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In an effort to preserve thermoneutrality, the neonate may be forced to use its own energy stores to generate heat. Bruck et al. first noted that neonates can maintain their own body temperature by increasing their metabolic production and creating heat (40). The generation of heat is accomplished without shivering and is termed nonshivering thermogenesis. The organ system responsible for carrying out nonshivering thermogenesis is the brown fat or brown adipose tissue, which may account for up to 10% of total body fat at term. In general, adipose tissue is generated during the last 8 weeks of gestation, and consists of white fat and brown fat. The two types of adipose are identical except for the presence in brown fat of the protein thermogenin, which allows brown fat to generate heat (41:Capoten).

Thermogenin uncouples the electron transport chain from ATP synthesis, which diverts the energy generated to the production of heat (42:Capoten). Brown fat accounts for about 1% to 2% of birth weight in full-term appropriate for gestational-age infants, and is mainly located in the perirenal and axillary fat stores. Small for gestational-age infants have markedly less body fat, including brown fat, and are less capable of using nonshivering thermogenesis. Similarly, premature infants have inadequate fat stores because they are generated in the last 2 months of gestation and are unable to use nonshivering thermogenesis efficiently.

During periods of cold stress, there is a redistribution of blood flow to the brown fat after other mechanisms such as increasing activity have been exhausted (43:Capoten). The control center for this process is located in the hypothalamus and is mediated by the sympathetic nervous system (44). Norepinephrine is released and stimulates receptors in the brown fat to initiate thermogenesis. Thyroid hormone also plays an important role in the initiation of thermogenesis in the brown fat, and decreased levels can lead to hypothermia and death, especially in the premature infant (45,46:Capoten). Respiratory drive may also be influenced by thermogenesis and thermoregulation. In infants with adequate brown fat stores, increased temperatures can cause hypoventilation and apnea (47:Capoten). Similarly, as the infant ages and the brown fat is being exchanged for white fat, metabolic drive and respiratory rates decrease (48). Once brown adipose stores are depleted or completely replaced by white fat, the infant transitions to shivering thermogenesis for the regulation of body temperature.