title: [Serum leptin in women during the third trimester of pregnancy].
abstract: Leptin is a small protein produced mainly by adipocytes. Recently, its relationship to obesity has been studied extensively. It was proved that obese individuals have either relative or absolute leptin deficiency. Several years ago, leptin was found to be produced also by the placenta. This stimulated us to study relationship between leptinemia and placental hormones in 85 women in the second gravidity trimester. Within the prenatal screening, these pregnant women were subjected to analysis of AFP, hCG, SP-1 glycoprotein and leptin and the results obtained were processed statistically. The control group consisted of 20 nonpregnant women with tetany. Women in the second gravidity trimester were found to have a significantly higher leptinemia than nongravid women (even with respect to body weight). This may be due to a larger amount of adipose tissue during gravidity and also leptin-resistance. Moreover, we recorded a negative correlation between leptinemia related to body weight and concentration of SP-1 glycoprotein. This finding supports the presumption that mother's leptinemia correlated negatively in the second gravidity trimester with quality and quantity of the placental syncytiotrophoblast. Our findings can be explained as follows: the biological effect of leptin is metabolically unfavourable for the growth of the foetus and the placenta. An increased leptinemia with advancing gravidity can be caused by a larger fatty mass and an increased activity of adipocytes when leptin presence increases in system circulation but the organism begins to be leptin-resistant and an "unfavourable" metabolic effect fort the gravid woman and the foetus is not distinct. These findings thus support the hypothesis postulating the nonsignificance of leptin production in human placenta and on the contrary the necessity of leptin-resistance for foetus development from the metabolic point of view. Thus, a decreased leptinemia immediately before and after the delivery could be caused by the still unclear regulators of leptin sensitivity. This is again a metabolically highly favourable state (reduced appetite, decreased body weight, increased energy output and others).
authors.affiliation: Metabolická a diabetologická jednotka Nemocnice, Sternberk.
authors.forename: D
authors.initials: D
authors.lastname: Stejskal
authors.forename: V
authors.initials: V
authors.lastname: Růzicka
authors.forename: J
authors.initials: J
authors.lastname: Novák
authors.forename: L
authors.initials: L
authors.lastname: Jedelský
authors.forename: J
authors.initials: J
authors.lastname: Bartek
authors.forename: D
authors.initials: D
authors.lastname: Horalík
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D005260:Female; D006801:Humans; D020738:Leptin; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy / Q000097:blood*; D011263:Pregnancy Trimester, Third; D011268:Pregnancy-Specific beta 1-Glycoproteins / Q000032:analysis; D011506:Proteins / Q000032:analysis*
chemical_list: D020738:Leptin; D011268:Pregnancy-Specific beta 1-Glycoproteins; D011506:Proteins
vernacular_title: Vysetrení leptinu v séru u zen v druhém trimestru gravidity.