Adipose tissue and fetal programming

• Published in: Diabetologia Vol. 55; no. 6; pp. 1597 - 1606
• Main Authors: Symonds, M. E., Pope, M., Sharkey, D., Budge, H.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01-06-2012; Springer; Springer Nature B.V
• Subjects: Adipocytes; Adipose Tissue, Brown - embryology; Adipose Tissue, Brown - metabolism; Adipose Tissue, White - embryology; Adipose Tissue, White - metabolism; Animals; Biological and medical sciences; Body fat; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Fetal Development - genetics; Fetal Development - physiology; Fetuses; Glucose; Heat; Homeostasis; Human Physiology; Humans; Insulin Resistance; Internal Medicine; Medical sciences; Medicine; Medicine & Public Health; Metabolic Diseases; Models, Biological; Musculoskeletal system; Nutrition research; Pregnancy; Proteins; Review; Pregnancy; White adipose tissue; Nutrition; Development; Brown adipose tissue; Fetus; Glucose; Review; Insulin; Fetal programming; Endocrinopathy; Pancreatic hormone; Adipose tissue; Diabetes mellitus; Programming
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/s00125-012-2505-5

Adipose tissue function changes with development. In the newborn, brown adipose tissue (BAT) is essential for ensuring effective adaptation to the extrauterine environment, and its growth during gestation is largely dependent on glucose supply from the mother to the fetus. The amount, location and type of adipose tissue deposited can also determine fetal glucose homeostasis. Adipose tissue first appears at around mid-gestation. Total adipose mass then increases through late gestation, when it comprises a mixture of white and brown adipocytes. BAT possesses a unique uncoupling protein, UCP1, which is responsible for the rapid generation of large amounts of heat at birth. Then, during postnatal life some, but not all, depots are replaced by white fat. This process can be utilised to investigate the physiological conversion of brown to white fat, and how it is re-programmed by nutritional changes in pre- and postnatal environments. A reduction in early BAT deposition may perpetuate through the life cycle, thereby suppressing energy expenditure and ultimately promoting obesity. Normal fat development profiles in the offspring are modified by changes in maternal diet at defined stages of pregnancy, ultimately leading to adverse long-term outcomes. For example, excess macrophage accumulation and the onset of insulin resistance occur in an adipose tissue depot-specific manner in offspring born to mothers fed a suboptimal diet from early to mid-gestation. In conclusion, the growth of the different fetal adipose tissue depots varies according to maternal diet and, if challenged in later life, this can contribute to insulin resistance and impaired glucose homeostasis.