Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin: lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin : lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients. / Hansen, L; Fjordvang, H; Rasmussen, S K; Vestergaard, H; Echwald, Søren Morgenthaler; Hansen, T; Alessi, D; Shenolikar, S; Saltiel, A R; Barbetti, F; Pedersen, O.

In: Diabetes, Vol. 48, No. 2, 02.1999, p. 403-7.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Hansen, L, Fjordvang, H, Rasmussen, SK, Vestergaard, H, Echwald, SM, Hansen, T, Alessi, D, Shenolikar, S, Saltiel, AR, Barbetti, F & Pedersen, O 1999, 'Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin: lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients', Diabetes, vol. 48, no. 2, pp. 403-7.

APA

Hansen, L., Fjordvang, H., Rasmussen, S. K., Vestergaard, H., Echwald, S. M., Hansen, T., Alessi, D., Shenolikar, S., Saltiel, A. R., Barbetti, F., & Pedersen, O. (1999). Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin: lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients. Diabetes, 48(2), 403-7.

Vancouver

Hansen L, Fjordvang H, Rasmussen SK, Vestergaard H, Echwald SM, Hansen T et al. Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin: lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients. Diabetes. 1999 Feb;48(2):403-7.

Author

Hansen, L ; Fjordvang, H ; Rasmussen, S K ; Vestergaard, H ; Echwald, Søren Morgenthaler ; Hansen, T ; Alessi, D ; Shenolikar, S ; Saltiel, A R ; Barbetti, F ; Pedersen, O. / Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin : lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients. In: Diabetes. 1999 ; Vol. 48, No. 2. pp. 403-7.

Bibtex

@article{e6e0bb463c704ac0b24bb5d399dc3147,
title = "Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin: lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients",
abstract = "The finding of a reduced insulin-stimulated glucose uptake and glycogen synthesis in the skeletal muscle of glucose-tolerant first-degree relatives of patients with NIDDM, as well as in cultured fibroblasts and skeletal muscle cells isolated from NIDDM patients, has been interpreted as evidence for a genetic involvement in the disease. The mode of inheritance of the common forms of NIDDM is as yet unclear, but the prevailing hypothesis supports a polygenic model. In the present study, we tested the hypothesis that the putative inheritable defects of insulin-stimulated muscle glycogen synthesis might be caused by genetic variability in the genes encoding proteins shown by biochemical evidence to be involved in insulin-stimulated glycogen synthesis in skeletal muscle. In 70 insulin-resistant Danish NIDDM patients, mutational analysis by reverse transcription-polymerase chain reaction-single strand conformation polymorphism-heteroduplex analysis was performed on genomic DNA or skeletal muscle-derived cDNAs encoding glycogenin, protein phosphatase inhibitor-1, phophatase targeting to glycogen, protein kinase B-alpha and -beta, and the phosphoinositide-dependent protein kinase-1. Although a number of silent variants were identified in some of the examined genes, we found no evidence for the hypothesis that the defective insulin-stimulated glycogen synthesis in skeletal muscle in NIDDM is caused by structural changes in the genes encoding the known components of the insulin-sensitive glycogen synthesis pathway of skeletal muscle.",
keywords = "3-Phosphoinositide-Dependent Protein Kinases, Carrier Proteins, DNA Mutational Analysis, Diabetes Mellitus, Type 2, Endoribonucleases, Female, Genetic Variation, Glucosyltransferases, Glycogen, Glycoproteins, Humans, Insulin, Intracellular Signaling Peptides and Proteins, Isomerism, Male, Middle Aged, Muscle, Skeletal, Phenotype, Phosphoprotein Phosphatases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, RNA-Binding Proteins",
author = "L Hansen and H Fjordvang and Rasmussen, {S K} and H Vestergaard and Echwald, {S{\o}ren Morgenthaler} and T Hansen and D Alessi and S Shenolikar and Saltiel, {A R} and F Barbetti and O Pedersen",
year = "1999",
month = feb,
language = "English",
volume = "48",
pages = "403--7",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association",
number = "2",

}

RIS

TY - JOUR

T1 - Mutational analysis of the coding regions of the genes encoding protein kinase B-alpha and -beta, phosphoinositide-dependent protein kinase-1, phosphatase targeting to glycogen, protein phosphatase inhibitor-1, and glycogenin

