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Impact of housing temperature on the adaptation of brown adipose tissue to pregnancy in lean and obese rats
Author(s) -
Budge Helen,
Dellschaft Neele,
Albustanji Layla,
AlHarethi Enas,
Perez G,
Peter Aldiss,
Symonds Michael
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.774.3
Subject(s) - brown adipose tissue , gestation , pregnancy , medicine , endocrinology , white adipose tissue , adipose tissue , biology , thermogenesis , leptin , thermogenin , obesity , genetics
Pregnancy has long been considered a physiological condition in which brown adipose tissue function is reduced. This was considered to represent a mechanism to enable energy conservation by the mother, although whether it is influenced by ambient temperature is unknown. It is now recognised that rodent studies examining brown fat function are conducted at a housing temperature well below thermoneutrality and as such are not immediately relevant to the human situation in which a majority of time is spent at thermoneutrality. The aim of our study was to examine the impact of an obesogenic diet on the mother prior to and during pregnancy and whether the housing temperature modulated the adaptations seen within interscapular brown fat through pregnancy. Methods Female rats were raised on a low fat (L) diet or a high fat, high sucrose diet (H) and housed at either a cool (20°C) or thermoneutral temperature (27°C) from 4 weeks of age, and 6 females of each group were tissue sampled at 10 weeks of age. The remaining females were mated and sampled at either 10d (mid‐gestation, n=6) or 19d gestation (late‐gestation, n=6). Gene expression and histological appearance of brown, interscapular adipose tissues was determined for brown (i.e. uncoupling protein (UCP)1) and white (i.e. leptin) characteristics as well as cell size. Results Gene expression for UCP1 was higher in unmated dams and at 19 but not 10 days of gestation in those animals maintained at 20°C, irrespective of diet. In these animals there was a marked decline in UCP1 at 10 days of gestation not seen in those kept at thermoneutrality. This was accompanied with a loss of UCP1 protein in obese, but not control dams. Gene expression for leptin was increased at thermoneutrality and rose through gestation in controls, but only increased in obese animals near to term. As expected the H diet raised white fat mass, but these animals had a similar body weight to controls, irrespective of rearing temperature. Brown fat mass was also higher with the H diet but only when maintained at 20°C, whereas mean cell size was increased at thermoneutrality. Conclusions The thermal environment has a major influence on the magnitude of loss of UCP1 through pregnancy. This adaptation does not occur when dams are maintained at thermoneutrality. Taken together these findings indicate that the impact of maternal obesity on the mother has been greatly under‐estimated in all studies to date which have been conducted at a standard (i.e. cool) thermal environment. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .