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Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology

Metabolic syndrome refers to obesity-associated metabolic disorders that increase the risk of type 2 diabetes, coronary diseases, stroke, and other disabilities. Environmental imbalance during the early developmental period affects health and increases susceptibility to non-communicable diseases, in...

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Autores principales: Itoh, Hiroaki, Ueda, Megumi, Suzuki, Misako, Kohmura-Kobayashi, Yukiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8850935/
https://www.ncbi.nlm.nih.gov/pubmed/35185805
http://dx.doi.org/10.3389/fendo.2022.839436
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author Itoh, Hiroaki
Ueda, Megumi
Suzuki, Misako
Kohmura-Kobayashi, Yukiko
author_facet Itoh, Hiroaki
Ueda, Megumi
Suzuki, Misako
Kohmura-Kobayashi, Yukiko
author_sort Itoh, Hiroaki
collection PubMed
description Metabolic syndrome refers to obesity-associated metabolic disorders that increase the risk of type 2 diabetes, coronary diseases, stroke, and other disabilities. Environmental imbalance during the early developmental period affects health and increases susceptibility to non-communicable diseases, including metabolic syndrome, in later life; therefore, the Developmental Origins of Health and Disease (DOHaD) theory was established. According to the DOHaD theory, the hypothesis of the energy-saving ‘Thrifty Phenotype’ in undernourished fetuses is one of the well-accepted schemes as a risk of developing metabolic syndrome. This phenotype is evolutionarily advantageous for survival of the fittest in a hangry environment after birth, a strong selection pressure, but increases the risk of developing metabolic syndrome under an obesogenic diet according to the ‘Mismatch’ hypothesis. Increasing evidences support that chronic inflammation pathophysiologically connects obesity to metabolic disorders in metabolic syndrome, leading to the concept of ‘Metaflammation’. ‘Metaflammation’ in humans is proposed to originate from the evolutionary conservation of crosstalk between immune and metabolic pathways; however, few studies have investigated the contribution of evolutionary maladaptation to the pathophysiology of ‘Metaflammation’. Therefore, it is promising to investigate ‘Metaflammation’ from the viewpoint of selective advantages and its ‘Mismatch’ to an unexpected environment in contemporary lifestyles, in consideration of the principal concept of evolutionarily conserved nutrient sensing and immune signaling systems.
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spelling pubmed-88509352022-02-18 Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology Itoh, Hiroaki Ueda, Megumi Suzuki, Misako Kohmura-Kobayashi, Yukiko Front Endocrinol (Lausanne) Endocrinology Metabolic syndrome refers to obesity-associated metabolic disorders that increase the risk of type 2 diabetes, coronary diseases, stroke, and other disabilities. Environmental imbalance during the early developmental period affects health and increases susceptibility to non-communicable diseases, including metabolic syndrome, in later life; therefore, the Developmental Origins of Health and Disease (DOHaD) theory was established. According to the DOHaD theory, the hypothesis of the energy-saving ‘Thrifty Phenotype’ in undernourished fetuses is one of the well-accepted schemes as a risk of developing metabolic syndrome. This phenotype is evolutionarily advantageous for survival of the fittest in a hangry environment after birth, a strong selection pressure, but increases the risk of developing metabolic syndrome under an obesogenic diet according to the ‘Mismatch’ hypothesis. Increasing evidences support that chronic inflammation pathophysiologically connects obesity to metabolic disorders in metabolic syndrome, leading to the concept of ‘Metaflammation’. ‘Metaflammation’ in humans is proposed to originate from the evolutionary conservation of crosstalk between immune and metabolic pathways; however, few studies have investigated the contribution of evolutionary maladaptation to the pathophysiology of ‘Metaflammation’. Therefore, it is promising to investigate ‘Metaflammation’ from the viewpoint of selective advantages and its ‘Mismatch’ to an unexpected environment in contemporary lifestyles, in consideration of the principal concept of evolutionarily conserved nutrient sensing and immune signaling systems. Frontiers Media S.A. 2022-02-03 /pmc/articles/PMC8850935/ /pubmed/35185805 http://dx.doi.org/10.3389/fendo.2022.839436 Text en Copyright © 2022 Itoh, Ueda, Suzuki and Kohmura-Kobayashi https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Itoh, Hiroaki
Ueda, Megumi
Suzuki, Misako
Kohmura-Kobayashi, Yukiko
Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology
title Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology
title_full Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology
title_fullStr Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology
title_full_unstemmed Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology
title_short Developmental Origins of Metaflammation; A Bridge to the Future Between the DOHaD Theory and Evolutionary Biology
title_sort developmental origins of metaflammation; a bridge to the future between the dohad theory and evolutionary biology
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8850935/
https://www.ncbi.nlm.nih.gov/pubmed/35185805
http://dx.doi.org/10.3389/fendo.2022.839436
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