TY - JOUR
T1 - PPAR-γ, TNF-α messenger RNA levels and lipase activity in the pregnant and lactating rat
AU - Kawaguchi, Kaoru
AU - Sugiyama, Takashi
AU - Hibasami, Hiroshige
AU - Toyoda, Nagayasu
N1 - Funding Information:
We thank Professor Yoshida T. of the Department of Pathology, Mie University School of Medicine, for technical assistance. This research was supported, in part, by a Grant-in-Aid from the Ministry of Education of Japan.
PY - 2003/2/21
Y1 - 2003/2/21
N2 - Dramatic alternations in maternal metabolism occur during gestation and lactation, especially glucose and fat metabolism. For example, in rats, the amount of body fat mass increases during gestation, then decreases just prior to delivery, and remains low after parturition. To investigate the factors involved in such changes in maternal fat mass, messenger ribonucleic acid (mRNA) levels of adipocytokines, peroxisome proliferator-activated receptor-γ (PPAR-γ) and tumor necrosis factor-α (TNF-α), were examined in the intraabdominal adipose tissue of non-pregnant rats, pregnant rats and postpartum rats. We also examined the issue of whether apoptosis, which could be promoted by PPAR-γ and TNF-α, is involved in any of the changes in maternal fat mass The activity of lipoprotein lipase (LPL) and hormone sensitive lipase (HSL) in adipose tissue was also measured. PPAR-γ and TNF-α mRNA levels remained constant during the gestational and postpartum periods. Apoptosis was not detected at any time as evidenced by DNA laddering and in situ staining. LPL activity was significantly increased at day 5 and remained elevated until day 14 of gestation. HSL activity was significantly increased at day 10 of gestation and then decreased after delivery, at day 10 of lactation. In conclusion, during the gestational and postpartum period of rats, changes in maternal fat mass did not directly correlate with the levels of expression of PPAR-γ and TNF-α mRNA. Apoptosis also does not appear to influence on fat mass change. The changes in LPL and HSL activities during gestation suggest that these enzymes might be regulators of maternal adipose tissue level.
AB - Dramatic alternations in maternal metabolism occur during gestation and lactation, especially glucose and fat metabolism. For example, in rats, the amount of body fat mass increases during gestation, then decreases just prior to delivery, and remains low after parturition. To investigate the factors involved in such changes in maternal fat mass, messenger ribonucleic acid (mRNA) levels of adipocytokines, peroxisome proliferator-activated receptor-γ (PPAR-γ) and tumor necrosis factor-α (TNF-α), were examined in the intraabdominal adipose tissue of non-pregnant rats, pregnant rats and postpartum rats. We also examined the issue of whether apoptosis, which could be promoted by PPAR-γ and TNF-α, is involved in any of the changes in maternal fat mass The activity of lipoprotein lipase (LPL) and hormone sensitive lipase (HSL) in adipose tissue was also measured. PPAR-γ and TNF-α mRNA levels remained constant during the gestational and postpartum periods. Apoptosis was not detected at any time as evidenced by DNA laddering and in situ staining. LPL activity was significantly increased at day 5 and remained elevated until day 14 of gestation. HSL activity was significantly increased at day 10 of gestation and then decreased after delivery, at day 10 of lactation. In conclusion, during the gestational and postpartum period of rats, changes in maternal fat mass did not directly correlate with the levels of expression of PPAR-γ and TNF-α mRNA. Apoptosis also does not appear to influence on fat mass change. The changes in LPL and HSL activities during gestation suggest that these enzymes might be regulators of maternal adipose tissue level.
KW - Adipose tissue
KW - Hormone sensitive lipase (HSL)
KW - Lipoprotein lipase (LPL)
KW - Peroxisome proliferator-activated receptor-γ (PPAR-γ)
KW - Pregnancy
KW - Tumor necrosis factor-α (TNF-α)
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U2 - 10.1016/S0024-3205(02)02445-1
DO - 10.1016/S0024-3205(02)02445-1
M3 - Article
C2 - 12551754
AN - SCOPUS:0037458428
VL - 72
SP - 1655
EP - 1663
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 14
ER -