Biomedical subjects

T Mampel

Publications and source records attributed to T Mampel.

44 records · Page 3Linked to original sources

PubMed1986

Brown adipose tissue activity in hypocaloric-diet fed lactating rats.

Hypocaloric diet feeding reduced the mitochondrial protein content and whole tissue GDP-binding in interscapular brown adipose tissue from both virgin and lactating rats. A reduction in brown fat lipoprotein lipase activity was also detected in underfed virgin and lactating animals. These results indicate that lactation in the rat, even though it produces a reduction in brown fat activity, does not impair the capacity of the tissue to respond to a diminished caloric intake by lowering its activity further.

Adipose Tissue, Brown↗

PubMed1986

Changes in brown adipose tissue lipoprotein lipase activity and lipogenesis rate during pregnancy and lactation in the rat.

Brown fat lipoprotein lipase activity did not change in the first two weeks of pregnancy whereas it decreased on day 18 of gestation and was lower during late pregnancy and lactation. Fatty acid synthesis rate, measured in vivo with (3H)H2O, showed a progressive increase until day 18 of gestation followed by a decrease on day 20 of pregnancy and a reduced lipogenesis rate throughout lactation. The early reduction in the pathways of fatty acid uptake and synthesis in brown fat during the breeding cycle of the rat suggests the possibility that a decline in the substrate supply was a factor contributing to the reduced thermogenic activity of brown adipose tissue after parturition.

Adipose Tissue, Brown↗

PubMed1985

Hepatectomy-nephrectomy effects in the pregnant rat and fetus.

Levels of circulating glucose, glycerol, and FFA concentrations were determined before and after hepatectomy-nephrectomy in 20 day pregnant rats and virgin controls. After evisceration, blood glucose levels decreased in a parallel way in both groups whereas in pregnant rats, the blood glycerol level increased less and plasma-FFA rose more than in controls. Maternal evisceration caused reduced blood glucose and enhanced glycerol levels in fetuses, whereas fetal plasma-FFA levels were unmodified. Results indicate that extrahepatic glucose utilization remained stable in the late pregnant rat. Fetal levels of circulating glycerol, but not of FFA, appeared directly dependent on maternal levels. It is proposed that under normal conditions, glycerol availability to the fetus is low, due to its preferential utilization by maternal gluconeogenic organs which reduced the amount available for possible placental transfer.

Animals↗

PubMed1985

Similar metabolic response to acute ethanol intake in pregnant and non-pregnant rats either fed or fasted.

Plasma ethanol concentration 3 hr after its oral administration (3 g/kg body wt) did not differ in 20 day pregnant rats with virgin controls, and in both groups values were higher when studied after 24 hr fasted than when fed. In fed animals, blood glucose and liver glycogen concentrations were lower in pregnant than in virgin rats, whereas ethanol intake in both groups enhanced blood glucose levels, it reduced liver glycogen content only in virgins. In fetuses, maternal ethanol intake enhanced blood glucose levels. In fasted animals, ethanol intake decreased blood glucose levels in pregnant and virgin animals but did not affect these levels in fetuses. Ethanol intake enhanced beta-hydroxybutyrate/acetoacetate ratio similarly in blood of pregnant and virgin rats when either fed or fasted, and it produced the same change in fetuses from fasted mothers. Results indicate that the metabolic response to acute ethanol does not differ between pregnant and non-pregnant animals, and it is proposed that fetuses passively follow the metabolic changes occurring in their mothers after receiving ethanol.

3-Hydroxybutyric Acid↗

PubMed1985

Effects of chronic ethanol treatment on glucose tolerance, insulin response and circulating metabolites in the pregnant rat.

The effects of chronic ethanol treatment on intravenous glucose tolerance and insulin response in non-pregnant and pregnant rats were studied. Basal circulating glucose, insulin, and ketone bodies levels were also determined during the treatment. Basal blood glucose concentration did not change during the ethanol treatment whereas plasma insulin levels were lower at the beginning of gestation and at the 15 and 18 days of pregnancy in ethanol-treated rats. Blood beta-OH-butyrate levels were higher and acetoacetate concentrations unchanged during the ethanol treatment, resulting in augmented beta-OH-butyrate/acetoacetate ratio. Intravenous glucose tolerance was not modified in ethanol-treated rats whilst the associated insulin response was lower in both non-pregnant and pregnant ethanol-treated rats. Data show that ethanol treatment during pregnancy alters glucose-insulin relationships despite being associated with unchanged maternal glycemia.

3-Hydroxybutyric Acid↗

PubMed1985

Glucose tolerance and insulin response in offspring of ethanol-treated pregnant rats.

The effects of maternal alcohol ingestion on oral glucose tolerance and insulin response were studied just after birth and in 3-day old offspring of rats given ethanol for drinking (25% w/v) during pregnancy. Offspring litter size, litter survival and body weight were reduced as a consequence of maternal alcohol treatment. Basal plasma insulin levels were augmented in pups from alcoholized mothers just after birth, despite the fact that blood glucose did not change. Maternal alcohol consumption caused glucose intolerance associated with unchanged insulin response in pups just after birth whereas 3-day old pups from alcoholized mothers showed normal glucose tolerance associated with increased insulin response. Data indicate that chronic maternal ethanol treatment may cause impaired insulin sensitivity in the offspring.

Animals↗

PubMed1985

Effects of insulin on the utilization of 14C-glycerol and 14C-glucose in hepatectomized nephrectomized rats.

Insulin (i.v.) administration to functionally hepatectomized-nephrectomized rats did not alter circulating levels of glycerol and only slightly affected plasma radioactivity when animals received (U-14C)-glycerol, whereas after (U-14C)-glucose administration insulin enhanced hypoglycemia and greatly accelerated the rate of radioactivity loss from plasma. At 15 min after i.v. injection of (U-14C)-glycerol, radioactivity in total lipids was reduced in heart and lungs by insulin administration and enhanced in carcass and brown adipose tissue. These effects involved the 14C-glyceride glycerol fraction in the case of heart and 14C-fatty acids in carcass and adipose tissue. When (U-14C)-glucose was administered, insulin enhanced the appearance of 14C-water-soluble material in heart and carcass and 14C-total lipids in heart, carcass, and both brown and white adipose tissue. The effect in heart corresponded mainly to the 14C-glyceride glycerol fraction whereas it corresponded to the 14C-fatty acids in the other tissues. Therefore, insulin effects on glycerol metabolism substantially differ from those on glucose. Opposite effects on heart and lung glycerol utilization as compared to those in carcass and brown adipose tissue may account for the difficulties in observing changes in plasma glycerol levels after insulin treatment.

Adipose Tissue↗

PubMed1981

Changes in circulating glycerol, free fatty acids and glucose levels following liver transplant in the pig.

Female pigs, fasted overnight, received an orthotopic liver transplant. During the nonhepatic phase, both blood glycerol and plasma free fatty acid concentrations increased, returning to basal values after the transplant, indicating that the liver is the main receptor of these products released in the blood from the glyceride breakdown in peripheral fat deposits. Blood glucose level rose during the nonhepatic phase, probably due in part to the perfusion of glucosated saline received by the animals during this phase. After liver transplant, blood glucose levels progressively decreased and this effect was greatly reduced by administering L-alanine. Our data indicate that metabolic changes in the donor's liver diminish the availability of gluconeogenetic substrates immediately following transplant, while administration of exogenous alanine permits faster restoration of gluconeogenetic function in the transplanted liver.

Animals↗