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At least 811 records · Page 45Linked to original sources
PubMed1994

Maternal protein reserves and their influence on lactational performance in rats. 4. Tissue protein synthesis and turnover associated with mobilization of maternal protein.

The present study was undertaken to investigate the changes in muscle protein turnover involved in the rapid mobilization of protein in rats subjected to severe protein restriction during lactation. Estimates of mammary gland and liver protein synthesis were also made during lactation. Multiparous female Sprague-Dawley rats, caged individually following mating, were offered a high-protein diet (H; 215 g crude protein (N x 6.25; CP)/kg dry matter (DM)) ad lib. until parturition. Following parturition, half the females continued to receive diet H, whilst the remainder were offered a diet low in protein (L; 90 g CP/kg DM) ad lib. On days 2, 4, 8 and 12 of lactation, groups of females were used in the estimation of tissue protein synthesis (flooding dose of [3H]phenylalanine) immediately after a milk sample had been obtained. Rates of muscle protein synthesis were unchanged during lactation in group H. The feeding of diet L during lactation reduced the muscle protein synthesis on day 12 to rates that were lower than group H and also the rate on diet L on day 2 (P < 0.01). However, this fall in muscle protein synthesis was not rapid and muscle fractional synthesis rate (FSR) was different from group H only from day 8 (P < 0.05). Estimated rates of mammary protein synthesis appeared to be generally unchanged by dietary treatment or stage of lactation. Liver FSR was also unchanged by dietary protein supply or stage of lactation. The effect of dietary protein restriction on liver size and protein content during lactation influenced liver absolute synthesis rate (ASR), and on days 8 and 12 of lactation liver ASR was lower in group L than in group H (P < 0.001). The loss of muscle protein in rats fed on diet L during lactation (133 mg) occurred mainly between days 2 and 8 of lactation and was primarily associated with a dramatic increase in degradation (13.0% per d), with the decline in synthesis having a much smaller role. A decline in muscle protein degradation during the latter half of lactation was part of the mechanism that prevented excessive muscle protein catabolism. It is thought that the estimation of mammary protein synthesis in the present study was impaired by the milk sampling procedure previously used.

Animals↗
PubMed1996

Maternal undernutrition during late pregnancy in sheep. Its relationship to maternal condition, gestation length, hepatic physiology and glucose metabolism.

There is a paucity of information on the metabolic effects of undernutrition of the ewe carrying multiple fetuses in late pregnancy. In the present study the effects of induction of ketosis from 132 d gestation in ewes carrying twin fetuses were compared with a control group. The ewes were well fed up to 132 d. Ketotic ewes showed a loss of condition score from 3.7 (SE 0.11) at 130 d gestation to 3.0 (SE 0.15) 10 d later after clinical recovery, compared with control twin-pregnant ewes (P < 0.01). The weight loss during the same time period was from 70.6 (SE 2.7) kg at 130 d to 64.2 (SE 2.7) kg at 140.d gestation. As expected, both groups lost weight and condition score in the first 28 d of lactation. Induction of ketosis caused a significant shortening of the gestation period to 142.8 (SE 0.7) d compared with 150 (SE 0.4) d in normal twin-pregnant ewes (P < 0.001). Ewes with induced ketosis recovered clinically and showed a normal feed intake by 3.4 (SE 0.07) d; three required treatment. Induction of ketosis resulted in reduction of hepatic uptake of bromosulphthalein (P < 0.01) and its biliary excretion (P < 0.05), metabolic clearance rate (P < 0.001), fractional clearance (P < 0.001) and 15 and 30 min retention compared with control twin-pregnant ewes. Most values had returned to normal by the first week of lactation. It is thought that in human pregnancy similar changes in bromosulphthalein clearance may be related to reduced binding sites for bromosulphthalein in the liver caused by increased circulating oestrogens. Induction of ketosis resulted in a significant hypoglycaemic (P < 0.01), ketotic (P < 0.001) state compared with well-fed twin-pregnant ewes. These changes could be correlated with the severity of the clinical signs, together with a significant rise in plasma urea (P < 0.001) and NH3 (P < 0.05) concentrations. Again, the return of most of these values to normal by the first week of lactation lends support to the reversibility of hepatic lesions caused by fatty infiltration of the liver. The severity of this condition in naturally occurring cases suggests that factors other than undernutrition may be contributory, such as the general body condition of the ewe and glucose metabolism by the liver, including the conversion of propionate to glucose.

Animals↗
PubMed1976

Maternal immunocompetence. II. Proliferative responses of maternal lymphocytes in vitro and inhibition by serum from pregnant rats.

Peripheral blood and splenic lymphocytes from interstrain (L X BN) or intrastrain (L X L) primigravida rats were equivalent to those from virgin L females in their in vitro DNA synthetic responses to paternal strain cells (BN), to unrelated allogeneic cells (ACI), and to the mitogen phytohemagglutinin (PHA). Heat-inactivated serum from pregnant L rats, when compared to serum from virgin or postpartum L rats, regularly suppressed the in vitro response of L lymphocytes to paternal and allogeneic cells. The response of L cells to PHA was not suppressed. The degree of inhibition was related to the final concentration of pregnant serum in culture, concentrations above 2% producing more than 80% inhibition of the mixed lymphocyte reaction. The inhibiting sera were not cytotoxic by a sensitive 51Cr release assay. Histoincompatibility between mother and fetus is not required for production of this inhibitory effect, since it is consistently present in intrastrain (L X L) pregnant rats. Among interstrain pregnant rats, the degree of inhibition is influenced by, but not specific for paternal-strain alloantigens. Thus, the proliferative function of thymus-derived (T) lymphocytes from pregnant rats is intrinsically normal, but the response to allogeneic cells can be altered by factors present in pregnant serum.

Animals↗