Search PubMed⌕ Search

Biomedical subjects

A B Steffens

Publications and source records attributed to A B Steffens.

At least 73 records · Page 4Linked to original sources
PubMed1986

Meal-induced increases in parasympathetic and sympathetic activity elicit simultaneous rises in plasma insulin and free fatty acids.

The aim of this study was to investigate sympathetic and parasympathetic activity during food intake in rats by measuring plasma norepinephrine (NE), epinephrine (E), insulin, free fatty acids. (FFA), glycerol and blood glucose. Therefore male Wistar rats were implanted with silastic jugular vein cannulas so that blood could be withdrawn from freely moving animals. Blood samples were frequently taken before, during and after intake of a test meal. The effects of the blood sampling procedure on above mentioned blood compounds was also determined. Insulin increased considerably within the first minutes of food intake before a rise in blood glucose which is mediated by a vagal mechanism. An increase in plasma NE could be observed during the whole period of ingestive behavior whereas E increased considerably only in the first minute. Plasma FFA level was augmented sharply during food intake and a few minutes afterwards, whereas plasma glycerol levels did not change. After termination of food intake sympathetic activation disappeared and both plasma FFA and glycerol levels declined significantly below levels as observed in control rats. In contrast, plasma insulin and blood glucose increased considerably. It is concluded that food intake in rats causes a simultaneous increase in both sympathetic and parasympathetic activity and because of that a rise in plasma FFA and insulin respectively. It is argued that augmented sympathetic activity elicits a rise in plasma FFA levels, which is not mediated by increased lipolysis but by either decreased FFA utilization or reduced reesterification.

Animals↗
PubMed1986

Autonomic innervation of the pancreas in diabetic and non-diabetic rats. A new view on intramural sympathetic structural organization.

Using histochemical and immunocytochemical methods the intramural neural tissue of the pancreas was investigated in non-diabetic and in alloxan-diabetic rats. It was demonstrated that the non-diabetic pancreas contains an average of 2.71 cells/mm3 tissue that react positive for activity of acetylcholinesterase and 2.38 cells/mm3 tissue that show monoamine oxidase activity. Both cholinergic and monoaminergic cells are found as solitary cells and in clusters of various sizes. All these cells are embedded in the exocrine tissue. Both histochemical methods revealed the presence of intra-insular fiber plexuses. Treatment with alloxan resulted in disappearance of intra-insular cholinergic and monoaminergic activity and also in a 68% reduction of the cholinergic cells and 54% of the monoaminergic cells in the diabetic pancreas. Application of immunocytochemical methods employing antibodies against norepinephrine and dopamine demonstrated the noradrenergic character of at least some of the monoaminergic cell groups. It is discussed how the present data and data from previous innervation studies provide evidence for an intramural ganglionic organization of the sympathetic innervation of the rat pancreas.

Acetylcholinesterase↗
PubMed1985

The course of paraventricular hypothalamic efferents to autonomic structures in medulla and spinal cord.

By application of the anterograde transport technique of Phaseolus vulgaris leuco-agglutinin the descending autonomic projection of the paraventricular hypothalamic nucleus was investigated. The Phaseolus lectin technique allowed the detection of the cells of origin in the paraventricular PVN, the precise position of two distinct descending axon pathways and the detailed morphology of terminal structures in midbrain, medulla oblongata and spinal cord.

Animals↗
PubMed1985

Interference of the nutritional condition of the rat with peripheral glucose regulation determined by CNS mechanisms.

Glucose and insulin levels of the cerebrospinal fluid (CSF) were changed by an infusion of either glucose, insulin or a mixture of glucose and insulin in the third ventricle of freely moving undisturbed rats. Before, during and after infusions venous blood samples were withdrawn to determine insulin- and glucose concentrations. In rats on carbohydrate rich food neither plasma insulin nor blood glucose changed during infusion of either glucose, insulin or a mixture of both. However, in rats on carbohydrate free food an immediate decline in blood glucose of about 7 mg/dl occurred 15 min after the start of the infusion. During infusion of a mixture of glucose and insulin, blood glucose rose slightly and reached a value which was in between those attained when glucose and insulin were infused separately. Plasma insulin did not change following central infusions. It is argued that the central nervous system (CNS) is sensitive to changes in CSF levels of glucose and insulin and affects peripheral glucose homeostasis mainly by changing glucose output from the liver. This action of the CNS, however, is dependent on the nutritional condition of the animal.

Animals↗
PubMed1984

Hypothalamically-induced insulin release and its potentiation during oral and intravenous glucose loads.

