>LING LI</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>SHIHONG WANG</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>YUNXIA ZHU</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>MINGLIANG ZHANG</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>JIYOON RYU</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>ZHIFANG XIE</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>DONGYUN SHI</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>ZHANG (Weiping J.)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>DONG (Lily Q.)</s1>
</fA11>
<fA11 i1="13" i2="1"><s1>WEIPING JIA</s1>
</fA11>
<fA14 i1="01"><s1>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road</s1>
<s2>Shanghai 200233</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Diabetes Institute, Shanghai Jiao Tong University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Shanghai Key Laboratory of Diabetes Mellitus</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>13 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive</s1>
<s2>San Antonio, TX 78229-3900</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Pathophysiology, Second Military Medical University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>9 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University</s1>
<s2>Shanghai</s2>
<s3>CHN</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>1999-2009</s1>
</fA20>
<fA21><s1>2013</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>13012</s2>
<s5>354000503689440190</s5>
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<fA44><s0>0000</s0>
<s1>© 2013 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>48 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>13-0281139</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Diabetologia : (Berlin)</s0>
</fA64>
<fA66 i1="01"><s0>DEU</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Aims/hypothesis Adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1) is an adapter protein that positively mediates adiponectin signalling. Deficiency of APPL1 in the target tissues of insulin induces insulin resistance. We therefore aimed, in the present study, to determine its role in regulating pancreatic beta cell function. Methods A hyperglycaemic clamp test was performed to determine insulin secretion in APPL1 knockout (KO) mice. Glucose- and adiponectin-induced insulin release was measured in islets from APPL1 KO mice or INS-1(832/13) cells with either APPL1 knockdown or overproduction. RT-PCR and western blotting were conducted to analyse gene expression and protein abundance. Oxygen consumption rate (OCR), ATP production and mitochondrial membrane potential were assayed to evaluate mitochondrial function. Results APPL1 is highly expressed in pancreatic islets, but its levels are decreased in mice fed a high-fat diet and db/db mice compared with controls. Deletion of the Appl1 gene leads to impairment of both the first and second phases of insulin secretion during hyperglycaemic clamp tests. In addition, glucose-stimulated insulin secretion (GSIS) is significantly decreased in islets from APPL1 KO mice. Conversely, overproduction of APPL1 leads to an increase in GSIS in beta cells. In addition, expression levels of several genes involved in insulin production, mitochondrial biogenesis and mitochondrial OCR, ATP production and mitochondrial membrane potential are reduced significantly in APPL1-knockdown beta cells. Moreover, suppression or overexproduction of APPL1 inhibits or stimulates adiponectin-potentiated GSIS in beta cells, respectively. Conclusions/interpretation Our study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.</s0>
</fC01>
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<s5>03</s5>
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<s5>03</s5>
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<s5>03</s5>
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<s5>04</s5>
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<s5>04</s5>
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<s5>05</s5>
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<s5>05</s5>
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<s5>07</s5>
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<s5>08</s5>
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<s5>08</s5>
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<s2>NM</s2>
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<s5>13</s5>
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<s5>14</s5>
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<s5>14</s5>
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<s5>69</s5>
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<s5>20</s5>
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<s5>21</s5>
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<s5>22</s5>
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<s2>NS</s2>
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<s2>NS</s2>
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<server><NO>PASCAL 13-0281139 INIST</NO>
<ET>Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function</ET>
<AU>CHEN WANG; XIAOWEN LI; KAIDA MU; LING LI; SHIHONG WANG; YUNXIA ZHU; MINGLIANG ZHANG; JIYOON RYU; ZHIFANG XIE; DONGYUN SHI; ZHANG (Weiping J.); DONG (Lily Q.); WEIPING JIA</AU>
<AF>Department of Endocrinology and Metabolism, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road/Shanghai 200233/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.); Diabetes Institute, Shanghai Jiao Tong University/Shanghai/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 13 aut.); Shanghai Key Laboratory of Diabetes Mellitus/Shanghai/Chine (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 13 aut.); Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive/San Antonio, TX 78229-3900/Etats-Unis (8 aut., 12 aut.); Department of Pathophysiology, Second Military Medical University/Shanghai/Chine (9 aut., 11 aut.); Department of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University/Shanghai/Chine (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Diabetologia : (Berlin); ISSN 0012-186X; Allemagne; Da. 2013; Vol. 56; No. 9; Pp. 1999-2009; Bibl. 48 ref.</SO>
<LA>Anglais</LA>
<EA>Aims/hypothesis Adaptor protein, phosphotyrosine interaction, pleckstrin homology domain and leucine zipper containing 1 (APPL1) is an adapter protein that positively mediates adiponectin signalling. Deficiency of APPL1 in the target tissues of insulin induces insulin resistance. We therefore aimed, in the present study, to determine its role in regulating pancreatic beta cell function. Methods A hyperglycaemic clamp test was performed to determine insulin secretion in APPL1 knockout (KO) mice. Glucose- and adiponectin-induced insulin release was measured in islets from APPL1 KO mice or INS-1(832/13) cells with either APPL1 knockdown or overproduction. RT-PCR and western blotting were conducted to analyse gene expression and protein abundance. Oxygen consumption rate (OCR), ATP production and mitochondrial membrane potential were assayed to evaluate mitochondrial function. Results APPL1 is highly expressed in pancreatic islets, but its levels are decreased in mice fed a high-fat diet and db/db mice compared with controls. Deletion of the Appl1 gene leads to impairment of both the first and second phases of insulin secretion during hyperglycaemic clamp tests. In addition, glucose-stimulated insulin secretion (GSIS) is significantly decreased in islets from APPL1 KO mice. Conversely, overproduction of APPL1 leads to an increase in GSIS in beta cells. In addition, expression levels of several genes involved in insulin production, mitochondrial biogenesis and mitochondrial OCR, ATP production and mitochondrial membrane potential are reduced significantly in APPL1-knockdown beta cells. Moreover, suppression or overexproduction of APPL1 inhibits or stimulates adiponectin-potentiated GSIS in beta cells, respectively. Conclusions/interpretation Our study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.</EA>
<CC>002B21E01A</CC>
<FD>Déficit; Glucose; Insuline; Sécrétion; Animal; Inhibition; Cellule β; Diabète; Mitochondrie; Adiponectine; Souris</FD>
<FG>Pancréas endocrine; Hormone pancréatique; Ilot Langerhans; Adipokine; Endocrinopathie; Rodentia; Mammalia; Vertebrata</FG>
<ED>Deficiency; Glucose; Insulin; Secretion; Animal; Inhibition; β Cell; Diabetes mellitus; Mitochondria; Adiponectin; Mouse</ED>
<EG>Endocrine pancreas; Pancreatic hormone; Langerhans islet; Adipokine; Endocrinopathy; Rodentia; Mammalia; Vertebrata</EG>
<SD>Déficiencia; Glucosa; Insulina; Secreción; Animal; Inhibición; Célula β; Diabetes; Mitocondria; Adiponectina; Ratón</SD>
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<ID>13-0281139</ID>
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Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function

Deficiency of APPL1 in mice impairs glucose-stimulated insulin secretion through inhibition of pancreatic beta cell mitochondrial function

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