Prenatal protein depletion and Δ9, Δ6 and Δ5 desaturases in the rat

Abstract

Pregnant rats were kept throughout gestation on a control diet (i.e., 25% protein), on a low protein diet (i.e., 5% protein) or on a fat-free diet. At 20--21 days of gestation, the rate of 9-, 6-, and 5-desaturation was measured, using microsomes from maternal and fetal livers and placenta microsomes. The effect of protein malnutrition was more evident upon delta 6-desaturase activity from maternal liver, while a less severe reduction in the activities of delta 9- and delta 5-desaturases was observed. No measurable activities of delta 5- and delta 6-desaturases were observed in fetal liver and placenta, while a low activity of delta 9-desaturase was detected in both tissues from the three groups under study. We concluded that delta 6-desaturation is greatly affected by maternal protein deprivation, and this fact could affect the normal supply of polyunsaturated fatty acids for the normal fetus growth and tissue development.

Comparative in vivo and in vitro Study of the Influence of Experimental Diabetes on Rat Liver Linoleic Acid Δ6- and Δ5-Desaturation

“…Streptozotocin diabetes leads to a partial inhibition of linoleic acid A6-desaturation, considered as an arachidonic acid biosynthe sis limiting step [9,16,18,31,32,41], We found, with a fat-free diet, in vitro (table III, IV), a medium inhibition ratio of 0.74, con firming the values of Friedmann et al [18] in vivo and those of Faas and Carter [17] in vitro. The inhibition ratio of A6-desaturation is strongly decreased in severe streptozotocin diabetes [42]; this desaturation is less dis turbed in marginal diabetes.…”

“…According to Mercuri et al [31,32] and Eck et al [16], linoleic acid microsomal desaturation, partially inhibited by streptozotocin diabetes, is corrected by moderate insulin treatment (table IV). Shortly before sacrifice the rats were hypoglycemic.…”

“…Gellhorn and Benjamin [19], Mercuri et al [31], Brenner et al [9] and Peluffo et al [4] used insulin-zinc to correct A9-and A6-desaturations. The duration of the treatment was comparable to ours, but the quantities administered and the number of injection changed according to the experiments and authors: from 0.2 [41] to 15 IU twice a day, for 48 h (the last ones were accompanied by 10 ml 5% isotonic glucose solution adminis tration, so as to compensate for the severe hypoglycemia induced by insulin) [31], Faas and Carter [17] used regular insulin (2 IU/6 h) for 48 h for restoring A9-and A6-desaturations and NPH insulin (4 IU/12h) for 48 h, for 'super' repairs.…”

“…We know [19] that insu lin injection for at least 24 h to alloxan-dia betic rats restores palmitic and stearic acid desaturation; the restoration rate and its du ration depend on the dose of insulin in jected [20], the in vitro administration being ineffective [19]. After 48 h, insulin also cor rects partial inhibition of linoleic acid A6-desaturation induced by alloxan diabetes [29], Mercuri et al [31] demonstrated that insulin-induced restoration of desaturation activities is better for palmitic and stearic acid than for linoleic and a-linolenic acid. According to Peluffo et al [41], restoration of linoleic acid desaturation to normal values is not proportional to insulin dose; hypogly cemic injection of insulin does not increase this A6-desaturation.…”

Long-Term Modification of the Excretion of Prostaglandin E₂ by Fetal Exposure to a Maternal Low Protein Diet in the Rat

“…Enzymes within the pathway leading to PG production are known to be susceptible to programming by prenatal diet. The desaturase activities, which convert linoleic acid to arachadonic acid, the immediate precursor of vasoactive PGs, exhibit long-term, postnatal changes in rats exposed to a low protein diet in utero [14,15].…”