Biomedical subjects

L Picon

Publications and source records attributed to L Picon.

At least 73 records · Page 4Linked to original sources

PubMed1985

Lipogenesis as related to endocrine control of adipose cellularity in the rat.

The incorporation rate of 3H from 3H2O in the total lipids of rat retroperitoneal adipose tissue (RPAT) according to age was followed in slightly hyperthyroid rats, in type-2 diabetic rats and in control rats. Until 12 weeks of age, the RPAT of the hyperthyroid animals exhibited hyperplasia and an increase in lipogenesis per g of wet weight or per whole fat pad. Fat cel number and lipogenesis per g of wet weight or per whole fat pad were reduced in adult diabetic rats. The concomitant changes in fat cell number and lipid synthesis in the RPAT of the two groups of treated rats have been discussed.

Adipose Tissue↗

PubMed1985

Insulin and glucagon during the perinatal period: secretion and metabolic effects on the liver.

Insulin and glucagon are detected in the plasma of most species early in gestation. In the fetus at term, insulin and glucagon secretion can be modified by long-term changes in glucose concentration but the responsiveness of A and B cells to glucose is lower than in the adult. The plasma insulin/glucagon molar ratio is high in the fetus at term, then decreases dramatically immediately after birth and remains low during the first hours of extrauterine life. This situation results in favored hepatic glycogen storage and prevented gluconeogenesis in utero, and sharp glycogen breakdown and active gluconeogenesis during the early postnatal period.

Animals↗

PubMed1985

Effects of gestational hyperglycemia on glucose metabolism and its hormonal control in the fasted, newborn rat during the early postnatal period.

To evaluate the effects of gestational hyperglycemia on glucose metabolism and its regulation in the fasted rat during the early postnatal period, unrestrained rats were continuously infused with glucose during the last week of pregnancy. Control rats were infused with distilled water. Newborns were studied during the first six postnatal hours. At birth, newborns from glucose-infused rats, compared with controls, showed higher plasma glucose levels, increased plasma insulin, and lower plasma glucagon and catecholamine concentrations. Between birth and 2 h postpartum, newborn rats from both groups exhibited a marked hypoglycemia, which was, however, more severe in newborns from glucose-infused rats (15 mg/dl) than in controls (26 mg/dl). During the first four postnatal hours, plasma insulin concentration remained higher, while plasma glucagon and catecholamine concentrations remained lower in newborns from hyperglycemic rats. At 6 h, the glycemia reached normal values and the concentrations of the different hormones were similar in controls and newborns from glucose-infused mothers. Concurrently, in the newborns from glucose-infused rats, hepatic glucose production was altered, as they were unable to mobilize liver glycogen stores during the six postnatal hours. Despite slightly delayed phosphoenolpyruvate carboxykinase induction, the rate of gluconeogenesis from 10 mmol/L lactate estimated on isolated hepatocytes was higher in newborns from hyperglycemic mothers than in controls. These results show that gestational hyperglycemia compromises the metabolic and hormonal adaptation of the newborn rat to early extrauterine life; the striking feature of these neonates is the absence of mobilization of liver glycogen stores, which can probably be explained by fetal and neonatal hyperinsulinism associated with the defect of counterregulatory hormones.

Age Factors↗

PubMed1984

Effects of thyroid hormones on adipose tissue development in Sherman and Zucker rats.

It has been reported that mild hyperthyroidism in the young Sherman rat induces adipose tissue hyperplasia, concomitant with cell size reduction, and that hypothyroidism induces opposite effects. The present experiments were designed to study the evolution of cellularity in retroperitoneal and epididymal adipose tissue during a long term thyroxine (T4) treatment or in T4-treated rats, after the treatment had been stopped. In both cases, hyperplasia was transient with the observation that the adipocyte number observed in 3-mo-old control rats was reached earlier in T4-treated rats. In hypothyroid rats, hypoplasia was also transient, because once the treatment was stopped, the cell number overtook that of controls. Zucker rats were also treated with T4, because hypoplasia has been observed in young obese (fa/fa) rats and these rats are reported to be hypothyroid. T4 treatment increased their adipocyte number up to the level of nonobese (Fa/fa) untreated rats, while hypertrophy, although reduced, was persistent. In Sherman and Zucker rats, adipose tissue lipoprotein lipase activity was decreased by T4 treatment in parallel with and perhaps because of adipocyte size reduction. We suggest that hyperplasia induced by thyroid hormones results from a precocious differentiation of preadipocytes and does not necessarily imply an increased preadipocytes multiplication.

