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L Aerts

Publications and source records attributed to L Aerts.

At least 37 records · Page 2Linked to original sources
PubMed1991

The effects of maternal diabetes on the offspring.

Diabetes in pregnancy has an influence on the development of the fetus. There are strong indications that the intrauterine diabetic milieu has long-lasting consequences. In the rat, mild diabetes during pregnancy induces decreased insulin secretion in later life, whereas severe diabetes is responsible for insulin resistance. In the human, data are available showing a long-term consequence in the offspring of type I diabetes and gestational diabetes mellitus.

Animals↗
PubMed1991

Absence of pregnancy-induced alterations in tissue insulin sensitivity in the offspring of diabetic rats.

We have previously demonstrated insulin resistance in the liver and peripheral tissues of the adult offspring of rats made diabetic with streptozotocin (SDF rats). In this study, a euglycaemic hyperinsulinaemic clamp was used to test the hypothesis that insulin resistance is further aggravated during pregnancy in SDF rats. Normal pregnancy was accompanied by a decrease in the sensitivity of the liver and peripheral tissues to insulin, with a normal responsiveness to insulin. In SDF rats no further decrease in the sensitivity of peripheral tissues to insulin occurred during pregnancy when compared with non-pregnant rats, and the dose-response curves of the glucose metabolic clearance rate during hyperinsulinaemia were similar in pregnant control and pregnant SDF rats. There was, however, a modest decrease in the sensitivity of the liver to insulin during pregnancy in SDF rats. The normal increase in plasma insulin levels during pregnancy was blunted in SDF rats: this resulted in increased glucose levels in maternal and fetal rats and increased fetal insulin concentrations, features compatible with mild 'gestation diabetes'. In conclusion, gestational diabetes develops in pregnant SDF rats, although there is no further deterioration in peripheral insulin resistance.

Animals↗
PubMed1991

Metabolic alterations in adulthood after intrauterine development in mothers with mild diabetes.

We studied the long-term effects of maternal diabetes mellitus on the offspring of experimentally induced diabetic Wistar rats. When stressed by an intravenous glucose load, the adult female offspring had impaired glucose tolerance and developed gestational diabetes mellitus when pregnant. Our results show that even mild diabetes mellitus induces an abnormal intrauterine milieu that causes morphological and functional changes in fetal development with consequences for later life.

Amino Acids↗
PubMed1991

Morphometric evaluation of B-cell function during glucose infusion in control and hyperresponsive rats.

According to their general appearance, the ultrastructural morphology of their organelles and their functional status, B cells can be divided into dark, unresponsive B cells with condensed mitochondria and narrow RER-cisternae, and pale activated B cells with orthodox mitochondria and distended RER. In control rats, during a three hour glucose infusion experiment, there is a shift from a majority of dark B cells to a majority of pale B cells, and a decrease in the proportion of dark and mixed islets in favour of the pale islets. No degranulation however (dark and light granules) occurs. In adult youngsters of severely diabetic mothers, known to be hyperresponsive to glucose stimulation, a more important mass of pale activated B cells is present in basal conditions, and is not augmented by stimulation. Dark and mixed islets are scarce in these animals and some degranulation occurs. The data illustrate that in control and in hyperresponsive rats, the B cells manage very well, to meet the increasing demand of insulin without any signs of exhaustion or damage. The data confirm in vivo, and at the morphological level, the concepts of functional heterogeneity and of dose-dependent recruitment of pancreatic B cells. Moreover functional heterogeneity of islets is suggested.

Animals↗
PubMed1989

Plasma amino acids in diabetic pregnant rats and in their fetal and adult offspring.

Amino acid profiles and total amino-acid concentrations are established in nonfasting plasma of pregnant control, mildly diabetic and severely diabetic rats, and of their fetal and adult offspring. In pregnant rats at day 20 of gestation plasma amino acids can be regarded as normal in mildly diabetic mothers, but are significantly decreased in severely diabetic mothers. In fetuses of control rats, amino acid levels are twice as high as in the mother (fetomaternal ratio 2.0); in the fetuses of mildly diabetic mothers they are significantly lower than normal (fetomaternal ratio 1.3); in the fetuses of severely diabetic mothers they are also significantly lower than normal but with a normal fetomaternal ratio (fetomaternal ratio 2.0). In adult offspring of mildly diabetic mothers the concentration of almost all amino acids as well as that of total amino acid pool is significantly lower than in the controls; in the offspring of severely diabetic mothers they can be regarded as normal. No specific amino acid or group of amino acids can be held responsible for any of these changes, since all differences with control values display an overall effect, involving all or almost all amino acids.

