دورية أكاديمية

Chorionic somatomammotropin RNA interference alters fetal liver glucose utilization.

التفاصيل البيبلوغرافية
العنوان: Chorionic somatomammotropin RNA interference alters fetal liver glucose utilization.
المؤلفون: Ali, Asghar, Swanepoel, Callie M., Winger, Quinton A., Rozance, Paul J., Anthony, Russell V.
المصدر: Journal of Endocrinology; Dec2020, Vol. 247 Issue 3, p169-180, 12p
مصطلحات موضوعية: SOMATOMEDIN C, LIVER, INSULIN receptors, GLUCOSE, LACTATE dehydrogenase
مستخلص: Chorionic somatomammotropin (CSH) is a placenta-specific hormone associated with fetal growth, and fetal and maternal metabolism in both humans and sheep. We hypothesized that CSH deficiency could impact sheep fetal liv er glucose utilization. To generate CSH-deficient pregnancies, day 9 hatched blastocysts were infected with lentiviral particles expressing CSH-specific shRNA (RNAi) or scr amble control shRNA (SC) and transferred to synchronized recipients. CSH RNAi generated two distinct phenotypes at 135 days of gestational age (dGA); pregnancies with IUGR (RN Ai-IUGR) or with normal fetal weight (RNAi-NW). Fetal body, fetal liver and placental w eights were reduced (P < 0.05) only in RNAi-IUGR pregnancies compared to SC. Umbilica l artery plasma insulin and insulin-like growth factor 1 (IGF1) concentrations were decreased, whereas insulin receptor beta (INSR) concentration in fetal liver was increased (P < 0.05) in both RNAi phenotypes. The mRNA concentrations of IGF1, IGF2, IGF binding protein 2 (IGFBP2) and IGFBP3 were decreased (P < 0.05) in fetal livers from both RNAi phenotypes. Fetal liver glycogen concentration and glycogen synthase 1 (GYS1) concentration were increased (P < 0.05), whereas fetal liver phosphorylated-GYS (inactive GYS) concentration was reduced (P < 0.05) in both RNAi phenotypes. Lactate dehydrogenase B (LDHB) concentration was increased (P < 0.05) and IGF2 concentration was decreased (P < 0.05) in RNAi-IUGR fetal livers only. Our findings suggest that fetal liver glucose utilization is impacted by CSH RNAi, independent of IUGR, and is likely tied t o enhanced fetal liver insulin sensitivity in both RNAi phenotypes. Determining the ph ysiological ramifications of both phenotypes, may help to differentiate direct effect of CS H deficiency or its indirect effect through IUGR. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:00220795
DOI:10.1530/JOE-20-0375