Adipose Tissue↗

PubMed1984

Glucagon secretion in rats with non-insulin-dependent diabetes: an in vivo and in vitro study.

Non-insulin-dependent diabetes ( NIDD ) was obtained in adult rats following a neonatal streptozotocin injection. Rats with NIDD exhibited a chronic low-insulin response to glucose in vivo, slightly elevated basal plasma glucose values (less than 2 g/l) and low pancreatic insulin stores (50% of the controls). Glucagon secretion was studied in this model, in vivo and in vitro using the isolated perfused pancreas technique. Normal basal plasma glucagon levels were observed in the fed state and were in accordance with normal basal glucagon release in vitro. The pancreatic glucagon stores were normal in the diabetics. In experiments with the perfused pancreas, the increased glucose concentration suppressed glucagon release as readily in the diabetics as in the controls. Moreover 5.5 mM glucose suppressed glucagon release stimulated by 19 mM arginine to the same extent in both groups. These data indicate that the suppression of A cell function by glucose is normal in rats with NIDD . Theophylline and isoproterenol also produced normal glucagon release in diabetics. By contrast, the glucagon secretion in response to arginine was lower in the diabetics. This was observed either in vivo (arginine infusion) or in vitro in the presence or the absence of glucose in the perfusate. But in the presence of theophylline the response to arginine was normalized in the diabetics. Impairment of A cell function of the diabetics is not limited to recognition of amino-acids, since acetylcholine evoked a lower glucagon response in the diabetics than in the controls. These defects are different from those described in their B cells.

Animals↗

PubMed1983

Experimental hypothalamic or genetic obesity in the non-insulin-dependent diabetic rat.

Non-insulin-dependent diabetes was obtained in adult rats by neonatal administration of streptozotocin (100 mg/kg). Obesity was obtained in the same animals either by a ventromedial hypothalamic lesion in adult non-insulin-dependent diabetic Wistar rats, or by using genetically obese Zucker rats. In diabetic rats, weight gain was similar to that in non-diabetic rats, whether hyperphagia was due to a ventromedial hypothalamic lesion or to a genetic factor. Glucose-induced insulin release in vivo was increased in obese diabetic rats compared with non-diabetic rats. Despite this enhanced insulin secretion, both diabetic 'fatty' Zucker rats and diabetic rats with hypothalamic obesity showed a deterioration of glucose tolerance. Moreover, about one-third developed overt diabetes with permanent or transient glycosuria. We conclude that when insulin-deficient rats are made hyperphagic, they are able to increase their insulin secretion and become obese. In some of these animals the occurrence of obesity aggravates the diabetes. The obese diabetic rat appears to be a suitable laboratory model for the study of the relationship between obesity and diabetes.

Animals↗

PubMed1983

Hyperglycaemia induced by glucose infusion in the unrestrained pregnant rat: effect on body weight and lipid synthesis in post-mature fetuses.

Mild hyperglycaemia was induced in unrestrained pregnant rats from day 20.5 to day 23.5 of pregnancy, using a continuous glucose infusion. Control rats were infused with distilled water. In post-mature fetuses from glucose-infused rats, raised plasma glucose and insulin concentrations were related to increased body weight (6.03 +/- 0.07 g) and total carcass fat (2.02 +/- 0.04% of fresh weight) compared with control fetuses of the same age (5.35 +/- 0.07 and 1.5 +/- 0.04 g, respectively). Concurrently, the rate of lipogenesis in the carcass, estimated from the incorporation of tritium from tritiated water into fatty acids, was significantly increased in fetuses from glucose infused rats compared with control rats (6.00 +/- 0.34 versus 2.62 +/- 0.27 and 3H2O X h-1 X g tissue-1, respectively.

Animals↗

PubMed1983

Decreased glucagon-stimulated cyclic AMP production by isolated liver cells of rats with type 2 diabetes.

