An immune origin of type 2 diabetes?

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Standard

An immune origin of type 2 diabetes? / Kolb, H; Mandrup-Poulsen, Thomas.

In: Diabetologia, Vol. 48, No. 6, 01.06.2005, p. 1038-50.

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

Harvard

Kolb, H & Mandrup-Poulsen, T 2005, 'An immune origin of type 2 diabetes?', Diabetologia, vol. 48, no. 6, pp. 1038-50. https://doi.org/10.1007/s00125-005-1764-9

APA

Kolb, H., & Mandrup-Poulsen, T. (2005). An immune origin of type 2 diabetes? Diabetologia, 48(6), 1038-50. https://doi.org/10.1007/s00125-005-1764-9

Vancouver

Kolb H, Mandrup-Poulsen T. An immune origin of type 2 diabetes? Diabetologia. 2005 Jun 1;48(6):1038-50. https://doi.org/10.1007/s00125-005-1764-9

Author

Kolb, H ; Mandrup-Poulsen, Thomas. / An immune origin of type 2 diabetes?. In: Diabetologia. 2005 ; Vol. 48, No. 6. pp. 1038-50.

Bibtex

@article{813755eb7d2d416bbff25b842f9501a5,
title = "An immune origin of type 2 diabetes?",
abstract = "Subclinical, low-grade systemic inflammation has been observed in patients with type 2 diabetes and in those at increased risk of the disease. This may be more than an epiphenomenon. Alleles of genes encoding immune/inflammatory mediators are associated with the disease, and the two major environmental factors the contribute to the risk of type 2 diabetes-diet and physical activity-have a direct impact on levels of systemic immune mediators. In animal models, targeting of immune genes enhanced or suppressed the development of obesity or diabetes. Obesity is associated with the infiltration and proinflammatory activity of macrophages in adipose tissue, and immune mediators may be important regulators of insulin resistance, mitochondrial function, ectopic lipid storage and beta cell dysfunction or death. Intervention studies targeting these pathways would help to determine the contribution of an activated innate immune system to the development of type 2 diabetes.",
keywords = "Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Disease Models, Animal, Humans, Inflammation, Macrophages, Obesity",
author = "H Kolb and Thomas Mandrup-Poulsen",
year = "2005",
month = jun,
day = "1",
doi = "10.1007/s00125-005-1764-9",
language = "English",
volume = "48",
pages = "1038--50",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "6",

}

RIS

TY - JOUR

T1 - An immune origin of type 2 diabetes?

AU - Kolb, H

AU - Mandrup-Poulsen, Thomas

PY - 2005/6/1

Y1 - 2005/6/1

N2 - Subclinical, low-grade systemic inflammation has been observed in patients with type 2 diabetes and in those at increased risk of the disease. This may be more than an epiphenomenon. Alleles of genes encoding immune/inflammatory mediators are associated with the disease, and the two major environmental factors the contribute to the risk of type 2 diabetes-diet and physical activity-have a direct impact on levels of systemic immune mediators. In animal models, targeting of immune genes enhanced or suppressed the development of obesity or diabetes. Obesity is associated with the infiltration and proinflammatory activity of macrophages in adipose tissue, and immune mediators may be important regulators of insulin resistance, mitochondrial function, ectopic lipid storage and beta cell dysfunction or death. Intervention studies targeting these pathways would help to determine the contribution of an activated innate immune system to the development of type 2 diabetes.

AB - Subclinical, low-grade systemic inflammation has been observed in patients with type 2 diabetes and in those at increased risk of the disease. This may be more than an epiphenomenon. Alleles of genes encoding immune/inflammatory mediators are associated with the disease, and the two major environmental factors the contribute to the risk of type 2 diabetes-diet and physical activity-have a direct impact on levels of systemic immune mediators. In animal models, targeting of immune genes enhanced or suppressed the development of obesity or diabetes. Obesity is associated with the infiltration and proinflammatory activity of macrophages in adipose tissue, and immune mediators may be important regulators of insulin resistance, mitochondrial function, ectopic lipid storage and beta cell dysfunction or death. Intervention studies targeting these pathways would help to determine the contribution of an activated innate immune system to the development of type 2 diabetes.

KW - Adipose Tissue

KW - Animals

KW - Diabetes Mellitus, Type 2

KW - Disease Models, Animal

KW - Humans

KW - Inflammation

KW - Macrophages

KW - Obesity

U2 - 10.1007/s00125-005-1764-9

DO - 10.1007/s00125-005-1764-9

M3 - Journal article

C2 - 15864529

VL - 48

SP - 1038

EP - 1050

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 6

ER -

ID: 33902430