Endocrine and nutritional regulation of fetal adipose tissue development

Abstract

In the fetus, adipose tissue comprises both brown and white adipocytes for which brown fat is characterised as possessing the unique uncoupling protein (UCP)1. The dual characteristics of fetal fat reflect its critical role at birth in providing lipid that is mobilised rapidly following activation of UCP1 upon cold exposure to the extrauterine environment. A key stage in the maturation of fetal fat is the gradual rise in the abundance of UCP1. For species with a mature hypothalamic-pituitary axis at birth there is a gradual increase in the amount and activity of UCP1 during late gestation, in conjunction with an increase in the plasma concentrations of catecholamines, thyroid hormones, cortisol, leptin and prolactin. These may act individually, or in combination, to promote UCP1 expression and, following the post-partum surge in each hormone, UCP1 abundance attains maximal amounts.Adipose tissue grows in the fetus at a much lower rate than in the postnatal period. However, its growth is under marked nutritional constraints and, in contrast to many other fetal organs that are unaffected by nutritional manipulation, fat mass can be significantly altered by changes in maternal and, therefore, fetal nutrition. Fat deposition in the fetus is enhanced during late gestation following a previous period of nutrient restriction up to mid gestation. This is accompanied by increased mRNA abundance for the receptors of IGF-I and IGF-II. In contrast, increasing maternal nutrition in late gestation results in less adipose tissue deposition but enhanced UCP1 abundance. The pronounced nutritional sensitivity of fetal adipose tissue to both increased and decreased maternal nutrition may explain why the consequences of an adverse nutritional environment persist into later life.

Maternal Dietary Patterns during Pregnancy Are Associated with Child Growth in the First 3 Years of Life

“…3 Represents a high probability of consuming apples, bananas, oranges, tomatoes, broccoli, spinach, carrots, green salads, whole-wheat bread, low-fat dairy, baked chicken, and water. 4 Represents a high probability of consuming white bread, red and processed meats, fried chicken, french fries, and vitamin C-rich drinks. 5 Adjusted for maternal age categories, maternal race, education at enrollment, income level, marital status, parity, smoking status, and prepregnancy BMI.…”

“…Moreover, childhood obesity has psychosocial correlates, including negative self-confidence and self-esteem, poor socialization, and depression during childhood and adolescence (2,3). Growing evidence suggests that development of adipocytes-the cells that regulate fat mass-begins before birth (4), and concentrations of inflammatory biomarkers are higher for children who are overweight starting as young as age 3 y (5). Therefore, identifying risk factors during fetal development that influence childhood growth and obesity could have substantial public health and clinical implications.…”

Influence of prematurity and growth restriction on the adipokine profile, IGF1, and ghrelin levels in cord blood: relationship with glucose metabolism

“…No anthropometric standards were available for infants below 26 weeks gestational age (nZ13), and exclusively raw data were used in these cases. Rohrer's ponderal index was calculated as weight (g)!100/(length (cm)) 3 . Those newborns from single pregnancies whose birth weight and/or length were below K2 SDS for gestational age and sex were classified as SGA for later comparison with AGA newborns (nZ141).…”

Association between serum lipoprotein lipase mass concentration and subcutaneous fat accumulation during neonatal period

“…In normal weight infants, subcutaneous adipose tissue grows rapidly during the first months of life in parallel with the change in fat cell size; however, the number of fat cells remains stable (Häger et al, 1977;Knittle et al, 1979;Soriguer Escofet et al, 1996). This process is regulated by several endocrine and nutritional factors (Symonds et al, 2003), including insulin-like growth factor-I (IGF-I) (Skalkidou et al, 2003).…”