Biomedical subjects

N Freund

Publications and source records attributed to N Freund.

23 records · Page 2Linked to original sources

PubMed1984

Fatty acid oxidation by developing rat kidney.

In view of the importance of free fatty acids (FFA) as substrates for the mature kidney, fatty acid oxidation by developing rat kidney has been investigated in vitro. Incubations of kidney slices from fetal stages (days 20 and 21 of gestation) and from days 1, 5, 10, 20, and 30 after birth have been carried out in Krebs-phosphate, pH 7.4, containing 0.5 or 1.5 mM U-14C-palmitate. Palmitate uptake and oxidation into CO2 were measured after 90 min incubation. At 0.5 mM concentration of palmitate in the incubation medium, fetal kidney exhibited a low uptake and a very low oxidation of palmitate into CO2. These two parameters increased only after birth and were maximum with slices from suckling rats between days 5 and 10 after birth. Palmitate oxidation increased only with postnatal days slices (maximum during the suckling period) and not with fetal slices. An increase in palmitate oxidation could be obtained with slices from kidneys of fetuses whose mothers had been starved 48h. These data suggest that the development of renal capacity for FFA oxidation during the perinatal period could be related to nutritional supply.

Animals↗

PubMed1982

Oxidative metabolism in fetal rat kidney during late gestation.

Slices of fetal rat kidney were incubated for 90 min at 37 degrees C in Krebs phosphate buffer containing [14C]glucose. Glucose uptake did not change significantly with age, but the 14CO2 evolved from [14C]-glucose dropped, and the lactate concentration at the end of incubation rose. The increasing development of the medulla during gestation was believed to be responsible for this. Higher glucose uptake and lower [14C]glucose incorporation into CO2 was observed in whole fetal slices compared to cortical slices from adult kidney, incubated following the same procedure. These results might be due to the smaller number of functionally differentiated nephrons present in fetal compared to adult kidney. Competition between glucose and lactate, normally found at high concentrations in fetal blood, and between glucose and beta-hydroxybutyrate, known to increase in circumstances such as starvation in the mother, showed a decrease in the 14CO2 evolved from [14C]glucose. This suggests that both these substrates might be oxidized by fetal kidney. This was confirmed by experiments in which lactate or beta-hydroxybutyrate replaced glucose in the incubation medium. Further, both these substrates seemed to be preferential fuels for oxidation compared to glucose, and their possible role in saving glucose is discussed.

3-Hydroxybutyric Acid↗

PubMed1980

Fetal metabolic response to phloridzin-induced hypoglycemia in pregnant rats.

Phloridzin, an inhibitor of renal sugar transport, produces an important loss of glucose in urine of treated animals. In order to reduce severely the maternal glucose supply to the fetuses in short-term experiments, we have combined phloridzin administration to pregnant rats with 18 h starvation. Fetuses from starved phloridzin-treated mothers were compared with fetuses from starved mothers. Combined treatment markedly decreases fetal blood glucose concentration (-36%) and fetal liver glycogen stores (-76%). These changes are associated with a decrease in plasma insulin (-25%), a rise in plasma glucagon (+120%) and a marked increase of hepatic PEPCK activity (+400%). It appears from these results that phloridzin treatment for a short duration is able to induce glycogenolysis and the premature appearance of PEPCK in the liver of rat fetuses.

Animals↗

PubMed1975

Sugar transport in the small intestine of obese hyperglycemic, fed and fasted mice.

1. The in vitro transport of 3-0-methyl-D-glucose was measured in the small intestine of obses-hyperglycemic (ob/ob) mice and their lean littermates, fed or fasted for 48 hrs. 2. Transport was much increased in the jejunum of obese animals and, to a lesser extent, in obese mice on a chronic restricted diet. 3. Kinetic studies indicate that the Vmax of transport was significantly greater in obese than in lean mice, whether fed or fasting. Fasting increase the Vmax in lean but not in obese animals. These changes were more prominent in the jejunum. The apparent Km of transport was the same in all four groups. 4. These findings are discussed in relation to the increase in intestinal absorptive functions in diabetes and in some conditions of food restriction or starvation. The results are consistent with the hypothesis that the effects of diabetes and of starvation on intestinal sugar transport reflect an alteration in the same controlling factor.

Animals↗

PubMed1975

Blood glucose and serum insulin levels in lean and genetically obese mice.

Fed and 24 hour fasted lean and genetically obese mice (ob/ob) were given a fixed glucose load per gm body weight by intraperitoneal and intragastric administration. Intraperitoneal glucose injection into the obese mice produced a prolonged elevated blood glucose level with a concomitant significant decrease of circulating insulin. Possible interpretations of this observation are discussed. In those obese animals in which glucose was administered intragastrically the fed obese mice had a blood glucose concentration of 450-500 mg% for a period of one hour but there was no increase in circulating insulin, however, in the fasted obese mice in which the glucose concentration was about 350 mg% for one hour, there was a significant increase in the circulating insulin levels. The fed and fasted lean mice showed normal glucose tolerance curves and the expected increase in circulating insulin following either intraperitoneal orintragastric glucose loads. It is concluded that hyperglycaemia in the ob/ob mice is unlikely to be the principal cause of hyperinsulinaemia.

Animals↗