Browsing by Author "Tavares do Carmo, Maria das Graças"

Effects of ethanol intake on lipid metabolism in the lactating rat. ALCOHOL 13(5) 443-448. 1996.-Femalc rals receiving alcohol (20%) in drinking water during lactation (AL) were compared lo pair-fed ,inimals (l'F) and normal controls (C) fed ad lib. All animals were killed on the 12th day of lactation. When compared to C mis, food intake decreased in both AL and PF groups. and this effect was followed by a lower body weight nnd mammary gland (MG). liver. and parametrial adipose tissue weights. Mammary glands tri,1cylglyceride concentration (TG) was much lower in l'F lhan in AL. although in the latter. values <.lid not reach lhose of C'. and had higher liver TG conccnlration than ;1ny of the other group.~. Both l'F and AL rats had lower plasma TG. glycerol, and free folly acid concentrations ur1<.I higher (3;-hydroxybutyrnte concenlrntion than C rats. When compared to C rals. the rnte of lipogencsis in MG was higher in bolh PF and AL mis. whereas in liver it was higher in PF and lower in AL rats, and in adipose tissue it wns higher in PF and unchanged in AL nils. The appearance of uc lipids 4 h after ornl (1 4 jlriolcin in both MG and liver was lower in AL and PF rnts and only lower in adipose tissue of AL rats as compared lo the C rnts. Lipopmtein lipase and hormone-sensitive lipase activities were lower in MG in holh PF and AL rats lhan in C. whereas in adipose tissue the activity of lipoprolein lipase did nol differ between AL and C rats and the activity of I ISL was lower in the former. These findings therefore show that in spite of re<.luce<.1 upt,1ke of ornlly administered lriglyceri<.les due lo decreased LPL aclivily, maternal alcohol feeding during lactation in the rat preserves the mammary !!land triglyceride content thanks to enhanced lipogcnetic activity. On the olher hand. it causes liver triglycerides accumulation. probably as a result of the decreased rate of triglycerides released into circulation. and these changes are not caused hy the reduced food in lake of the animals.

From parturition, lactating Wistar rats were given 20% ethanol in drinking water and solid diet ad lihitum (ET group) or were pair-fed to the ET group (PF group) or were given water and solid diet ad lihitum (control group, C). Animals were studied on day 12 of lactation and/or treatment, when dams were separated from their litters and 2-4 hours latter they were i.p. injected with oxytocin for milk collection under anaesthesia. Maternal food intake, weight gain and pup's body weight were lower in ET than in C rats. When compared to C rats, milk of ET dams had a decreased proportion of C14:0 and C22:6 n-3 fatty acids while an increase in C18:0, C16:1 and C18:1 n-9 was detected, whereas when compared to PF it had higher CS:0, Cl0:0, C18:0, C18:1 n-9, C18:2 n-6 and lower C20:5 n-3 and C22:6 n-3. Body weight was lower in pups from ET than in those from C or PF, and whereas brain weight and brain lipid content was lower in ET and PF pups than in C, total phospholipid (PL) brain content was similar among the groups. The ratio of C20:3 n-9 to C20:4 n-6 in brain PL was higher in ET pups than in either C or PF, indicating an essential fatty acid deficiency in the formers. Ethanol treatment also decreased the proportional amount of C18:2 n-6, C18:3 n-3, C20:4 n-6, C20:5 n-3 and C22:6 n-3 in brain PL as compared to C, whereas from these fatty acids only C18:3 n-3, C20:5 n-3 and C22:6 n-3 were decreased in PF. On the other hand, the proportion of C22:6 n-3 was significantly lower in the pups of ET group than in PF animals. Present results show that maternal intake of ethanol during lactation in the rat modifies milk lipid composition and that these effects are not caused by the undemutrition condition of the animals. These effects alter fatty acid composition of brain PL in pups, and such effect may contribute to its abnormal development.

From parturition, lactating Wistar rats were given 20% alcohol in drinking water and fed a solid diet ad lib (group AL). Pair-fed (PF) and control (C) rats were fed solid diet and given water ad lib (C). All animals were sacrificed on the 12th day of lactation. Ethanol treatment decreased food intake and milk production in lactating rats to a greater level than in PF rats, and a greater reduction in body weight of the AL pups was noted. Brain weight, protein concentration, and DNA content were also lower in pups of AL dams than of PF dams, whereas liver glycogen concentration was higher in the former. Pups from AL dams had higher circulating levels of [3-OH-butyrate, triglyceride, and free fatty acids than those from either C or PF dams. Plasma glucose concentration was lower in both PF and AL than in C pups, whereas the AL group had lower plasma protein concentration than any of the other groups. We conclude that maternal alcohol intake during lactation greatly impairs milk production, and although the known increase of lipid content in milk in rats studied under similar conditions allows an enhanced lipidic components in the pups, this adaptation does not allow normal growth and brain development.