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Low birth weight and endocrine dysfunction in postnatal life
1Institute of Maternal and Child Research, Faculty of Medicine, University of Chile, Santiago. vmericq@med.uchile.cl
Insights
Small size at birth and reduced early growth are linked to endocrine issues like insulin resistance and abnormal puberty. These developmental origins may explain long-term health problems, including type 2 diabetes and cardiovascular disease.
Area of Science:
- Endocrinology
- Developmental Biology
- Public Health
Background:
- Small size at birth increases neonatal morbidity and mortality.
- Reduced early-life growth is linked to endocrine dysfunctions, including insulin insensitivity, gonadal and somatotropic axis abnormalities, and premature adrenarche.
- These alterations are associated with increased prevalence of type 2 diabetes (T2DM) and cardiovascular disease (CHD).
Purpose of the Study:
- To review the factors involved in fetal and infant programming.
- To understand the development of endocrine dysfunction in postnatal life.
Main Methods:
- Literature review of studies on early life growth and endocrine outcomes.
- Analysis of the
- Fetal Origins
- and
- Developmental Origins
- hypotheses.
Main Results:
- Early life growth patterns influence long-term endocrine health.
- The
- thrifty phenotype
- hypothesis suggests adaptive responses to in utero malnutrition.
- Developmental Origins
- incorporates postnatal growth contributions.
Conclusions:
- Factors influencing fetal and infant development play a critical role in programming postnatal endocrine function.
- Understanding these programming factors is essential for preventing long-term health issues.
- Early life interventions may mitigate risks associated with endocrine dysfunction.
Abstract:
Small size at birth has long been recognized as a factor increasing neonatal morbidity and mortality. During the last decade, reduced growth in early life has also been strongly linked with a number of endocrine dysfunctions. Included among the most important alterations are insulin insensitivity, gonadal and somatotropic axis abnormalities and premature adrenarche. These have been associated with an escalating prevalence of T2DM and CHD abnormal gonads and genitalia, growth hormone resistance and decreased growth as well as early puberty. The usual hypothesis proposed to explain the development of these long term alterations relates to the thrifty phenotype as an adaptive response to in utero malnutrition and modifications thereof; called "Fetal Origins" and updated to "Developmental Origins" which include the additional contributions of the patterns of growth in infancy and childhood. In this paper the factors that participate in the programming of the fetus and infants that lead to endocrine dysfunction in postnatal life is reviewed.
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