Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.

A number of epidemiological studies demonstrated that postprandial hyperglycemia is a risk factor for cardiovascular disease in individuals with impaired glucose tolerance. Although several laboratory studies have addressed the plausible causal role of postprandial acute hyperglycemia (glucose spike...

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Main Authors: Yuki Shuto, Akira Asai, Mototsugu Nagao, Hitoshi Sugihara, Shinichi Oikawa
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2015-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4552094?pdf=render
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author Yuki Shuto
Akira Asai
Mototsugu Nagao
Hitoshi Sugihara
Shinichi Oikawa
author_facet Yuki Shuto
Akira Asai
Mototsugu Nagao
Hitoshi Sugihara
Shinichi Oikawa
author_sort Yuki Shuto
collection DOAJ
description A number of epidemiological studies demonstrated that postprandial hyperglycemia is a risk factor for cardiovascular disease in individuals with impaired glucose tolerance. Although several laboratory studies have addressed the plausible causal role of postprandial acute hyperglycemia (glucose spikes) in the development of atherosclerosis, there is little convincing evidence in vivo whether the atherosclerotic lesion formation can be accelerated solely by glucose spikes. Here, we assessed the effect of repetitive glucose spikes on atherosclerotic lesion formation in mice.Female C57BL/6 mice were fed an atherogenic diet from 8 to 28 weeks of age. During the atherogenic diet feeding period, the mice orally received a glucose solution (50 mg glucose/mouse; G group) or water (W group) twice daily, 6 days a week. Atherosclerotic lesion formation in the aortic sinus was quantitatively analyzed in serial cross-sections by oil red O staining.G group mice showed transient increases in blood glucose level (~5 mmol/L above W group), and the levels returned to levels similar to those in W group mice within 60 min. No significant differences in glucose tolerance, insulin sensitivity, and plasma lipid profiles were observed after the 20-week repetitive administration between the 2 groups. G group mice showed an approximately 4-fold greater atherosclerotic lesion size in the aortic sinus than W group mice. Gene expression levels of Cd68 and Icam1 in the thoracic aorta were higher in G group mice than in W group mice.These results indicate that glucose spikes can accelerate atherosclerotic lesion formation, with little influence on other metabolic disorders. Repetitive glucose administration in wild-type mice may serve as a simple and useful approach to better understanding the causal role of glycemic spikes in the development of atherosclerosis.
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spelling doaj.art-5858a0a797d84d449bc367688ee6ac982022-12-22T01:34:20ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01108e013684010.1371/journal.pone.0136840Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.Yuki ShutoAkira AsaiMototsugu NagaoHitoshi SugiharaShinichi OikawaA number of epidemiological studies demonstrated that postprandial hyperglycemia is a risk factor for cardiovascular disease in individuals with impaired glucose tolerance. Although several laboratory studies have addressed the plausible causal role of postprandial acute hyperglycemia (glucose spikes) in the development of atherosclerosis, there is little convincing evidence in vivo whether the atherosclerotic lesion formation can be accelerated solely by glucose spikes. Here, we assessed the effect of repetitive glucose spikes on atherosclerotic lesion formation in mice.Female C57BL/6 mice were fed an atherogenic diet from 8 to 28 weeks of age. During the atherogenic diet feeding period, the mice orally received a glucose solution (50 mg glucose/mouse; G group) or water (W group) twice daily, 6 days a week. Atherosclerotic lesion formation in the aortic sinus was quantitatively analyzed in serial cross-sections by oil red O staining.G group mice showed transient increases in blood glucose level (~5 mmol/L above W group), and the levels returned to levels similar to those in W group mice within 60 min. No significant differences in glucose tolerance, insulin sensitivity, and plasma lipid profiles were observed after the 20-week repetitive administration between the 2 groups. G group mice showed an approximately 4-fold greater atherosclerotic lesion size in the aortic sinus than W group mice. Gene expression levels of Cd68 and Icam1 in the thoracic aorta were higher in G group mice than in W group mice.These results indicate that glucose spikes can accelerate atherosclerotic lesion formation, with little influence on other metabolic disorders. Repetitive glucose administration in wild-type mice may serve as a simple and useful approach to better understanding the causal role of glycemic spikes in the development of atherosclerosis.http://europepmc.org/articles/PMC4552094?pdf=render
spellingShingle Yuki Shuto
Akira Asai
Mototsugu Nagao
Hitoshi Sugihara
Shinichi Oikawa
Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.
PLoS ONE
title Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.
title_full Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.
title_fullStr Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.
title_full_unstemmed Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.
title_short Repetitive Glucose Spikes Accelerate Atherosclerotic Lesion Formation in C57BL/6 Mice.
title_sort repetitive glucose spikes accelerate atherosclerotic lesion formation in c57bl 6 mice
url http://europepmc.org/articles/PMC4552094?pdf=render
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AT mototsugunagao repetitiveglucosespikesaccelerateatheroscleroticlesionformationinc57bl6mice
AT hitoshisugihara repetitiveglucosespikesaccelerateatheroscleroticlesionformationinc57bl6mice
AT shinichioikawa repetitiveglucosespikesaccelerateatheroscleroticlesionformationinc57bl6mice