This study was undertaken to investigate the effect of experimental type 2 diabetes in the rat on the insulin and glucagon receptors and on the early steps of glucagon action. The binding of insulin and glucagon and the glucagon-stimulated cyclic AMP accumulation in the presence of a phosphodiesterase inhibitor (IBMX, 0.1 mmoles/l) were studied in liver cells isolated from 7-9-month-old rats with chronic type 2 diabetes and from control rats. No significant change was observed in [125I] insulin binding and [125I]glucagon binding of diabetic liver cells as compared to controls. Scatchard analysis of the competition experiments indicated that affinity and number of insulin and glucagon receptors were not significantly changed in the liver cells of diabetic rats. The basal cyclic AMP level was significantly lower in the diabetic hepatocytes (2.3 +/- 0.9 pmoles/10(6) cells) than in the controls (4.0 +/- 0.6 pmoles/10(6) cells). Cyclic AMP response to physiological concentrations of glucagon (0.1-1 nmoles/l) was about 2 times lower in the diabetic hepatocytes than in the controls. Furthermore, the basal liver membrane adenylate cyclase activity and the fluoride-activatable adenylate cyclase activity were about 2 times lower in the diabetics as compared to control rats, while the liver cyclic AMP and cyclic GMP phosphodiesterase activities were unchanged. The ability of glucagon to stimulate liver membrane adenylate cyclase over a 10(-12)-10(-6) M concentration range was decreased in diabetic rats. Taken together, these data are consistent with the thesis that the impairment of the liver cyclic AMP response to glucagon in rats with type 2 diabetes is caused by a decrease in the amount of adenylate cyclase in the liver plasma membranes.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1983

Glucose insensitivity and amino-acid hypersensitivity of insulin release in rats with non-insulin-dependent diabetes. A study with the perfused pancreas.

Non-insulin-dependent diabetes (NIDDM) was obtained in adult rats following a neonatal streptozotocin injection. Rats with NIDDM exhibited slightly lowered plasma insulin, slightly elevated basal plasma glucose values (less than 200 mg/dl), and low pancreatic insulin stores (50% of the controls). Insulin secretion was studied in this model using the isolated perfused pancreas technique. Insulin response to glucose stimulation over the range 5.5-22 mM was lacking, thus indicating complete loss of B-cell sensitivity to glucose. Even in presence of theophylline, the B-cells remained insensitive to glucose. In contrast, glyceraldehyde elicited an insulin release as important as that obtained in the control pancreata. This could possibly suggest that the B-cell dysfunction in rats with NIDDM involves a block in glucose metabolism in the early steps of glycolysis prior to the triose-phosphate. Mannose stimulated insulin secretion less in the diabetics than in the controls. The insulin secretion obtained in response to isoproterenol indicated that the ability of the adenylcyclase to generate cAMP in the B-cells of the diabetics was not decreased. The insulinotropic actions of acetylcholine and tolbutamide were normal and increased, respectively, as compared with the controls. In the absence of glucose, the B-cells of the diabetics were unexpectedly hypersensitive to arginine and leucine. The alpha-ketoisocaproate effect in the diabetics was not significantly different from that obtained in the controls. The possibility that enhancement of insulin response to leucine in the diabetics might be related to a more active conversion of leucine to ketoisocaproate along the first steps of intraislet leucine metabolism is proposed.

Acetylcholine↗

PubMed1983

[Maternal hyperglycemia and fetal development in the rat: effects of a continuous glucose perfusion in the rat at the end of gestation].

Continuous glucose infusion was used to induce mild hyperglycemia in unrestrained pregnant rats during the last three days of pregnancy. Control rats were infused with distilled water. Compared with the controls, fetuses from glucose-infused rats showed higher plasma glucose levels, increased plasma insulin and lower plasma glucagon concentrations. Pregnancy prolonged until day 23.5 resulted in a sharp decrease in plasma insulin concentrations and a dramatic increase in plasma glucagon concentrations. In 23.5-day old fetuses from both groups, plasma insulin concentration rose when phentolamine was injected but not when propanolol was injected. Plasma glucagon concentration in 23.5-day old fetuses from glucose-infused rats dropped with propanolol injection. In fetuses from control rats, liver phosphoenolpyruvate activity increased markedly and liver glycogen stores decreased sharply. In fetuses from glucose-infused rats, liver phosphoenolpyruvate carboxykinase activity rose and glycogen content decreased, but to a lesser degree. Moreover, in postmature fetuses from glucose-infused rats, elevated plasma glucose and insulin concentrations were related to increased body weight and total carcass fat. Concurrently, the rate of lipogenesis in the carcass of these fetuses (estimated from the incorporation of 3H from 3H2O into fatty acids) was significantly increased.

Animals↗

PubMed1982

Effect of diet on glucose tolerance and insulin response in chemically diabetic rats.