Male Wistar rats were provided with bilateral cannulas in the lateral hypothalamic area (LHA) and cannulas in the left and right jugular vein. Freely moving rats provided in this way with cannulas were infused with transmitters in the LHA and with various substances in the blood circulation during simultaneous sampling of blood without disturbing the animals. Infusion of norepinephrine (NE) in the LHA resulted in increased insulin levels while plasma glucagon and blood glucose were nearly not affected. This LHA mediated insulin release was suppressed by atropine injection in the blood circulation suggesting a vagal contribution to the observed phenomenon. Administration of either an oral or i.v. glucose load during noradrenergic stimulation of the LHA elicited an exaggerated insulin response when compared to their controls. This LHA potentiated insulin response during an oral and i.v. glucose load could be suppressed by atropinization of the rats. It is concluded that meal-related stimuli are relayed to the NE-stimulated area of the LHA and that these stimuli modulate the output from this area of the LHA that is concerned with the release of insulin.

Animals↗
PubMed1984

Preganglionic innervation of the pancreas islet cells in the rat.

The position and number of preganglionic somata innervating the insulin-secreting beta-cells of the endocrine pancreas were investigated in Wistar rats. This question was approached by comparing the innervation of the pancreas of normal rats with the innervation of the pancreas in alloxan-induced diabetic animals. The presumption was made that alloxan treatment destroys the beta-cells of the islet of Langerhans and results in a selective degeneration of the beta-cells innervation. Cell bodies of preganglionic fibers innervating the pancreas were identified by retrograde transport of horseradish peroxidase following pancreas injections. It was found that 25% of the cells innervating the pancreas in the left dorsal vagal motor nucleus, 50% of the cells in the ambiguous nucleus and 50% of the cells innervating the pancreas, that originate in segments C3-C4 of the spinal cord, fail to become labeled after alloxan treatment. The position and distribution of these cell groups are described in detail and are assumed to be involved in preganglionic beta-cell innervation. A second cell population in the ventral horn and intermediolateral column of the segments T3-L2 of the cord also was labeled in normal rats and was not affected by the alloxan treatment. These thoracic cell groups are thus considered as sympathetic preganglionic somata that maintain direct connections to the pancreas. Additional preliminary information is presented dealing with the general aspects of sympathetic and parasympathetic organization of the pancreas innervation.

Acetylcholinesterase↗
PubMed1984

Circulating free fatty acids, insulin, and glucose during chemical stimulation of hypothalamus in rats.

The aim of this study was to investigate plasma free fatty acids (FFA), insulin, and blood glucose during chemical stimulation of the lateral and ventromedial hypothalamic areas (LHA and VMH) in rats. Therefore male Wistar rats were implanted with bilateral cannulas in the LHA or the VMH and into the left and right jugular veins. Freely moving rats were then infused into the LHA and VMH with norepinephrine (NE), epinephrine (E), or acetylcholine or intravenously with NE or E. Before, during, and after the infusions, simultaneous blood samples were taken without disturbing the animals. Infusion of NE into the LHA resulted in a decrease of plasma FFA and a simultaneous increase of insulin. NE infusion in the VMH elicited an increase of plasma FFA, plasma insulin, and blood glucose. E infusion into the LHA did not lead to a change of plasma FFA, whereas insulin and glucose showed an increase. E infusion into the VMH evoked increases of plasma FFA and insulin. Peripheral administration of NE led to a sharp increase of FFA, whereas plasma insulin and blood glucose did not change. E in the periphery elicited an augmentation of plasma FFA and blood glucose and a suppression of insulin during infusion. After termination of E infusion, plasma FFA and glucose levels decreased, whereas plasma insulin showed a sharp increase.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1983

Influence of peripheral and intracerebroventricular glucose and insulin infusions on peripheral and cerebrospinal fluid glucose and insulin levels.

There is much evidence that glucose and insulin are related to the regulation of food intake and the maintenance of peripheral glucose homeostasis through actions of the central nervous system. However, evidence concerning the penetration of peripheral glucose and insulin into the cerebrospinal fluid (CSF) and the relationship between both peripheral and CSF glucose and insulin levels is still missing. In the reported experiments it is shown that insulin is present in the CSF (17 +/- 3.6 microU/ml CSF versus 44 +/- 6.0 microU/ml plasma) but that CSF insulin does not follow rises of peripheral insulin to 136 microU/ml plasma during 4.5 hours. On the other hand CSF glucose (55 +/- 3.1 mg/dl CSF) follows rises of peripheral glucose levels with a delay of about 30 min. Increase of CSF glucose by infusing glucose into the third brain ventricle elicits a prolonged decrease in peripheral glucose levels. Infusion into the third ventricle of insulin only does not change peripheral glucose. However, infusion of a combination of insulin and glucose in the third ventricle leads to a gradual increase in peripheral glucose and elicits a disappearance of the decrease in peripheral glucose after glucose only infusion into the CSF. During third ventricle infusion experiments no change in peripheral insulin could be observed. It will be argued that changes in CSF glucose and insulin contribute to maintenance of peripheral glucose homeostasis.

