| pubmed-article:3972153 | pubmed:abstractText | Overt diabetes and gestational diabetes (1-2.5% of all pregnancies) has been related to perinatal mortality, increased macrosomia and increased frequency of other pregnancy complications. Human placental lactogen (hPL), a hormone similar to growth hormone, is produced by the placenta and is a potent antagonist to insulin action. While hPL's presence in maternal circulation induces a sparing effect on nutrients including glucose, it exacerbates diabetes during pregnancy and may well relate to other clinical complications. To explore possible regulation of hPL in diabetic pregnancy and specifically to examine gestational diabetes, we have evaluated the levels of placental mRNA coding for hPL synthesis as well as other parameters from diabetic and normal term patients. By in vitro translation assays using nuclease-treated reticulocyte lysate, no substantial differences in translatable hPL-mRNA were observed when comparing normal term (3.5% of total synthesis), gestational diabetic (3.4%) and Type C diabetic (3.5%). However, translatable hPL-mRNA in Type R diabetes which was 2.7% of total synthesis was slightly reduced in comparison to normal term. To determine more directly hPL-mRNA levels in gestational diabetic placentas and normal term placentas, total RNA preparations were evaluated qualitatively by northern blot and quantitatively by dot blot of RNA and cDNA hybridization to a nick-translated hPL-pMB9 plasmid. The northern blot revealed no major size differences of the mRNA and the dot blot hybridization was quantitatively similar for both gestational diabetics and normal terms per unit of total RNA. By direct analysis of DNA per g tissue we found the DNA content of placentas from gestational diabetics and normal term to be statistically the same.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
