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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Adult-Onset Diseases in Low Birth Weight Infants: Association with Adipose Tissue Maldevelopment
1Department of Pediatrics, Showa University School of Medicine.
Insights
Low birth weight (LBW) infants face increased risks of insulin resistance due to adipose tissue maldevelopment. This study explores how a smaller number of fat cells in LBW infants may lead to impaired adipose tissue function.
Area of Science:
- Endocrinology
- Developmental Biology
- Metabolic Syndrome Research
Background:
- Low birth weight (LBW) infants exhibit a heightened risk for developing insulin resistance and associated metabolic disorders later in life.
- The developmental origins of health and disease (DOHaD) paradigm highlights the critical role of intrauterine and early postnatal environments in shaping long-term health outcomes.
- Adipose tissue maldevelopment, characterized by altered body composition and increased visceral fat, is implicated in metabolic syndrome and may contribute to adult-onset diseases in LBW individuals.
Purpose of the Study:
- To investigate the hypothesis that a reduced number of adipocytes (fat cells) in low birth weight infants contributes to impaired adipose tissue expandability and function.
- To explore the potential mechanisms underlying adipose tissue maldevelopment in low birth weight infants.
- To identify critical developmental windows, such as intrauterine life or up to term-equivalent age, for adipose tissue development in relation to birth weight.
Main Methods:
- Longitudinal evaluation of adiponectin levels in early life.
- Analysis of body composition and fat distribution in low birth weight infants.
- Review of existing literature and theoretical frameworks on adipose tissue development and metabolic programming.
Main Results:
- Low birth weight infants may not always be overweight or obese, suggesting a 'thrifty phenotype' linked to impaired growth potential and reduced lean body mass.
- A smaller adipocyte number in LBW infants could lead to overloading of individual fat cells.
- Impaired adipose tissue expandability in LBW infants may be a key factor in their increased risk of metabolic dysfunction.
Conclusions:
- Adipose tissue maldevelopment, particularly a reduced number of adipocytes and impaired expandability, is a significant factor in the metabolic risks faced by low birth weight infants.
- The intrauterine period and early postnatal development up to term-equivalent age appear crucial for adipose tissue development and may represent key targets for intervention.
- Understanding these mechanisms is vital for developing strategies to mitigate the long-term health consequences of low birth weight.
Abstract:
Low birth weight (LBW) infants have higher risk of developing insulin resistance and its comorbidities later in life. The concept of "developmental origins of health and disease" suggests that intrauterine and postnatal environments have an important role in increasing these risks. The risk of such adult-onset diseases in LBW infants might be associated with adipose tissue maldevelopment including altered body composition and increased amount of visceral fat, which is the same mechanism as that in children and adults with metabolic syndrome. However, LBW infants often have different characteristics: they are not always overweight or obese over their life course. The inconsistency might be associated with the thrifty phenotype, which is produced in response to impaired growth potential and decreased lean body mass. LBW infants tend to be obese within the limits of impaired growth potential. Through our previous investigations evaluating longitudinal changes in adiponectin levels at an early stage of life, we speculated that probably, the intrauterine life of term infants or the period up to term-equivalent age in preterm infants might be the key age for the development of adipose tissues including fat cells. Because of that, we hypothesized that the smaller number of adipocytes in LBW infants might be associated with overloading of single adipocytes and impaired adipose tissue expandability. The possible mechanisms are discussed from the perspective of adipose tissue maldevelopment in LBW infants.
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