Browsing by Author "Martín, A."

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.

In the late pregnant rat, blood glucose levels were lower and plasma RIA-insulin levels were slightly higher than in virgin animals. Oral and intravenous glucose tolerance tests produced parallel changes in blood glucose in both groups whereas plasma RIA-insulin increased more in the pregnant animals. Blood glucose levels after either low (0.1-1 IU/Kg) or high (10 IU/Kg) doses of intravenous insulin decreased more slowly and less in pregnant than in virgin rats. Feta! blood glucose levels were not affected by maternal insulin treatment. Results show that in the unanaesthesized late pregnant rat both insulin sensitivity and responsiveness decreased and it is proposed that this insulin resistance may represent a mechanism to delay disposal of ingested nutrients by maternal tissues, ensuring their availability to the fetus.

Radioinmunoassayable somatostatin content was measured in stomach antrum and fundus, and in colon mucosa from virgin and 20-day pregnant rats made diabetic with streptozotocin treatment before gestation, and which either did or did not receive daily insulin substitution therapy. They were compared with normal untreated rats. Somatostatin content in both antrum and fundus was lower in normal pregnant animals than in virgin animals. Diabetes produced an increase in somatostatin content, and insulin therapy caused a reduction in antrum, fundus and colon somatostatin content in the virgin animals, only in the fundus and colon in pregnant rats. It is proposed that these findings may be related to changes in gastric acid secretion and digestive cell proliferation known to occur during diabetes and pregnancy although their precise physiological significance remains to be established.