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Biomedical subjects

M Benito

Publications and source records attributed to M Benito.

At least 145 records · Page 8Linked to original sources
PubMed1983

Regulation of lipogenesis in vivo by glucose availability and insulin secretion in maternal and foetal tissues during late gestation in the rat. Effect of glucose intubation, streptozotocin-induced diabetes and starvation.

Administration of an oral load of glucose did not change the rate of lipogenesis in maternal liver during late gestation. However, streptozotocin-induced diabetes or starvation decreased maternal liver lipogenesis at 20-22 days of gestation. Glucose intubation, on the other hand, increased foetal lipogenesis at 21-22 days. In addition, maternal starvation decreased foetal lipogenesis and plasma insulin concentration. However, chronic hyperglycaemia induced by streptozotocin administration to the mother did not change foetal liver lipogenesis.

Adipose Tissue↗
PubMed1983

The effect of chronic ethanol administration on lipogenesis in liver and adipose tissue in the rat.

Rates of lipogenesis de novo have been studied in liver and epididymal fat pads of male rats chronically treated with ethanol. A solution of ethanol (150 ml/l) was administered as the only drinking fluid for 3 months with a standard solid diet; both food and drink were available ad lib. Lipogenesis in vivo was measured by the incorporation of tritiated water into lipid fractions: non-saponifiable lipid and fatty acids. Non-saponifiable lipid, both in liver and in adipose tissue, was unaffected by ethanol treatment. However, fatty acid synthesis de novo was significantly enhanced in both liver and adipose tissue, by 150 and 300% respectively. Plasma triacylglycerol and non-esterified fatty acid levels were unchanged and plasma glucose concentration slightly increased by ethanol administration. The rate of lipogenesis increased when insulin: glucagon increased twofold due to the effect of ethanol.

Adipose Tissue↗
PubMed1983

Effect of postnatal hypoxia on the energy homeostasis of the newborn rat during the early neonatal period.

Newborn rats breathing a low-oxygen mixture showed similar rates of glycogenolysis to newborns breathing air. However, hypoxia prevented the decrease of plasma glucose and lactate concentrations which occurred in newborns breathing air immediately after delivery. The time-course of plasma alanine was not affected by experimental hypoxia. The decrease in the liver lactate/pyruvate ratio observed in control newborns immediately after delivery was prevented by hypoxia. Lower blood oxygen concentrations were observed in hypoxic animals throughout the observation period. Lower ATP concentrations were observed in hypoxic newborns during the first hour after delivery but similar values were observed in both groups thereafter.

Adenine Nucleotides↗
PubMed1982

Relationship between lipogenesis and glycogen synthesis in maternal and foetal tissues during late gestation in the rat. Effect of dexamethasone.

Treatment with dexamethasone enhanced 3H2O incorporation into liver and blood lipid, and also increased plasma glucose, insulin, non-esterified fatty acid and triacylglycerol concentrations during late gestation in the mother rat. An inverse relationship between glycogen and lipid synthesis in foetal liver and lung was observed in control rats. This relationship was also observed in foetal liver, but not in foetal lung, after treatment with dexamethasone.

Animals↗
PubMed1982

[Profile of the capacity for lipid synthesis in vivo in various rat tissues: effect of age].

Changes in 3H2O incorporation in vivo to lipid fractions have been studied in rats 1, 3 and 13 months old. The incorporation of tritiated water into non-saponifiable fraction showed and age-dependent decrease in liver. The values were 4.32, 2.91 and 2.56 mumol 3H2O incorporated/g wet weight of liver/hour, at 1, 3 and 13 months respectively. Similar variations could be observed in adipose tissue and in blood. The rates of lower lipogenesis increase markedly from 1 to 3 months (7.02 to 13.36 mumol 3H2O/g/h) and decrease sharply from the 3rd to 13th months (13.36 to 3.75 mumol 3H2O/g/h). The incorporation of radioactivity into blood and adipose tissue fatty acids, also decrease by age.

