Jørgen Frøkiær

Tissue Renin-Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperReviewResearchpeer-review

Standard

Tissue Renin-Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease. / Skov, Jeppe; Persson, Frederik; Frøkiær, Jørgen; Christiansen, Jens Sandahl.

In: Frontiers in Endocrinology, Vol. 5, No. 23, 2014.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperReviewResearchpeer-review

Harvard

APA

CBE

MLA

Vancouver

Author

Skov, Jeppe ; Persson, Frederik ; Frøkiær, Jørgen ; Christiansen, Jens Sandahl. / Tissue Renin-Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease. In: Frontiers in Endocrinology. 2014 ; Vol. 5, No. 23.

Bibtex

@article{ffb5bd68ce4a438ab2e19d32f4b7807b,
title = "Tissue Renin-Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease",
abstract = "The actions of angiotensin peptides are diverse and locally acting tissue renin-angiotensin systems (RAS) are present in almost all tissues of the body. An activated RAS strongly correlates to metabolic disease (e.g., diabetes) and its complications and blockers of RAS have been demonstrated to prevent diabetes in humans. Hyperglycemia, obesity, hypertension, and cortisol are well-known risk factors of metabolic disease and all stimulate tissue RAS whereas glucagon-like peptide-1, vitamin D, and aerobic exercise are inhibitors of tissue RAS and to some extent can prevent metabolic disease. Furthermore, an activated tissue RAS deteriorates the same risk factors creating a system with several positive feedback pathways. The primary effector hormone of the RAS, angiotensin II, stimulates reactive oxygen species, induces tissue damage, and can be associated to most diabetic complications. Based on these observations, we hypothesize that an activated tissue RAS is the principle cause of metabolic syndrome and type 2 diabetes, and additionally is mediating the majority of the metabolic complications. The involvement of positive feedback pathways may create a self-reinforcing state and explain why metabolic disease initiate and progress. The hypothesis plausibly unifies the major predictors of metabolic disease and places tissue RAS regulation in the center of metabolic control.",
author = "Jeppe Skov and Frederik Persson and J{\o}rgen Fr{\o}ki{\ae}r and Christiansen, {Jens Sandahl}",
year = "2014",
doi = "10.3389/fendo.2014.00023",
language = "English",
volume = "5",
journal = "Frontiers in Endocrinology",
issn = "1664-2392",
publisher = "Frontiers Media S.A",
number = "23",

}

RIS

TY - JOUR

T1 - Tissue Renin-Angiotensin Systems: A Unifying Hypothesis of Metabolic Disease

AU - Skov, Jeppe

AU - Persson, Frederik

AU - Frøkiær, Jørgen

AU - Christiansen, Jens Sandahl

PY - 2014

Y1 - 2014

N2 - The actions of angiotensin peptides are diverse and locally acting tissue renin-angiotensin systems (RAS) are present in almost all tissues of the body. An activated RAS strongly correlates to metabolic disease (e.g., diabetes) and its complications and blockers of RAS have been demonstrated to prevent diabetes in humans. Hyperglycemia, obesity, hypertension, and cortisol are well-known risk factors of metabolic disease and all stimulate tissue RAS whereas glucagon-like peptide-1, vitamin D, and aerobic exercise are inhibitors of tissue RAS and to some extent can prevent metabolic disease. Furthermore, an activated tissue RAS deteriorates the same risk factors creating a system with several positive feedback pathways. The primary effector hormone of the RAS, angiotensin II, stimulates reactive oxygen species, induces tissue damage, and can be associated to most diabetic complications. Based on these observations, we hypothesize that an activated tissue RAS is the principle cause of metabolic syndrome and type 2 diabetes, and additionally is mediating the majority of the metabolic complications. The involvement of positive feedback pathways may create a self-reinforcing state and explain why metabolic disease initiate and progress. The hypothesis plausibly unifies the major predictors of metabolic disease and places tissue RAS regulation in the center of metabolic control.

AB - The actions of angiotensin peptides are diverse and locally acting tissue renin-angiotensin systems (RAS) are present in almost all tissues of the body. An activated RAS strongly correlates to metabolic disease (e.g., diabetes) and its complications and blockers of RAS have been demonstrated to prevent diabetes in humans. Hyperglycemia, obesity, hypertension, and cortisol are well-known risk factors of metabolic disease and all stimulate tissue RAS whereas glucagon-like peptide-1, vitamin D, and aerobic exercise are inhibitors of tissue RAS and to some extent can prevent metabolic disease. Furthermore, an activated tissue RAS deteriorates the same risk factors creating a system with several positive feedback pathways. The primary effector hormone of the RAS, angiotensin II, stimulates reactive oxygen species, induces tissue damage, and can be associated to most diabetic complications. Based on these observations, we hypothesize that an activated tissue RAS is the principle cause of metabolic syndrome and type 2 diabetes, and additionally is mediating the majority of the metabolic complications. The involvement of positive feedback pathways may create a self-reinforcing state and explain why metabolic disease initiate and progress. The hypothesis plausibly unifies the major predictors of metabolic disease and places tissue RAS regulation in the center of metabolic control.

U2 - 10.3389/fendo.2014.00023

DO - 10.3389/fendo.2014.00023

M3 - Review

C2 - 24592256

VL - 5

JO - Frontiers in Endocrinology

JF - Frontiers in Endocrinology

SN - 1664-2392

IS - 23

ER -