Relationship Between Plasma Free Fatty Acid Levels and Human Placental Lactogen Secretion in Late Pregnancy

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Abstract
In order to determine whether changes in free fatty acid (FFA)-levels affect hPL [human placental lactogen] secretion in late human pregnancy in the same way as they affect human growth hormone (hGH) secretion, 2 types of experiments were performed: 1 g of nicotinic acid (NA) was infused for 60 min in 11 patients and 1.5 g of NA was infused for 90 min in 8 additional patients; triglycerides and heparin were administered i.v. for 120 min in 5 control cases and, in 11 other patients 0.3 U [units] insulin/kg BW [body weight] was injected at the 45th min of the triglyceride-heparin infusion. Maternal blood glucose (BG), plasma triglycerides (TG), FFA, immunoreactive insulin (IRI) and hPL levels were sequentially determined in the course of these experiments. In both series of patients, the NA infusion resulted in substantial depression of FFA levels to around 50% of mean basal levels. The hPL levels displayed only negligible fluctuations, although FFA depression persisted for more than 2 h. During the lipid-heparin infusion, an increase in plasma TG and an accompanying rise in FFA levels (from 629 .+-. 48 to 1,919 .+-. 301 .mu.eq/l) were recorded. When insulin was infused together with lipids, the ensuing hypoglycemia (average glycemia, 32.3 .+-. 3 mg/100 ml) resulted in a significant increase in hPL levels (mean peak rise: + 26.3% of mean preinsulin values, P values between < 0.05 and < 0.005 from 15 to 105 min after insulin). The elevation of hPL levels in response to insulin-induced hypoglycemia was similar in amplitude to the one observed in previous experiments in which plasma FFA levels were in the normal range. No significant change in hPL levels was discernible in the control study when saline was injected in place of insulin. Marked and sustained plasma FFA depressions or elevations do not influence hPL circulating levels in late human pregnancy and high FFA levels cannot blunt the hPL response to insulin-induced hypoglycemia. In this respect, the metabolic mechanisms controlling hGH and hPL secretion are different.

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