Adipose Tissue↗
PubMed1982

[In vivo study of lipogenesis and glycogen synthesis in fetal tissues of the rat. Effect of dexamethasone].

Foetal rat liver lipogenesis in vivo decreased during the last two days of gestation. Whereas glycogen synthesis of the same tissue had increased between 20-21 days and sharply decreased during the last day. Treatment with dexamethasone increased glycogen synthesis and decreased lipid synthesis at the same time. Conversely, foetal rat lung lipogenesis increased and glycogen synthesis decreased during the last two days of gestation. Treatment with dexamethasone decreased both the rates of lipogenesis and the glycogen synthesis in the same observation period.

Animals↗
PubMed1981

Lipogenesis in vivo in maternal and foetal tissues during late gestation in the rat.

The rate of 3H2O incorporation into lipid in vivo progressively decreased in liver but increased in parametrial adipose tissue during the last 3 days of gestation. These changes seem to be related to those occurring in plasma insulin and progesterone concentrations during the same period. Foetal liver showed a high rate of lipogenesis, which sharply decreased before parturition. foetal lung lipogenesis increased during days 20 and 21 of gestation.

Adipose Tissue↗
PubMed1981

Regulation of glycogenolysis in the liver of the newborn rat in vivo. Inhibitory effect of glucose.

Newborn rats were injected immediately after delivery with glucose or glucose plus mannoheptulose, and the time-courses of liver glycogen, plasma glucose insulin and glucagon concentration were studied. The administration of glucose prevented both liver glycogenolysis and the increase in plasma glucagon concentration, which normally occurs immediately after delivery. In addition, the administration of glucose prevented the decrease of plasma glucose and insulin concentration which normally occurs during the first hour of extrauterine life. Supplementation of glucose with mannoheptulose prevented the increase of plasma insulin concentrations caused by the administration of glucose; liver glycogenolysis, however, was not stimulated in these circumstances. The increase in the rate of glycogenolysis caused by the administration of glucagon was prevented in newborn rats previously treated with glucose. These results suggest that glucose exerts an inhibitory effect on the stimulation of neonatal liver glycogenolysis by glucagon.

Animals↗
PubMed1980

Prematurity in the rat. II. Effect of hypothermia.

The time-courses of liver glycogen, plasma glucose, lactate, alanine and glycerol concentrations in term and preterm rats undergoing hypothermia (30 degrees C) during the first 2 h after delivery have been studied. Hypothermia prevented liver glycogenolysis and the neonatal decrease of plasma glucose concentration in term and preterm rats during the first 2 h after delivery. Hypothermia decreased plasma glucose, lactate and alanine utilization but increased plasma glycerol concentration. These results suggest that hypothermia blunts the utilization of the main metabolic substrates but increases brown adipose tissue lipolysis for thermogenesis.

Adipose Tissue, Brown↗
PubMed1979

Regulation of ketogenesis during the suckling-weanling transition in the rat. Studies with isolated hepatocytes.

The rates of ketogenesis from endogenous substrates, butyrate or oleate, have been measured in isolated hepatocytes from suckling and weanling rats. Ketogenesis from endogenous substrate and from oleate decreased on weaning, whereas the rate from butyrate remained unchanged. It is concluded that the major site of regulation of ketogenesis during this period of development involves the disposal of long-chain fatty acyl-CoA between the esterification and beta-oxidation pathways. Modulators of lipogenesis [dihydroxyacetone and 5-(tetradecyloxy)-2-furoic acid] did not alter the rate of ketogenesis in hepatocytes from suckling rats, and it is suggested that this is due to the low rate of lipogenesis in these cells. Hepatocytes from fed weanling rats have a high rate of lipogenesis and evidence is presented for a reciprocal relationship between ketogenesis and lipogenesis, and ketogenesis, and esterification in these cells. Dibutyryl cyclic AMP stimulated ketogenesis from oleate in hepatocytes from fed weanling rats, even in the presence of an inhibitor of lipogenesis [5-(tetradecyloxy)-2-furoic acid], but not in cells from suckling rats. It is suggested that cyclic AMP may act via inhibition of esterification and that in hepatocytes from suckling rats ketogenesis is already maximally stimulated by the high basal concentrations of cyclic AMP [Beaudry, Chiasson & Exton (1977) Am. J. Physiol. 233, E175--E180].