Animals↗
PubMed1981

The modulatory effect of the hypothalamus on glucagon and insulin secretion in the rat.

Rats were provided both with brain cannulas, to permit infusion in the ventromedial and lateral hypothalamic areas (resp. VMH and LH), and with two heart catheters. In this way infusions of fluids and withdrawal of blood could be done in unanesthetized free moving animals. Infusion of norepinephrine (NE) in the VMH elicited glucagon release during the whole period of NE infusion whereas insulin levels did not change. This glucagon release could not be suppressed by alpha- and beta-receptor blockade but it was suppressed by hexamethonium, a blocking agent of signal transmission in peripheral ganglia of the autonomic nervous system. On the other hand, infusion of NE in the LH elicited insulin release during the whole period of NE infusion whereas glucagon levels remained unchanged. It is argued that [1] the sympathetic nervous system is involved in glucagon release, [2] no alpha- and beta-receptor mechanisms are involved during this glucagon release, [3] the parasympathetic nervous system is involved in insulin release during noradrenergic LH stimulation.

Animals↗
PubMed1977

Blood glucose levels in portal and peripheral circulation and their relation to food intake in the rat.

Rats weighing about 450 g were provided with permanent catheters in the portal vein and the right auricle. This method allows blood sampling from the portal and peripheral circulation at the same moment in the nondisturbed unanesthetized rat. In the ad lib condition the portal glucose level was higher than that in the general circulation before, during, and after the meal. After a fast of 22 hr premeal portal vein levels were equal to those of the general circulation. During the meal the portal glucose levels rose to about 150 mg per 100 ml whereas those of the general circulation did not exceed 130 mg/100 ml. Experiments with glucose infusions systemically and intraportally show that, under conditions of mild deprivation, the level of glucose in the portal vein plays no or only a very minor role in the termination of feeding.

Animals↗
PubMed1977

Hypothalamic influence on insulin and glucagon release in the rat.

Blood glucose, plasma insulin, and glucagon levels were measured in undisturbed and free-moving rats. The insulin and glucagon levels rise in the 1st min after the beginning of food ingestion, whereas the glucose level begins to increase only in the 3rd min if carbohydrate-rich food is eaten. This early rise in insulin and glucagon level is also observed under conditions in which carbohydrate-free food is eaten. A similar release of insulin and glucagon can be obtained by injection of 0.1 microgram of norepinephrine into the ventromedial hypothalamus, but the same injection made into the lateral hypothalamus causes release of insulin only, whereas injections in other hypothalamic areas are nearly without effect. Similar injections of isoproterenol did not cause changes in insulin, glucagon, and glucose levels. It is suggested that the early insulin and glucagon responses are of reflex origin and that the ventromedial and lateral hypothalamic areas are relay stations in the reflex pathways. The lack of effect of atropine to block the insulin and glucagon responses to noradrenergic stimulation of the ventromedial hypothalamus indicates that the efferent pathway is not cholinergic.

Animals↗
PubMed1977

Involvement of a humoral factor in regulation of body weight in parabiotic rats.

Excessive food intake and obesity was induced in one member of parabiotic pairs by electrical stimulation (three 30-min sessions/day for 2 wk) of the lateral hypothalamus (LH). The nonstimulated partners reduced spontaneous food intake the fatter the stimulated animals became. This reduced food intake resulted in a decreased body weight, fat content, and fat-free solid body mass. The decrease of food intake was not due to changed social behavior of the obese partner. It must be attributed to transmission of a humoral satiety factor. The very first stimulation of the LH in the stimulated partners resulted in a large increase in blood glucose and glucagon level without much change in the insulin level. These changes in blood parameters were probably due to strong sympathetic arousal. In the nonstimulated animals there were practically no changes in these parameters. One week of fattening resulted in increased basal glucose and insulin levels in the stimulated animals and decreased glucose levels in the nonstimulated partners, in which the basal insulin levels remained nearly normal. Basal glucagon levels were the same in both partners and did not differ from the prefattening situation. At that time during stimulation the obese animals showed a large increase in glucose and glucagon levels and a decrease in insulin level. On the other hand the nonstimulated animals showed a slow gradual increase in glucose and insulin level due to transmission from their fat partners because of the large gradient in these substances between the animals. These phenomena were still more pronounced after 2 wk of fattening. It is tentatively concluded that the humoral satiety factor is neither circulating insulin nor glucagon nor one of the major circulating nutrients.

Animals↗