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Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice

BACKGROUND: Chronic hyperglycemia in diabetes causes atherosclerosis and progresses to diabetic macroangiopathy, and can lead to coronary heart disease, myocardial infarction and cerebrovascular disease. Palmitoleic acid (POA) is a product of endogenous lipogenesis and is present in fish and vegetab...

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Autores principales: Takenouchi, Yasuhiro, Seki, Yoshie, Shiba, Sachiko, Ohtake, Kazuo, Nobe, Koji, Kasono, Keizo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014575/
https://www.ncbi.nlm.nih.gov/pubmed/35436932
http://dx.doi.org/10.1186/s12902-022-01018-2
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author Takenouchi, Yasuhiro
Seki, Yoshie
Shiba, Sachiko
Ohtake, Kazuo
Nobe, Koji
Kasono, Keizo
author_facet Takenouchi, Yasuhiro
Seki, Yoshie
Shiba, Sachiko
Ohtake, Kazuo
Nobe, Koji
Kasono, Keizo
author_sort Takenouchi, Yasuhiro
collection PubMed
description BACKGROUND: Chronic hyperglycemia in diabetes causes atherosclerosis and progresses to diabetic macroangiopathy, and can lead to coronary heart disease, myocardial infarction and cerebrovascular disease. Palmitoleic acid (POA) is a product of endogenous lipogenesis and is present in fish and vegetable oil. In human and animal studies, POA is reported as a beneficial fatty acid related to insulin sensitivity and glucose tolerance. However, few studies have reported its effects on aortic function in diabetes. Here, we investigated the effects of POA administration on vascular function in KKAy mice, a model of type 2 diabetes. METHODS: Male C57BL/6 J (control) and KKAy (experimental) mice at the age of 14 weeks were used in the present study. For each mouse strain, one group was fed with reference diet and a second group was fed POA-containing diet for 2 weeks. The vascular reactivities of prepared aortic rings were then measured in an organ bath to determine if POA administration changed vascular function in these mice. RESULTS: KKAy mice treated with POA exhibited decreased plasma glucose levels compared with mice treated with reference diet. However, endothelium-dependent vasorelaxant responses to acetylcholine and protease-activated receptor 2 activating protein, which are attenuated in the aorta of KKAy mice compared to C57BL/6 J mice under a reference diet, were not affected by a 2-week POA treatment. In addition, assessment of vasoconstriction revealed that the phenylephrine-induced vasoconstrictive response was enhanced in KKAy mice compared to C57BL/6 J mice under a reference diet, but no effect was observed in KKAy mice fed a POA-containing diet. In contrast, there was an increase in vasoconstriction in C57BL/6 J mice fed the POA-containing diet compared to mice fed a reference diet. Furthermore, the vasoconstriction in aorta in both C57BL/6 J and KKAy mice fed a POA-containing diet were further enhanced under hyperglycemic conditions compared to normal glucose conditions in vitro. In the hyperinsulinemic, and hyperinsulinemic combined with hyperglycemic conditions, vasoconstriction was increased in KKAy mice fed with POA. CONCLUSION: These results suggest that POA intake enhances vasoconstriction under hyperglycemic and hyperinsulinemic conditions, which are characteristics of type 2 diabetes, and may contribute to increased vascular complications in diabetes.
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spelling pubmed-90145752022-04-19 Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice Takenouchi, Yasuhiro Seki, Yoshie Shiba, Sachiko Ohtake, Kazuo Nobe, Koji Kasono, Keizo BMC Endocr Disord Research BACKGROUND: Chronic hyperglycemia in diabetes causes atherosclerosis and progresses to diabetic macroangiopathy, and can lead to coronary heart disease, myocardial infarction and cerebrovascular disease. Palmitoleic acid (POA) is a product of endogenous lipogenesis and is present in fish and vegetable oil. In human and animal studies, POA is reported as a beneficial fatty acid related to insulin sensitivity and glucose tolerance. However, few studies have reported its effects on aortic function in diabetes. Here, we investigated the effects of POA administration on vascular function in KKAy mice, a model of type 2 diabetes. METHODS: Male C57BL/6 J (control) and KKAy (experimental) mice at the age of 14 weeks were used in the present study. For each mouse strain, one group was fed with reference diet and a second group was fed POA-containing diet for 2 weeks. The vascular reactivities of prepared aortic rings were then measured in an organ bath to determine if POA administration changed vascular function in these mice. RESULTS: KKAy mice treated with POA exhibited decreased plasma glucose levels compared with mice treated with reference diet. However, endothelium-dependent vasorelaxant responses to acetylcholine and protease-activated receptor 2 activating protein, which are attenuated in the aorta of KKAy mice compared to C57BL/6 J mice under a reference diet, were not affected by a 2-week POA treatment. In addition, assessment of vasoconstriction revealed that the phenylephrine-induced vasoconstrictive response was enhanced in KKAy mice compared to C57BL/6 J mice under a reference diet, but no effect was observed in KKAy mice fed a POA-containing diet. In contrast, there was an increase in vasoconstriction in C57BL/6 J mice fed the POA-containing diet compared to mice fed a reference diet. Furthermore, the vasoconstriction in aorta in both C57BL/6 J and KKAy mice fed a POA-containing diet were further enhanced under hyperglycemic conditions compared to normal glucose conditions in vitro. In the hyperinsulinemic, and hyperinsulinemic combined with hyperglycemic conditions, vasoconstriction was increased in KKAy mice fed with POA. CONCLUSION: These results suggest that POA intake enhances vasoconstriction under hyperglycemic and hyperinsulinemic conditions, which are characteristics of type 2 diabetes, and may contribute to increased vascular complications in diabetes. BioMed Central 2022-04-18 /pmc/articles/PMC9014575/ /pubmed/35436932 http://dx.doi.org/10.1186/s12902-022-01018-2 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visithttp://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Takenouchi, Yasuhiro
Seki, Yoshie
Shiba, Sachiko
Ohtake, Kazuo
Nobe, Koji
Kasono, Keizo
Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
title Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
title_full Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
title_fullStr Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
title_full_unstemmed Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
title_short Effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
title_sort effects of dietary palmitoleic acid on vascular function in aorta of diabetic mice
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014575/
https://www.ncbi.nlm.nih.gov/pubmed/35436932
http://dx.doi.org/10.1186/s12902-022-01018-2
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