Cellular basis of diabetic nephropathy: III. In vitro GLUT1 mRNA expression and risk of diabetic nephropathy in Type 1 diabetic patients

C. Huang; Y. Kim; M. L. Caramori; A. J. Fish; S. S. Rich; M. E. Miller; G. B. Russell; M. Mauer

doi:10.1007/s00125-004-1533-1

Cellular basis of diabetic nephropathy: III. In vitro GLUT1 mRNA expression and risk of diabetic nephropathy in Type 1 diabetic patients

C. Huang, Y. Kim, M. L. Caramori, A. J. Fish, S. S. Rich, M. E. Miller, G. B. Russell, M. Mauer

Research output: Contribution to journal › Article › peer-review

9 Scopus citations

Abstract

Aims/hypothesis. Altered glucose transporter expression has been implicated in the pathogenesis of diabetic nephropathy. There is increasing evidence that genetic factors convey risk of, or protection from, diabetic nephropathy and that the behaviour of cultured skin fibroblasts from Type 1 diabetic patients may reflect these genetic influences. This study aimed to compare GLUT1 mRNA expression levels in skin fibroblasts from Type 1 diabetic patients with either rapid ("fast-track", n=25) or slow ("slow-track", n=25) development of diabetic nephropathy and from non-diabetic normal control subjects (controls, n=25). Methods. Skin fibroblasts were cultured in Dulbecco's Modified Eagle's Medium with 25 mmol/1 glucose for 36 h. Total RNA was isolated, and GLUT1 mRNA levels were estimated by microarray analysis and RT-PCR. Results. Levels of GLUT1 mRNA expression in skin fibroblasts from "slow-track" patients were greater than those from "fast-track" patients (p=0.02), as initially detected by microarray. GLUT1 inRNA expression levels were confirmed by RT-PCR to be higher in skin fibroblasts from "slow-track" patients (4.59± 2.04) than in those from "fast-track" patients (3.34± 1.2, p=0.02), and were also higher than in skin fibroblasts from control subjects (3.52±1.66, p=0.03). There was no statistically significant difference between levels of expression in the "fast-track" patients and the control subjects. Conclusions/interpretation. This finding is consistent with the presence of cellular protection factors against diabetic nephropathy in the "slow-track" patients. These factors could be associated with the regulation of the GLUT1 pathway and may be genetically determined.

Original language	English (US)
Pages (from-to)	1789-1794
Number of pages	6
Journal	Diabetologia
Volume	47
Issue number	10
DOIs	https://doi.org/10.1007/s00125-004-1533-1
State	Published - Oct 2004

Bibliographical note

Funding Information:
Acknowledgements. C. Huang was supported by a mentor-based research fellowship from the American Diabetes Association. M. L. Caramori was initially supported by the Foundation for the Coordination of Higher Education and Graduate Training (CAPES) from the Brazilian Government and subsequently by a research fellowship grant from Juvenile Diabetes Foundation International. This work was supported by grants from the National Institutes of Health (DK 13083 and DK 54638), the National Center for Research Resources (M01-RR00400) and the Viking Children’s Fund (Eden Prairie, Minn., USA). We are especially grateful to P. Walker for his help with the RT-PCR. We also thank J. Basgen and T. Groppoli for performing the morphometric studies, K. Pinkham for the cell culture, M. Watrin for patient recruitment and S. Kupcho-Sandberg for AER measurements.

