Abstract
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.
Highlights
Metabolic syndrome refers to the co-occurrence of cardiovascular risk factors, including obesityassociated metabolic disorders, such as insulin resistance, atherogenic dyslipidemia, and hypertension, and is a global public health issue despite being initially reported in Western countries [1]
According to the Developmental Origins of Health and Disease (DOHaD) theory, one of the well-accepted proposals for the risk of developing metabolic syndrome is the hypothesis of the energysaving ‘Thrifty Phenotype’ in undernourished fetuses, which is evolutionarily advantageous for survival of the fittest in a starved environment after birth, a strong selection pressure, but increases the risk of metabolic syndrome under an obesogenic diet according to the ‘Mismatch’ hypothesis [7]
The DOHaD theory is partly derived from retrospective epidemiological observations of susceptibilities to metabolic disorders in offspring that experienced maternal starvation during gestation, such as in the Dutch Famine in World War II [13, 51] and the Great Chinese Famine [52, 53]
Summary
Metabolic syndrome refers to the co-occurrence of cardiovascular risk factors, including obesityassociated metabolic disorders, such as insulin resistance, atherogenic dyslipidemia, and hypertension, and is a global public health issue despite being initially reported in Western countries [1]. According to the DOHaD theory, one of the well-accepted proposals for the risk of developing metabolic syndrome is the hypothesis of the energysaving ‘Thrifty Phenotype’ in undernourished fetuses, which is evolutionarily advantageous for survival of the fittest in a starved environment after birth, a strong selection pressure, but increases the risk of metabolic syndrome under an obesogenic diet according to the ‘Mismatch’ hypothesis [7].
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