The long term effect of dietary carbohydrate content on the course of noninsulin-dependent diabetes has been assessed in rats with experimental chemical diabetes (CD) obtained as spontaneous evolution of neonatal streptozotocin acute diabetes. Glucose tolerance and insulin secretion were serially tested before and during high carbohydrate diet (2 and 6 mo) or high lipid diet (1 mo) in control and in CD males. In none of the control or CD groups, did the high sucrose diet significantly affect the weight gain as compared to that obtained upon the standard diet. The high sucrose diet increased the insulin response to glucose and slightly improved the glucose tolerance in the normal rats. In CD rats, it increased the insulin secretion and the insulinogenic index; glucose tolerance was unaffected. In control rats receiving the high lipid diet, the weight gain was significantly increased as compared to that obtained upon the standard diet. Their plasma insulin levels were increased both in basal and glucose stimulated states while glucose tolerance remained unchanged. In the CD rats receiving the high lipid diet, weight gain was significantly increased as compared to that obtained upon the standard diet. But in these CD rats, the insulin secretion was not significantly enhanced by the high fat diet and the glucose tolerance deteriorated. These findings indicated a beneficial long-term effect of high carbohydrate diet in the CD rats as far as their insulin response to glucose was concerned. By contrast high lipid diet may be regarded as an aggravating factor of glucose handling in chemical diabetes. The results are discussed with regard to; (1) the increased insulin production and/or release on the high sucrose diet, and (2) the decreased insulin sensitivity on the high lipid diet.

Animals↗

PubMed1982

Plasma corticosterone during perinatal period in postmature rats.

In the fetal rat, plasma corticosterone concentration (PCC) decreases dramatically on the 20th day of gestation and remains low until birth even if the parturition is delayed until 23.5 days postcoitus. In the normal term newborn, there is an increase of PCC in the 1st h after birth. In postmature newborn rats this increase is not present but PCC can be increased towards normal term values if the adrenal cortex is stimulated with cosyntropin or lysine-vasopressin. This suggests that the lack of elevation of PCC in the postmature newborn is not due to the lack of responsiveness of the adrenal cortex but rather an impairment of the hypophyseal stimulation. The absence of PCC elevation at birth could contribute to the metabolic disorders observed in the postmature newborn rat.

Animals↗

PubMed1982

Experimental chemical diabetes and pregnancy in the rat. Evolution of glucose tolerance and insulin response.

The effect of pregnancy on the course of experimental chemical diabetes (CD) has been studied in the rat. Glucose tolerance tests (0.5 g/kg i.v.) have been performed serially in the virgin state (2 mo), late pregnancy (20.5 day of gestation), and 1 and 2 mo after delivery, in control and in CD female rats. During gestation in the controls basal plasma glucose is decreased, and plasma glucose levels after glucose load, and also lower than levels found in the virgin state. Glucose tolerance is not significantly affected. Nevertheless, glucose-induced insulin secretion in pregnant animals is increased compared with the virgin state. Glucose tolerance remains unchanged 1 and 2 mo postpartum, but insulin response to glucose becomes significantly lower than in the virgin state. In the pregnant CD rats basal plasma glucose is decreased, but plasma glucose levels after glucose load are similar to values found in the virgin state, thus suggesting decreased glucose tolerance. Glucose-induced insulin secretion is increased compared with the virgin state. Glucose tolerance remains deteriorated 1 and 2 mo postpartum, but insulin secretion is no longer significantly different. These findings indicate that in CD female rats glucose tolerance is and remains deteriorated by pregnancy, while in normal female rats it is and remains unchanged. Thus, despite increased insulin response to glucose during late gestation in the CD rats, the diabetogenicity of pregnancy is confirmed with this experimental model.

Animals↗

PubMed1982

Insulin treatment improves the spontaneous remission of neonatal streptozotocin diabetes in the rat.

Neonatal rats injected with streptozotocin (STZ, 100 mg/kg) at birth exhibit an acute diabetes that is characterized by a spontaneous and incomplete remission. The short- and long-term effect of exogenous insulin on the course of this neonatal diabetes has been studied. Insulin treatment (20 mU/g body wt./day, for 4 days) diminished the percentage of glycosuric animals on day 5 after birth (10%) as compared with the percentage in the non-insulin-treated diabetics (STZ) (67%). On the 14th day, the body weight and the pancreatic insulin content of insulin-treated animals (STZ + I) were significantly higher than the corresponding values in the STZ animals. Glucose tolerance tests performed sequentially indicated that from 21 days to 7 mo, the plasma insulin response in the (STZ + I) females was clearly increased as compared with that observed in the STZ group. However, it did not reach the insulin response of the controls except in the 21-day-old females and, as a function of age, it declined progressively at variance with the normal age-related pattern. These findings indicate that insulin treatment (sufficient to reduce daily glycosuria) applied during the overtly diabetic period markedly improved the recovery of the insulin stores in the pancreas. Moreover, the long-term effect of the treatment was a long lasting if not permanent improvement of the in vivo insulin response to glucose.