Keywords

Cellular marker
Diabetic nephropathy
GLUT1
Skin fibroblasts
mRNA expression

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "Cellular basis of diabetic nephropathy: III. In vitro GLUT1 mRNA expression and risk of diabetic nephropathy in Type 1 diabetic patients",

abstract = "Aims/hypothesis. Altered glucose transporter expression has been implicated in the pathogenesis of diabetic nephropathy. There is increasing evidence that genetic factors convey risk of, or protection from, diabetic nephropathy and that the behaviour of cultured skin fibroblasts from Type 1 diabetic patients may reflect these genetic influences. This study aimed to compare GLUT1 mRNA expression levels in skin fibroblasts from Type 1 diabetic patients with either rapid ({"}fast-track{"}, n=25) or slow ({"}slow-track{"}, n=25) development of diabetic nephropathy and from non-diabetic normal control subjects (controls, n=25). Methods. Skin fibroblasts were cultured in Dulbecco's Modified Eagle's Medium with 25 mmol/1 glucose for 36 h. Total RNA was isolated, and GLUT1 mRNA levels were estimated by microarray analysis and RT-PCR. Results. Levels of GLUT1 mRNA expression in skin fibroblasts from {"}slow-track{"} patients were greater than those from {"}fast-track{"} patients (p=0.02), as initially detected by microarray. GLUT1 inRNA expression levels were confirmed by RT-PCR to be higher in skin fibroblasts from {"}slow-track{"} patients (4.59± 2.04) than in those from {"}fast-track{"} patients (3.34± 1.2, p=0.02), and were also higher than in skin fibroblasts from control subjects (3.52±1.66, p=0.03). There was no statistically significant difference between levels of expression in the {"}fast-track{"} patients and the control subjects. Conclusions/interpretation. This finding is consistent with the presence of cellular protection factors against diabetic nephropathy in the {"}slow-track{"} patients. These factors could be associated with the regulation of the GLUT1 pathway and may be genetically determined.",

keywords = "Cellular marker, Diabetic nephropathy, GLUT1, Skin fibroblasts, mRNA expression",

author = "C. Huang and Y. Kim and Caramori, {M. L.} and Fish, {A. J.} and Rich, {S. S.} and Miller, {M. E.} and Russell, {G. B.} and M. Mauer",

note = "Funding Information: Acknowledgements. C. Huang was supported by a mentor-based research fellowship from the American Diabetes Association. M. L. Caramori was initially supported by the Foundation for the Coordination of Higher Education and Graduate Training (CAPES) from the Brazilian Government and subsequently by a research fellowship grant from Juvenile Diabetes Foundation International. This work was supported by grants from the National Institutes of Health (DK 13083 and DK 54638), the National Center for Research Resources (M01-RR00400) and the Viking Children{\textquoteright}s Fund (Eden Prairie, Minn., USA). We are especially grateful to P. Walker for his help with the RT-PCR. We also thank J. Basgen and T. Groppoli for performing the morphometric studies, K. Pinkham for the cell culture, M. Watrin for patient recruitment and S. Kupcho-Sandberg for AER measurements.",

year = "2004",

month = oct,

doi = "10.1007/s00125-004-1533-1",

language = "English (US)",

volume = "47",

pages = "1789--1794",

journal = "Diabetologia",

issn = "0012-186X",

publisher = "Springer Science and Business Media Deutschland GmbH",

number = "10",

}

TY - JOUR

T1 - Cellular basis of diabetic nephropathy

T2 - III. In vitro GLUT1 mRNA expression and risk of diabetic nephropathy in Type 1 diabetic patients

AU - Huang, C.

AU - Kim, Y.

AU - Caramori, M. L.

AU - Fish, A. J.

AU - Rich, S. S.

AU - Miller, M. E.

AU - Russell, G. B.

AU - Mauer, M.

N1 - Funding Information: Acknowledgements. C. Huang was supported by a mentor-based research fellowship from the American Diabetes Association. M. L. Caramori was initially supported by the Foundation for the Coordination of Higher Education and Graduate Training (CAPES) from the Brazilian Government and subsequently by a research fellowship grant from Juvenile Diabetes Foundation International. This work was supported by grants from the National Institutes of Health (DK 13083 and DK 54638), the National Center for Research Resources (M01-RR00400) and the Viking Children’s Fund (Eden Prairie, Minn., USA). We are especially grateful to P. Walker for his help with the RT-PCR. We also thank J. Basgen and T. Groppoli for performing the morphometric studies, K. Pinkham for the cell culture, M. Watrin for patient recruitment and S. Kupcho-Sandberg for AER measurements.