Amino Acids↗
PubMed1988

The diabetic intrauterine milieu has a long-lasting effect on insulin secretion by B cells and on insulin uptake by target tissues.

From our previous work, it appears that fetal development in the abnormal intrauterine milieu of a mother with diabetes results in impaired glucose tolerance in adult life. In adult Wistar rats that were the offspring of mildly or severely diabetic mothers, in vitro islet stimulation and in vivo insulin uptake studies were undertaken to distinguish between alterations in glucose sensitivity and insulin secretion at the B cell level and alterations in insulin sensitivity and uptake at the level of the peripheral tissues. Insulin output after glucose stimulation by isolated islets was lower than normal in the rats of mothers with mild diabetes and higher than normal in the animals of severely diabetic mothers, confirming the results of previous in vivo studies. Insulin binding by the liver was normal in both groups. Insulin uptake by the kidney was normal in rats with mildly diabetic mothers but was increased in rats of severely diabetic mothers, suggesting decreased uptake of insulin by the peripheral tissues. Impaired glucose tolerance in rats of mildly diabetic mothers, resulting from decreased responsiveness to glucose, is interpreted as a consequence of hyperactivity of these B cells during the intrauterine life. Impaired glucose tolerance in rats of severely diabetic mothers, associated with insulin hypersecretion and decreased insulin uptake by the peripheral tissues might result from intrauterine alterations of the peripheral receptor or postreceptor system induced by the abnormal intrauterine milieu. These data on experimental diabetes in the rat demonstrate that the maternal diabetic environment exerts a diabetogenic influence on the offspring.

Animals↗
PubMed1987

Research priorities in diabetic pregnancy today: the role of animal models.

Strict metabolic control has resulted in a striking fall in the rates for stillbirths, neonatal deaths and neonatal morbidity in diabetic pregnancy. However, clinical problems and challenges for research remain, particularly in relation to a high incidence of congenital malformation, low birth weight, and early growth delay; the detection and management of gestational diabetes; insulin delivery systems; the consequences of maternal hypoglycaemia on organogenesis and fetal well-being; the mechanisms underlying various categories of neonatal morbidity, and possible long-term morbidity in the children born to diabetic mothers. The nature of these problems determines that certain fundamental aspects of reproduction which are difficult to study in human pregnancy will have high priority for research. Progress in this field will be heavily dependent on animal models in the foreseeable future.

Animals↗
PubMed1986

Direct and indirect influences of a 14 days oestradiol-17 beta treatment on the endocrine pancreas of the female rat.

The relationship between the hyperinsulinism induced by 14-days oestradiol treatment and the trophic action of this hormone on the endocrine pancreas was studied. The possible interference of the adrenal glands in these effects of oestradiol was investigated using comparisons between adrenalectomized and/or ovariectomized rats. Oestradiol increased the dry weight of the islets of Langerhans and enhanced total incorporation of [3H] leucine into newly synthetized proteins during a glucose stimulation independently of the presence of the adrenal glands. Conversely, the presence of the adrenal glands was necessary for the expression of the enhancing actions of oestradiol such as the production of insulin hypersecretion, increased insulin biosynthesis and a higher proportion of light granules inside the B cells. These results were in favour of a direct trophic role of oestradiol on the endocrine pancreas, but also of an indirect role of this hormone in the stimulation of the insulin secretion and biosynthesis, mediated by glucocorticoids.

Adrenalectomy↗
PubMed1985

Effect of ritodrine on the maternal and fetal endocrine pancreas of the rat.

Pregnant Wistar rats received four high-dose intramuscular injections of ritodrine per day during the last 6 days of pregnancy. The injections provoked an immediate but transient increase in plasma insulin level, without affecting the plasma glucose concentration. At the end of the treatment, the morphology of the endocrine pancreas and the ultrastructure of the B cells of the ritodrine-treated mothers were similar to those of the control mothers. No lasting influence of the treatment was seen in the fetuses of these rats: body weights, blood glucose and insulin levels, morphology of the endocrine pancreas and ultrastructure of the B cells were all normal.