T2 - lessons from a search for genetic variability of the insulin-stimulated glycogen synthesis pathway of skeletal muscle in NIDDM patients

AU - Hansen, L

AU - Fjordvang, H

AU - Rasmussen, S K

AU - Vestergaard, H

AU - Echwald, Søren Morgenthaler

AU - Hansen, T

AU - Alessi, D

AU - Shenolikar, S

AU - Saltiel, A R

AU - Barbetti, F

AU - Pedersen, O

PY - 1999/2

Y1 - 1999/2

N2 - The finding of a reduced insulin-stimulated glucose uptake and glycogen synthesis in the skeletal muscle of glucose-tolerant first-degree relatives of patients with NIDDM, as well as in cultured fibroblasts and skeletal muscle cells isolated from NIDDM patients, has been interpreted as evidence for a genetic involvement in the disease. The mode of inheritance of the common forms of NIDDM is as yet unclear, but the prevailing hypothesis supports a polygenic model. In the present study, we tested the hypothesis that the putative inheritable defects of insulin-stimulated muscle glycogen synthesis might be caused by genetic variability in the genes encoding proteins shown by biochemical evidence to be involved in insulin-stimulated glycogen synthesis in skeletal muscle. In 70 insulin-resistant Danish NIDDM patients, mutational analysis by reverse transcription-polymerase chain reaction-single strand conformation polymorphism-heteroduplex analysis was performed on genomic DNA or skeletal muscle-derived cDNAs encoding glycogenin, protein phosphatase inhibitor-1, phophatase targeting to glycogen, protein kinase B-alpha and -beta, and the phosphoinositide-dependent protein kinase-1. Although a number of silent variants were identified in some of the examined genes, we found no evidence for the hypothesis that the defective insulin-stimulated glycogen synthesis in skeletal muscle in NIDDM is caused by structural changes in the genes encoding the known components of the insulin-sensitive glycogen synthesis pathway of skeletal muscle.

AB - The finding of a reduced insulin-stimulated glucose uptake and glycogen synthesis in the skeletal muscle of glucose-tolerant first-degree relatives of patients with NIDDM, as well as in cultured fibroblasts and skeletal muscle cells isolated from NIDDM patients, has been interpreted as evidence for a genetic involvement in the disease. The mode of inheritance of the common forms of NIDDM is as yet unclear, but the prevailing hypothesis supports a polygenic model. In the present study, we tested the hypothesis that the putative inheritable defects of insulin-stimulated muscle glycogen synthesis might be caused by genetic variability in the genes encoding proteins shown by biochemical evidence to be involved in insulin-stimulated glycogen synthesis in skeletal muscle. In 70 insulin-resistant Danish NIDDM patients, mutational analysis by reverse transcription-polymerase chain reaction-single strand conformation polymorphism-heteroduplex analysis was performed on genomic DNA or skeletal muscle-derived cDNAs encoding glycogenin, protein phosphatase inhibitor-1, phophatase targeting to glycogen, protein kinase B-alpha and -beta, and the phosphoinositide-dependent protein kinase-1. Although a number of silent variants were identified in some of the examined genes, we found no evidence for the hypothesis that the defective insulin-stimulated glycogen synthesis in skeletal muscle in NIDDM is caused by structural changes in the genes encoding the known components of the insulin-sensitive glycogen synthesis pathway of skeletal muscle.

KW - 3-Phosphoinositide-Dependent Protein Kinases

KW - Carrier Proteins

KW - DNA Mutational Analysis

KW - Diabetes Mellitus, Type 2

KW - Endoribonucleases

KW - Female

KW - Genetic Variation

KW - Glucosyltransferases

KW - Glycogen

KW - Glycoproteins

KW - Humans

KW - Insulin

KW - Intracellular Signaling Peptides and Proteins

KW - Isomerism

KW - Male

KW - Middle Aged

KW - Muscle, Skeletal

KW - Phenotype

KW - Phosphoprotein Phosphatases

KW - Protein-Serine-Threonine Kinases

KW - Proto-Oncogene Proteins

KW - Proto-Oncogene Proteins c-akt

KW - RNA-Binding Proteins

M3 - Journal article

C2 - 10334321

VL - 48

SP - 403

EP - 407

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 2

ER -

ID: 92192413