Age-related inflammation and insulin resistance: a review of their intricate interdependency

Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation, adipose tissue function, mitochondrial function, and causes endoplasmic reticulum (ER)...

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Published inArchives of pharmacal research Vol. 37; no. 12; pp. 1507 - 1514
Main Authors Park, Min Hi, Kim, Dae Hyun, Lee, Eun Kyeong, Kim, Nam Deuk, Im, Dong Soon, Lee, Jaewon, Yu, Byung Pal, Chung, Hae Young
Format Journal Article
LanguageEnglish
Published Heidelberg Pharmaceutical Society of Korea 01.12.2014
대한약학회
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ISSN0253-6269
1976-3786
1976-3786
DOI10.1007/s12272-014-0474-6

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Abstract Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation, adipose tissue function, mitochondrial function, and causes endoplasmic reticulum (ER) stress, which lead to insulin resistance. However, some studies show that insulin resistance itself amplifies chronic inflammation. The activity of the insulin-dependent Akt signaling pathway is highlighted because of its decrease in insulin-sensitive organs, like liver and muscle, which may underlie insulin resistance and hyperinsulinemia, and its increased levels in non-metabolic organs, such as kidney and aorta. In that the prevalence of obesity has increased substantially for all age groups in recent years, our review summarizes the data showing the involvement of chronic inflammation in obesity-induced insulin resistance, which perpetuates reciprocal interactions between the chronic inflammatory process and increased adiposity, thereby accelerating the aging process.
AbstractList Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation, adipose tissue function, mitochondrial function, and causes endoplasmic reticulum (ER) stress, which lead to insulin resistance. However, some studies show that insulin resistance itself amplifies chronic inflammation. The activity of the insulin-dependent Akt signaling pathway is highlighted because of its decrease in insulin-sensitive organs, like liver and muscle, which may underlie insulin resistance and hyperinsulinemia, and its increased levels in non-metabolic organs, such as kidney and aorta. In that the prevalence of obesity has increased substantially for all age groups in recent years, our review summarizes the data showing the involvement of chronic inflammation in obesity-induced insulin resistance, which perpetuates reciprocal interactions between the chronic inflammatory process and increased adiposity, thereby accelerating the aging process.
Chronic inflammation is a major risk factorunderlying aging and the associated diseases of aging; ofparticular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation,adipose tissue function, mitochondrial function, and causesendoplasmic reticulum (ER) stress, which lead to insulinresistance. However, some studies show that insulinresistance itself amplifies chronic inflammation. Theactivity of the insulin-dependent Akt signaling pathway ishighlighted because of its decrease in insulin-sensitiveorgans, like liver and muscle, which may underlie insulinresistance and hyperinsulinemia, and its increased levels innon-metabolic organs, such as kidney and aorta. In that theprevalence of obesity has increased substantially for all agegroups in recent years, our review summarizes the datashowing the involvement of chronic inflammation inobesity-induced insulin resistance, which perpetuatesreciprocal interactions between the chronic inflammatoryprocess and increased adiposity, thereby accelerating theaging process. KCI Citation Count: 75
Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation, adipose tissue function, mitochondrial function, and causes endoplasmic reticulum (ER) stress, which lead to insulin resistance. However, some studies show that insulin resistance itself amplifies chronic inflammation. The activity of the insulin-dependent Akt signaling pathway is highlighted because of its decrease in insulin-sensitive organs, like liver and muscle, which may underlie insulin resistance and hyperinsulinemia, and its increased levels in non-metabolic organs, such as kidney and aorta. In that the prevalence of obesity has increased substantially for all age groups in recent years, our review summarizes the data showing the involvement of chronic inflammation in obesity-induced insulin resistance, which perpetuates reciprocal interactions between the chronic inflammatory process and increased adiposity, thereby accelerating the aging process.Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging. Chronic inflammation impairs normal lipid accumulation, adipose tissue function, mitochondrial function, and causes endoplasmic reticulum (ER) stress, which lead to insulin resistance. However, some studies show that insulin resistance itself amplifies chronic inflammation. The activity of the insulin-dependent Akt signaling pathway is highlighted because of its decrease in insulin-sensitive organs, like liver and muscle, which may underlie insulin resistance and hyperinsulinemia, and its increased levels in non-metabolic organs, such as kidney and aorta. In that the prevalence of obesity has increased substantially for all age groups in recent years, our review summarizes the data showing the involvement of chronic inflammation in obesity-induced insulin resistance, which perpetuates reciprocal interactions between the chronic inflammatory process and increased adiposity, thereby accelerating the aging process.
Author Lee, Eun Kyeong
Yu, Byung Pal
Im, Dong Soon
Kim, Nam Deuk
Park, Min Hi
Chung, Hae Young
Kim, Dae Hyun
Lee, Jaewon
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Issue 12
Keywords Aging
Molecular inflammation
Insulin resistance
Language English
License Open AccessThis article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
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PublicationCentury 2000
PublicationDate 2014-12-01
PublicationDateYYYYMMDD 2014-12-01
PublicationDate_xml – month: 12
  year: 2014
  text: 2014-12-01
  day: 01
PublicationDecade 2010
PublicationPlace Heidelberg
PublicationPlace_xml – name: Heidelberg
– name: Korea (South)
PublicationTitle Archives of pharmacal research
PublicationTitleAbbrev Arch. Pharm. Res
PublicationTitleAlternate Arch Pharm Res
PublicationYear 2014
Publisher Pharmaceutical Society of Korea
대한약학회
Publisher_xml – name: Pharmaceutical Society of Korea
– name: 대한약학회
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Snippet Chronic inflammation is a major risk factor underlying aging and the associated diseases of aging; of particular interest is insulin resistance during aging....
Chronic inflammation is a major risk factorunderlying aging and the associated diseases of aging; ofparticular interest is insulin resistance during aging....
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SubjectTerms adipose tissue
adiposity
Aging - immunology
aorta
Cytokines - biosynthesis
Cytokines - immunology
endoplasmic reticulum
Endoplasmic Reticulum Stress - immunology
Humans
hyperinsulinemia
Inflammation
insulin resistance
Insulin Resistance - immunology
kidneys
Lipid Metabolism - immunology
liver
Medicine
muscles
obesity
Obesity - immunology
Pharmacology/Toxicology
Pharmacy
Proto-Oncogene Proteins c-akt - biosynthesis
Proto-Oncogene Proteins c-akt - immunology
Review
risk factors
Signal Transduction
약학
Title Age-related inflammation and insulin resistance: a review of their intricate interdependency
URI https://link.springer.com/article/10.1007/s12272-014-0474-6
https://www.ncbi.nlm.nih.gov/pubmed/25239110
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https://www.proquest.com/docview/1733503963
https://pubmed.ncbi.nlm.nih.gov/PMC4246128
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Volume 37
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