A developmental perspective on the origins of obesity and metabolic syndrome

ABSTRACT

Metabolic syndrome comprises central obesity, dyslipidemia, hypertension, glucose intolerance, and insulin resistance. Children sometimes develop metabolic syndrome, and it is strongly associated with the same syndrome in adulthood. Recently, there is evidence that obesity and metabolic syndrome originate from fetal life. Possible explanations of fetal and developmental origin of metabolic syndrome are the thrifty genotype and thrifty phenotype hypothesis, which together confer insulin resistance on developing fetus. Poor nutrition in utero as well as extrauterine growth restriction of preterm infants are important triggers of this hypothesis. Like metabolic syndrome in adulthood, the high levels of inflammatory cytokines and adipokines are certainly characteristic in pediatric patients. Increased fat mass was also observed in these patients, although their birth weight was lower than average. The mitochondrial genome is responsible for the inheritance of obesity from the maternal line. This can be a key as to why the phenotypes of obesity and metabolic syndrome start in fetal life with an association with poor maternal nutrition. In such circumstances, catch-up growth with an over-nutrition strategy can aggravate those features, suggesting that rapid catch-up growth in early infancy should not be encouraged.