Animals↗
PubMed1985

Long-term effect of diabetes and pregnancy in the rat.

Islet hyperplasia and B-cell degranulation were found in the fetuses of the third generation from mothers (second generation) born to a diabetic mother (first generation) regardless of the origin of the father, while pancreatic islets were normal in fetuses from control mothers, even when the father was an offspring of a diabetic mother. These data support the hypothesis that in our experimental model overstimulation of the fetal endocrine pancreas results in long-term consequences to the third generation.

Animals↗
PubMed1983

The endocrine pancreas during pregnancy and lactation in the rat.

The percentage of endocrine tissue in the whole pancreas, the volume density of the insulin producing beta-cells, the non-fasting plasma glucose level and the plasma insulin level were studied in pregnant rats and in puerperal lactating and non-lactating rats. During pregnancy there was a progressive rise in the percentage of endocrine tissue, in the volume density of the beta-cells and in the insulin level in peripheral blood. Plasma glucose levels declined during pregnancy. A lower plasma glucose level, a lower plasma insulin level, a lower percentage of endocrine tissue and a lower volume density of the beta-cells was found in lactating compared to non-lactating rats.

Animals↗
PubMed1981

Endocrine pancreas in the offspring of rats with experimentally induced diabetes.

At birth newborn rats from mothers with experimentally induced diabetes show hypertrophy and degranulation of the pancreatic islets. With birth the maternal hyperglycaemic stimulus is removed and during the lactation period the overstimulated B cells can restore their normal secretory activity. The increase of B-cell mass, however, remains retarded for several weeks. By adulthood the endocrine pancreas of offspring from mildly diabetic mothers seems to have recovered from the influence of the abnormal intra-uterine milieu, at least as judged by morphometric examination. In offspring from severely diabetic mothers an increased secretory activity of the individual B cells might be responsible for their sustained hypoglycaemia.

Aging↗
PubMed1980

Immunocytochemical study of the endocrine pancreas in the rat during normal pregnancy and during experimental diabetic pregnancy.

The distribution of different celltypes (A, B, D and PP cells) of the endocrine pancreas was studied in both the normal and in the experimental diabetic non-pregnant and pregnant rat. In the normal rat the head (juxta duodenal part) of the pancreas contained more PP cells than the tail (12.5 +/- 1.1 versus 5.2 +/- 2.2) but fewer glucagon cells (19.0 +/- 3.5 versus 14.3 +/- 3.6). This difference disappeared during pregnancy, when the total B cell mass increased (2.05 versus 0.82). In the diabetic rat no difference was found in the number of endocrine cells between the tail and the juxta duodenal part of the pancreas. Unlike the non-diabetic rat, the number of B cells did not increase in the pancreas of the pregnant diabetic rat. An absolute increase in the number of glucagon (A) cells was demonstrated in the islets of the pregnant diabetic rat as compared to the non-diabetic rat (35 versus 21.2).

Animals↗
PubMed1980

Effects of treatment with progesterone and oestradiol-17 beta on the endocrine pancreas in ovariectomized rats: ultrastructural variations in the B cells.

The effects of progesterone and/or oestradiol treatment on the ultrastructural appearance of the pancreatic B cells has been studied in ovariectomized Wistar rats. A morphometric examination of the numberical density of dark and high granules in the B cells was therefore performed in each group of experimental rats as well as in control (olive oil-injected) rats. In the oestradiol-treated rats, and especially in the rats with combined oestradiol/progesterone treatment, the proportions of light and dark granules in the pancreatic B cells changed, compared with control values, in favour of the light granules. This increase in light granule content was comparable to changes in B cells during a pregnancy and it is suggested that the secretory activity of the B cells increases during pregnancy in a manner similar to that seen during oestradiol treatment.

Animals↗
PubMed1979

Morphological changes in the endocrine pancreas in pregnant rats with experimental diabetes.

This present study has demonstrated that during normal pregnancy in the rat the number of beta-cells is increased (hyperplasia) and the volume of the individual beta-cells is increased (hypertrophy). During experimental diabetes, however, the endocrine pancreas has an impaired capacity to compensate during pregnancy. In the experimental diabetic pregnant rat the beta-cells cannot replicate due to the unfavourable metabolic environment. This could reflect the complications caused by diabetes during human pregnancy.

Animals↗