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[Fetal weight at weight as predisposing risk factor for type 2 diabetes in adulthood]
M Hernández Valencia1, A Zárate
1Unidad de Investigación en Enfermedades Endocrinas, Centro Médico Nacional, Siglo XXI, Instituto Mexicano del Seguro Social, México D.F.
Insights
Fetal development in adverse conditions, such as maternal diabetes or undernutrition, can lead to low birth weight and predispose individuals to metabolic disorders like type 2 diabetes later in life.
Area of Science:
- Endocrinology
- Developmental Biology
- Metabolic Syndrome
Context:
- Adverse intrauterine environments, including maternal diabetes and undernutrition, impact fetal development.
- Epidemiological studies link low birth weight to impaired glucose metabolism in adulthood.
- High birth weight in relation to gestational age is also associated with metabolic impairments.
Purpose:
- To explore the long-term implications of intrauterine environmental exposures on metabolic health.
- To investigate the role of fetal programming in the development of adult-onset metabolic diseases.
- To understand the mechanisms linking intrauterine conditions to pancreatic islet function and insulin metabolism.
Summary:
- Fetal exposure to unfavorable intrauterine environments can lead to permanent changes in pancreatic islet structure and function, termed "programmed changes".
- Low birth weight is associated with a 13-25% prevalence of type 2 diabetes, while overnutrition conditions show an 8-18% prevalence.
- Maternal hyperglycemia can cause fetal beta-cell hyperplasia, increasing fetal weight and potentially altering genetic factors.
Impact:
- Findings highlight critical developmental periods where intrauterine factors permanently alter metabolic trajectories.
- Suggests a need for further molecular research into pancreatic islets to elucidate lifelong insulin metabolism changes.
- Informs potential interventions aimed at mitigating metabolic disease risk originating from early life exposures.
Abstract:
When the fetus growth in an unfavorable intrauterine environment, this process has implications in the adult life, that predisposes to suffer metabolic abnormalities as obesity, hypertension and non-insulin dependent diabetes mellitus. The unfavorable intrauterine environment includes the pregnancy with diabetes mellitus, pregnancy with gestational diabetes, and pregnancy with maternal undernutrition. Multiple epidemiological studies developed in North America and Europe appear to broadly confirm the association of the low birth weight in babies borne at term, with the glucose metabolism impairments in the adult life. An implication of metabolic impairments on high birth weight for the gestational age has been founded. This alteration could start when there are changes in nutritional habits in migrate populations, having number and function of the pancreatic islets altered, maybe because during fetal life they were faced to blood fluid decreased, and nutrients also decrease as well as the differentiation of cells was modified, as an important intent for fetal survival. The prevalence of type 2 diabetes has been reported in 13 to 25% for low birth weight. On the other hand, maternal hyperglycemia leads to beta-cell hyperplasia in the fetus, by a constant stimulus over the insulin production which stimulates the use of glucose as nutrients, leading to the increase in fetal weight and determining genetic changes. In overnutrition conditions, the prevalence of type 2 diabetes has been reported of 8 to 18%. Growth of tissues has critical periods at different times and intrauterine environment can be one mechanism for may permanently changes in pancreas structure and hormonal secretion patterns. Thus, the hypothesis that autoprotective fetal changes during the intrauterine life occur, took place, specially during the critical period of development, leaves to permanent changes called "programmed changes", including an endocrine disturbance of pancreatic functions, appearing in adult life. Further molecular studies of pancreatic islets are necessary in order to determine the mechanisms for lifelong changes and insulin metabolism due to intrauterine growth.
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