Slices of caruncular endometrium from steroid-treated ovariectomized sheep were incubated with myo-[2-3H]inositol to label tissue phosphatidylinositol. Effects of oxytocin were determined on the rate of incorporation of radioactivity into phosphatidylinositol and on the hydrolysis of phosphoinositides to inositol phosphates and diacylglycerol. Incorporation of radioactivity into phosphatidylinositol was linear during 2 h incubations; 10(-7) M (100 nM)-oxytocin caused a 2.8-fold increase in the rate of incorporation. In the presence of Li+, addition of 10(-7) M-oxytocin to slices in which phosphatidylinositol was pre-labelled caused mean increase of 40-fold in the incorporation of radioactivity into inositol mono-, bis- and tris-phosphates. Inositol 1,3,4-trisphosphate was quantitatively the major trisphosphate formed. The action of oxytocin on phosphoinositide hydrolysis was dose- and time-dependent, occurring at concentrations within the range observed in plasma during episodes of secretion in vivo, and with a time course comparable with that of the action of oxytocin on uterine prostaglandin production. The effect of oxytocin on incorporation of radioactivity into inositol phosphates was not affected by inhibitors of prostaglandin synthesis. Diacylglycerol 1- and 2-lipases in caruncular endometrium converted up to 72% of added 2-[3H]arachidonyldiacylglycerol into [3H]arachidonic acid during 30 min incubations at pH 7.0. Caruncular endometrium contained 1.49 mumol of phosphatidylinositol/g, representing approx. 0.2 mumol/g of phosphatidylinositol arachidonic acid. It is proposed that the stimulation of endometrial prostaglandin synthesis by oxytocin is accounted for by increased hydrolysis of phosphoinositides to diacylglycerol and inositol phosphates with subsequent release of arachidonic acid from diacylglycerol.

The effect of bile and pancreatic juice on the pattern of lipids in the intestinal digesta of the sheep has been examined using animals suitably prepared with chronic intestinal fistulae. The major lipid of digesta collected anterior to the common bile duct was the free fatty acid fraction composed mainly of palmitic and stearic acids. Digesta collected immediately posterior to the common bile duct contained, in addition, polyunsaturated fatty acids and lecithin, indicating that these lipids originated in the mixed secretions of bile and pancreatic juice. In the mid jejunum the major phospholipid was lysolecithin derived from the hydrolysis of lecithin by pancreatic enzymes. In the duodenum and jejunum the free fatty acids were associated mainly with the particulate matter of digesta, but in the ileum the free fatty acids were more evenly distributed between the particulate and aqueous phases. Negligible amounts of monoglyceride were present in digesta of the small intestine. Diversion of bile and pancreatic juice from the intestine resulted in the disappearance of lysolecithin and a decrease in the content of unsaturated fatty acids in the digesta of the jejunum. The digestion of lipids in the sheep intestine is discussed in relation to the possible role of bile and pancreatic juice. It is suggested that a major function of pancreatic juice is to provide, by interaction with biliary lecithin, the lysolecithin required for optimum micelle formation and lipid absorption.

1. The fatty acid compositions of the plasma lipids of newborn unsuckled lambs, kids, calves and piglets have been determined and compared with those of maternal plasma lipids at parturition. 2. The predominating plasma fatty acids in the newborn of all species are palmitic acid, C(16:1) acid, stearic acid and C(18:1) acid. This finding is consistent with the synthesis of the major proportion of fatty acids from non-lipid sources within the foetus. 3. Very small amounts of C(18:2) acid and C(18:3) acid are present in the plasma lipids of newborn ruminants, although considerable amounts of these fatty acids are contained in maternal plasma. The plasma fatty acids of the newborn piglet contained 5.5% of C(18:2) acid, those of the calf 2.0%, and those of the lamb and kid less than 1.0%. This finding is discussed in relation to the higher content of C(18:2) acid in the plasma non-esterified fatty acid fraction of the sow (15%) compared with that of the ruminant (less than 4%). 4. In the lamb and kid, but not in the calf or piglet, a C(20:3) acid was detected in plasma lipids that was very similar to, if not identical with, the C(20:3) acid that accumulates in the plasma of animals given diets low in essential fatty acids. The possible significance of this finding is discussed. 5. The cholesteryl esters of cow plasma were found to contain a higher percentage (43%) of C(18:3) acid than those of goat and sheep plasma (5-10%). The possible reasons for this difference are discussed.

Rats were reared into a third generation on diets deficient in essential fatty acids supplemented with linoleic acid (18:2 n-6) or linolenic acid (18:3 n-3) with the object of depleting the retina of n-6 or n-3 fatty acids. In the rats fed 18:2 n-6 the percentage by weight of 22:6 n-3 in retinal fatty acids fell from 22.5 to 8.5% in first-generation animals but then remained unchanged in second and third generations. There was no difference in b-wave amplitudes of the electroretinogram between the rats fed 18:2 n-6 and those fed 18:3 n-3. In guinea-pigs fed purified diets low in 18:3 n-3 the percentage by weight of 22:6 n-3 in retinas fell from 8 to < 0.5% by the third generation. However, there were no statistical differences in the b-wave amplitudes between these animals and those reared on a commercial diet. It is concluded that if n-3 fatty acids are involved in retinal function their role is too subtle to be detected by standard electroretinographic techniques.

SUMMARYIn two experiments a total of twelve male rats were reared from weaning for up to 63 weeks on an essential fatty acid (EFA)-deficient diet alone (2 x two animals) or supplemented with the methyl esters of linoleic acid (18: 2w6) (2 x two animals) or linolenic acid (18: 3w3) (2 x two animals). Testicular development was normal in rats given 18:2w6, but in rats fed the EFAdeficient diet alone, and in those supplemented with 18:3w3 the testes were reduced in size. Histologically, a degeneration of the seminiferous tubules was noted, with progressive loss of the germinal cells, and with an absence of spermatozoa in the lumina of the seminiferous tubules and epididymides. Leydig cells appeared unaffected, and were prominent. The six rats in Experiment 1 were capable of mating with females reared on commercial diets, but only the two 18: 20)6 supplemented animals were fertile. There was a marked reduction in the percentage of arachidonic acid (20:4wj6) and docosapentaenoic acid (22: 516) in the total fatty acids of the atrophic testes. There was no compensatory increase in long-chain derivatives of 18: 3w3 in the 18: 3w3 fed rats and it is concluded that linolenic acid cannot replace linoleic acid in the development of the rat testis.