The Endocrine Control of the Fetus 1988
DOI: 10.1007/978-3-642-72975-1_27
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Perinatal Activation of Brown Adipose Tissue

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Cited by 21 publications
(22 citation statements)
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“…A reduction in UCP1 protein as a result of elevated prolactin is in accord with previous findings in adult females (Chan & Swaminathan, 1990), but is in direct contrast to the response of fetal and neonatal rat pups following chronic maternal prolactin administration (Budge et al 2002). The most likely explanation for these divergent responses to raised prolactin relate to the parallel postnatal development of the hypothalamic-pituitary axis that is necessary for brown adipose tissue maturation (Cannon et al 1988). The fetal rat pup has an immature hypothalamic-pituitary axis with plasma prolactin and UCP1 abundance remaining low, thereby making the fetus more responsive to exogenous prolactin exposure.…”
Section: Discussionsupporting
confidence: 68%
See 1 more Smart Citation
“…A reduction in UCP1 protein as a result of elevated prolactin is in accord with previous findings in adult females (Chan & Swaminathan, 1990), but is in direct contrast to the response of fetal and neonatal rat pups following chronic maternal prolactin administration (Budge et al 2002). The most likely explanation for these divergent responses to raised prolactin relate to the parallel postnatal development of the hypothalamic-pituitary axis that is necessary for brown adipose tissue maturation (Cannon et al 1988). The fetal rat pup has an immature hypothalamic-pituitary axis with plasma prolactin and UCP1 abundance remaining low, thereby making the fetus more responsive to exogenous prolactin exposure.…”
Section: Discussionsupporting
confidence: 68%
“…The fetal rat pup has an immature hypothalamic-pituitary axis with plasma prolactin and UCP1 abundance remaining low, thereby making the fetus more responsive to exogenous prolactin exposure. A gradual increase in prolactin then occurs postnatally (Yamamuro et al 1999) coincident with the maturation of the hypothalamic-pituitary axis and the recruitment of non-shivering thermogenesis in brown adipose tissue (Cannon et al 1988). Further prolactin exposure either at the time of, or following, maximal recruitment of UCP1 does not therefore appear to promote UCP1 abundance.…”
Section: Discussionmentioning
confidence: 99%
“…However, can these maladaptations be programmed in utero ? In relation to the relative importance of the prenatal and the postnatal diet in excess fat deposition, a majority of small and large mammals are born with minimal fat reserves in which the major component is brown adipose tissue rather than white adipose tissue (Cannon et al 1988;Bispham et al 2005). Critically, brown adipose tissue is located in very different regions in small and large mammals; it is found in the intrascapular region in rodents but around the central organs such as the kidney in young sheep and infants.…”
Section: Nutritional Programming Of the Kidney And Its Relationship Wmentioning
confidence: 99%
“…In ruminants, BAT is rapidly being used following birth and quickly disappears, typically being absent in the adult. Rodents however typically huddle together in a nest after birth and UCP1 does not reach maximal levels until approximately two weeks after birth and are able to maintain functional BAT throughout their lifetime (Cannon et al 1988). Because of this unique characteristic, rodents are an excellent model for studying nutritional regulation of BAT and its effects.…”
Section: Nutritional Regulation Of Bat and Thermogenic Capacitymentioning
confidence: 99%