Adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice

Wing Tak Wong; Xiao Yu Tian; Aimin Xu; Jun Yu; Chi Wai Lau; Ruby L.C. Hoo; Yu Wang; Vivian W.Y. Lee; Karen S.L. Lam; Paul M. Vanhoutte; Yu Huang

doi:10.1016/j.cmet.2011.05.009

Adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice

Wing Tak Wong, Xiao Yu Tian, Aimin Xu, Jun Yu, Chi Wai Lau, Ruby L.C. Hoo, Yu Wang, Vivian W.Y. Lee, Karen S.L. Lam, Paul M. Vanhoutte, Yu Huang

Research output: Journal Publications and Reviews › RGC 21 - Publication in refereed journal › peer-review

111 Citations (Scopus)

Abstract

Rosiglitazone is a PPARγ agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. © 2011 Elsevier Inc.

Original language	English
Pages (from-to)	104-115
Journal	Cell Metabolism
Volume	14
Issue number	1
DOIs	https://doi.org/10.1016/j.cmet.2011.05.009
Publication status	Published - 6 Jul 2011
Externally published	Yes

Bibliographical note

Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

UN SDGs

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

SDG 3 Good Health and Well-being

Access Output

10.1016/j.cmet.2011.05.009Licence: Elsevier user license

Other Access Options

Check CityUHK Library

Permanent Link

Right click to copy link

Cite this

@article{8494e7bcfc264e828b760281ccc76581,

title = "Adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice",

abstract = "Rosiglitazone is a PPARγ agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. {\textcopyright} 2011 Elsevier Inc.",

author = "Wong, {Wing Tak} and Tian, {Xiao Yu} and Aimin Xu and Jun Yu and Lau, {Chi Wai} and Hoo, {Ruby L.C.} and Yu Wang and Lee, {Vivian W.Y.} and Lam, {Karen S.L.} and Vanhoutte, {Paul M.} and Yu Huang",

note = "Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].",

year = "2011",

month = jul,

day = "6",

doi = "10.1016/j.cmet.2011.05.009",

language = "English",

volume = "14",

pages = "104--115",

journal = "Cell Metabolism",

issn = "1550-4131",

publisher = "Cell Press",

number = "1",

}

TY - JOUR

T1 - Adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice

AU - Wong, Wing Tak

AU - Tian, Xiao Yu

AU - Xu, Aimin

AU - Yu, Jun

AU - Lau, Chi Wai

AU - Hoo, Ruby L.C.

AU - Wang, Yu

AU - Lee, Vivian W.Y.

AU - Lam, Karen S.L.

AU - Vanhoutte, Paul M.

AU - Huang, Yu

N1 - Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

PY - 2011/7/6

Y1 - 2011/7/6

N2 - Rosiglitazone is a PPARγ agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. © 2011 Elsevier Inc.

AB - Rosiglitazone is a PPARγ agonist commonly used to treat diabetes. In addition to improving insulin sensitivity, rosiglitazone restores normal vascular function by a mechanism that remains poorly understood. Here we show that adiponectin is required to mediate the PPARγ effect on vascular endothelium of diabetic mice. In db/db and diet-induced obese mice, PPARγ activation by rosiglitazone restores endothelium-dependent relaxation of aortae, whereas diabetic mice lacking adiponectin or treated with an anti-adiponectin antibody do not respond. Rosiglitazone stimulates adiponectin release from fat explants, and subcutaneous fat transplantation from rosiglitazone-treated mice recapitulates vasodilatation in untreated db/db recipients. Mechanistically, adiponectin activates AMPK/eNOS and cAMP/PKA signaling pathways in aortae, which increase NO bioavailability and reduce oxidative stress. Taken together, these results demonstrate that adipocyte-derived adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetes. Thus, the adipose tissue represents a promising target for treating diabetic vasculopathy. © 2011 Elsevier Inc.

UR - http://www.scopus.com/inward/record.url?scp=79960018147&partnerID=8YFLogxK

UR - https://www.scopus.com/record/pubmetrics.uri?eid=2-s2.0-79960018147&origin=recordpage

U2 - 10.1016/j.cmet.2011.05.009

DO - 10.1016/j.cmet.2011.05.009

M3 - RGC 21 - Publication in refereed journal

C2 - 21723508

SN - 1550-4131

VL - 14

SP - 104

EP - 115

JO - Cell Metabolism

JF - Cell Metabolism

IS - 1

ER -

Adiponectin is required for PPARγ-mediated improvement of endothelial function in diabetic mice

Abstract

Bibliographical note

UN SDGs

Access Output

Other Access Options

Permanent Link

Other Files and Links

Fingerprint

Cite this