PY - 2004/10

Y1 - 2004/10

N2 - Aims/hypothesis. Altered glucose transporter expression has been implicated in the pathogenesis of diabetic nephropathy. There is increasing evidence that genetic factors convey risk of, or protection from, diabetic nephropathy and that the behaviour of cultured skin fibroblasts from Type 1 diabetic patients may reflect these genetic influences. This study aimed to compare GLUT1 mRNA expression levels in skin fibroblasts from Type 1 diabetic patients with either rapid ("fast-track", n=25) or slow ("slow-track", n=25) development of diabetic nephropathy and from non-diabetic normal control subjects (controls, n=25). Methods. Skin fibroblasts were cultured in Dulbecco's Modified Eagle's Medium with 25 mmol/1 glucose for 36 h. Total RNA was isolated, and GLUT1 mRNA levels were estimated by microarray analysis and RT-PCR. Results. Levels of GLUT1 mRNA expression in skin fibroblasts from "slow-track" patients were greater than those from "fast-track" patients (p=0.02), as initially detected by microarray. GLUT1 inRNA expression levels were confirmed by RT-PCR to be higher in skin fibroblasts from "slow-track" patients (4.59± 2.04) than in those from "fast-track" patients (3.34± 1.2, p=0.02), and were also higher than in skin fibroblasts from control subjects (3.52±1.66, p=0.03). There was no statistically significant difference between levels of expression in the "fast-track" patients and the control subjects. Conclusions/interpretation. This finding is consistent with the presence of cellular protection factors against diabetic nephropathy in the "slow-track" patients. These factors could be associated with the regulation of the GLUT1 pathway and may be genetically determined.

AB - Aims/hypothesis. Altered glucose transporter expression has been implicated in the pathogenesis of diabetic nephropathy. There is increasing evidence that genetic factors convey risk of, or protection from, diabetic nephropathy and that the behaviour of cultured skin fibroblasts from Type 1 diabetic patients may reflect these genetic influences. This study aimed to compare GLUT1 mRNA expression levels in skin fibroblasts from Type 1 diabetic patients with either rapid ("fast-track", n=25) or slow ("slow-track", n=25) development of diabetic nephropathy and from non-diabetic normal control subjects (controls, n=25). Methods. Skin fibroblasts were cultured in Dulbecco's Modified Eagle's Medium with 25 mmol/1 glucose for 36 h. Total RNA was isolated, and GLUT1 mRNA levels were estimated by microarray analysis and RT-PCR. Results. Levels of GLUT1 mRNA expression in skin fibroblasts from "slow-track" patients were greater than those from "fast-track" patients (p=0.02), as initially detected by microarray. GLUT1 inRNA expression levels were confirmed by RT-PCR to be higher in skin fibroblasts from "slow-track" patients (4.59± 2.04) than in those from "fast-track" patients (3.34± 1.2, p=0.02), and were also higher than in skin fibroblasts from control subjects (3.52±1.66, p=0.03). There was no statistically significant difference between levels of expression in the "fast-track" patients and the control subjects. Conclusions/interpretation. This finding is consistent with the presence of cellular protection factors against diabetic nephropathy in the "slow-track" patients. These factors could be associated with the regulation of the GLUT1 pathway and may be genetically determined.

KW - Cellular marker

KW - Diabetic nephropathy

KW - GLUT1

KW - Skin fibroblasts

KW - mRNA expression

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SN - 0012-186X

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EP - 1794

JO - Diabetologia

JF - Diabetologia

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ER -

Cellular basis of diabetic nephropathy: III. In vitro GLUT1 mRNA expression and risk of diabetic nephropathy in Type 1 diabetic patients

Abstract

Bibliographical note

Keywords

UN SDGs

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