Animals↗
PubMed1979

Long-term effect of glucagon administration on rat liver L-type pyruvate kinase.

After 5 h of treatment with glucagon, liver L-type pyruvate kinase (ATP: pyruvate 2-0-phosphotransferase; EC 2.7.1.40) showed a significant decrease of K0.5 and the Hill coefficient (nH) in the absence of fructose 1,6-diphosphate. However, in the presence of fructose 1,6-diphosphate, liver enzymes from treated rats showed a slight decrease of K0.5 but nH remained unchanged. In both circumstances, no changes of Vmax were observed after treatment. These changes in the kinetic properties of liver L-type pyruvate kinase are consistent with the dephosphorylation of the enzyme caused by insulin release in response to treatment with glucagon.

Animals↗
PubMed1978

Evidence for a reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed virgin and lactating rats.

Lipogenesis is increased in hepatocytes from fed lactating rats compared with virgin rats. Inhibition of lipogenesis with 5-(tetradecyloxy)-2-furoic acid resulted in increased ketogenesis from endogenous substrate, but not from oleate. Dihydroxyacetone increased ketogenesis from endogenous substrate, but not from oleate. Dihydroxyacetone increased lipogenesis and esterification of [1--14C]oleate and decreased ketogenesis; these changes were reversed by the inhibitor. The reciprocal relationship between lipogenesis and ketogenesis in hepatocytes from fed rats may be due to alterations in [malonyl-CoA] [McGarry, Mannaerts & Foster (1977) J. Clin. Invest. 60, 265--270; Cook, King & Veech (1978) J. Biol. Chem. 253, 2529--2531], but this mechanism is not considered to be sufficient to explain the increased ketogenesis in starvation completely.

Animals↗
PubMed1978

Changes in the liver lactate dehydrogenase isozyme profile after induced glycogenolysis.

Treatment with cystamine, phlorrhizin or nicotinic acid, which induced liver glycogenolysis, resulted in the increase of liver lactate dehydrogenase activity. This increase was counteracted by the administration of cycloheximide or actinomycin D and coincided with the increase os isozymes 4 and 3 and the decrease of isozyme 5. The enhancement of liver lactate dehydrogenase activity and the changes observed in the isozyme profile were similar to those observed after starvation. These results suggest that the changes in the lactate dehydrogenase isozyme profile found after cystamine, phlorrhizin or nicotinic acid administration may be related to the glycogenolytic effect of these compounds. These result in an adaptation of the liver lactate dehydrogenase to gluconeogenesis.

Animals↗
PubMed1978

Stimulation of ketogénesis after glycogen depletion by nicotinic acid in perfused rat liver.

Treatment with nicotinic acid produced an enhancement of ketone bodies production from endogenous, substrates, either oleate or octanotate. The enhancement was accounted for by an increase of acetoacetate synthesis. These results suggest that the increase of acetoacetate production may be due to the enhancement of extramitochondrial ketogenesis as a consequence of the inhibition of lipogenesis.

Animals↗
PubMed1976

Pyruvate kinase activity and gluconeogenesis in rat liver after glycogen depletion with nicotinic acid.

Nicotinic acid administration, which depletes liver glycogen, leads to an increase of both pyruvate kinase L and phosphoenolypyruvate carboxykinase in liver by a factor of nearly two. The former is not prevented by either cycloheximide or actinomycin D. L-Cysteine, an allosteric inhibitor of pyruvate kinase L, favors gluconeogenesis from lactate in both nicotinic acid treated and starved animals.

Animals↗