Aging↗

PubMed1981

[Disparity between the effect of glucose and arginine on insulin secretion from the perfused pancreas of non insulin dependent diabetic rats].

Insulin secretion was evaluated with the isolated perfused pancreas in a Rat model of non insulin-dependent diabetes (type II diabetes). In the diabetic Rats, pancreatic insulin stores were twice as low as in the controls. The amount of insulin release was expressed as a percentage of the insulin content in each pancreas. With perfusate glucose at 5.5 mM, the basal insulin secretion in the diabetics was not significantly different from that in the controls. With perfusate glucose at 16.2 mM, the diabetic pancreases exhibited 2 distinct patterns of response: in some Rats the insulin output expressed as a percentage of the insulin content of the pancreas was not different from the controls, while in the others there was no response to glucose. By contrast, with arginine (19.2 mM) the response was decreased to the same extent in all the diabetics. Thus some diabetic Rats exhibit a selective functional defect concerning the response to glucose contrasting with the preservation of the basal insulin release and of the response to arginine.

Animals↗

PubMed1981

Effect of early and chronic hypoinsulinism on adipose tissue cellularity in the rat.

The effect of chronic hypoinsulinism on the development of retroperitoneal adipose tissue was studied in rats injected with streptozotocin at birth. The streptozotocin injection induced an acute neonatal diabetes which regressed spontaneously after one week and led to a chronic state of chemical diabetes in the young and in the adult rat. Growth of chemically diabetic rats was normal although the retroperitoneal adipose tissue showed a relative hypoplasia which appeared at two months and evolved with age so that at 10 months the number of adipose cells in the retroperitoneal adipose tissue was largely decreased with respect to control animals (1.34 +/- 0.12 x 10(6) versus 2.23 +/- 0.11 x 10(6)). This relative hypoplasia was still present at 20 months. Whereas the hypoplasia associated with the chemical diabetes was highly reproducible, the mean adipocyte size was modified in a variable manner but was never significantly decreased in chemically diabetic rats. These findings indicate that insulin is involved in the control of retroperitoneal adipose tissue cellularity and suggest that the effect of hypoinsulinism on adipocyte number does not depend on a decrease of the mean adipocyte volume.

Adipose Tissue↗

PubMed1981

Hyperglycaemia induced by glucose infusion in the unrestrained pregnant rat during the last three days of gestation: metabolic and hormonal changes in the mother and the fetuses.

Continuous glucose infusion was used to induced mild hyperglycaemia in unrestrained pregnant rats during the last three days of pregnancy. Control pregnant rats were infused with distilled water. Fetuses were studied after normal or prolonged pregnancy. Fetuses from glucose-infused rats, compared with controls, showed higher plasma glucose levels, increased plasma insulin and lower plasma glucagon concentrations. Pregnancy prolonged until day 23.5 resulted in a rise in the glucagon/insulin ratio from 6.5 to 67 in fetuses from control rats and from 1.3 to 13 in fetuses from glucose-infused rats. Concurrently in fetuses from control rats, liver phosphoenolpyruvate carboxykinase activity increased markedly and liver glycogen stores decreased sharply. In fetuses from glucose-infused rats, liver phosphoenolpyruvate carboxykinase activity rose and glycogen content decreased, but to a lesser extent. These results show that both the A and B cells of the rat fetal pancreas are sensitive to chronic glucose stimulation.

Animals↗

PubMed1981

Histogenesis of the endocrine pancreas in newborn rats after destruction by streptozotocin. An immunocytochemical study.

Endocrine pancreatic tissue in newborn rats was studied 1 to 17 days after the destruction of B cells by an injection of streptozotocin. Regeneration of insulin cells was observed four days after streptozotocin injection, which was followed by recovery from the diabetic state and an increased pancreatic insulin content. Regeneration was characterised by new islets budding from small ducts. The pancreas of newborn rats, like the embryonic pancreas, thus retains a capacity to form endocrine tissue, although some degree of reduplication of preexisting B cells may also be involved in the process. Newborn rats injected with streptozotocin constitute an interesting model for the study of factors which may act on the regenerative potential of pancreatic endocrine tissue in the diabetic state.

Animals↗