Early-life programming of adipose tissue

Abstract

Worldwide obesity is increasing at an alarming rate in children and adolescents, with the consequent emergence of co-morbidities. Moreover, the maternal environment during pregnancy plays an important role in obesity, contributing to transgenerational transmission of the same and metabolic dysfunction. White adipose tissue represents a prime target of metabolic programming induced by maternal milieu. In this article, we review adipose tissue physiology and development, as well as maternal influences during the perinatal period that may lead to obesity in early postnatal life and adulthood. First, we describe the adipose tissue cell composition, distribution and hormonal action, together with the evidence of hormonal factors participating in fetal/postnatal programming. Subsequently, we describe the critical periods of adipose tissue development and the relationship of gestational and early postnatal life with healthy fetal adipose tissue expansion. Furthermore, we discuss the evidence showing that adipose tissue is an important target for nutritional, hormonal and epigenetic signals to modulate fetal growth. Finally, we describe nutritional, hormonal, epigenetic and microbiome changes observed in maternal obesity, and whether their disruption alters fetal growth and adiposity. The presented evidence supports the developmental origins of health and disease concept, which proposes that the homeostatic system is affected during gestational and postnatal development, impeding the ability to regulate body weight after birth, thereby resulting in adult obesity. Consequently, we anticipate that promoting a healthy early-life programming of adipose tissue and increasing the knowledge of the mechanisms by which maternal factors affect the health of future generations may offer novel strategies for explaining and addressing worldwide health problems such as obesity.

Nutrition and Metabolic Adaptations in Physiological and Complicated Pregnancy: Focus on Obesity and Gestational Diabetes

“…Obesity in pregnancy is characterised by dyslipidemia, hyperleptinemia, hyperinsulinemia and a proinflammatory state, that may enhance adipogenesis and lipogenesis, resulting in higher white adipose tissue mass and adipocyte hypertrophy in offspring (157). Higher leptin levels were found in macrosomic newborns and are related to insulin levels and adiposity (158); this may explain how fetuses of obese mothers develop insulin-resistance in the womb and are born with higher adiposity (159).…”

To measure growth—pediatrician’s dilemma

“…After this initial period, there is a constant level of fat intake during the first 2 years, and ultimately increasing intake and oxidation of protein and carbohydrate [7]. Adipose tissue is an important target for nutritional, hormonal, and epigenetic signals to modulate fetal growth [8,9].…”

“…It is mandatory to know adipose tissue cells composition, distribution and action, together with adipose tissue development and relationship with fat free mass and bone mineral content. Specific and precise body composition assessment could explain the body weight regulation and the dis-regulation of the homeostatic system [4,8,10]. Unfortunately, all the measurements of body composition are indirect and we have limitations related to the intraindividual variability as a consequence of changes in fat free mass occurring with growth, maturation, and disease statues [9].…”

Plasma Adipokines Profile in Prepubertal Children with a History of Prematurity or Extrauterine Growth Restriction

“…It is known that abnormal adipokine profile may be observed in obese children [15]. Moreover, it was suggested that impaired growth during critical periods, such as in the third trimester of pregnancy can lead the programming of adipose tissue, conferring a high subsequent cardiometabolic risk later in life [16]. In fact, an abnormal production of some adipokines was described in children with intrauterine growth restriction (IUGR) [17] who, in turn, may present an elevated risk of inflammatory chronic diseases [4,18].…”

“…In fact, an abnormal production of some adipokines was described in children with intrauterine growth restriction (IUGR) [17] who, in turn, may present an elevated risk of inflammatory chronic diseases [4,18]. Similarly, an early postnatal environment with EUGR might be associated with a higher vulnerability to an adipose tissue disturbance [16]. However, there is scarce literature about the role of the antecedents of EUGR in the later adipokines status, although it could be similar to obesity or IUGR condition.…”