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A B Steffens

Publications and source records attributed to A B Steffens.

84 records · Page 5Linked to original sources
PubMed1976

Influence of the oral cavity on insulin release in the rat.

Blood glucose and insulin levels were measured in undisturbed and free-moving rats. The insulin level rose in the 1st min after the start of food intake; the glucose level began to increase only in the 3rd min if a fluid carbohydrate-rich food was eaten. The insulin release followed a biphasic pattern. If the same quantity of food ingested orally was injected into the stomach in the same time as the animals needed to complete oral ingestion, delayed insulin release could be seen and the second phase of insulin release was exaggerated. The glucose level, which started to rise in the 3rd min, increased much more than during oral ingestion. With respect to insulin release the same phenomena could be observed if carbohydrate-free fluid food was used instead of carbohydrate-rich fluid food. It is argued that the oral cavity plays a major role in the first phase of insulin release, which in its turn seems to be important in the homeostasis of the blood glucose and insulin levels.

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PubMed1975

Influence of reversible obesity on eating behavior, blood glucose, and insulin in the rat.

Excessive food intake, resulting in extreme obesity, was induced in rats by electrical stimulation (three 30-min sessions per day for 3 wk) of the lateral hypothalamus (LH). Outside the stimulation sessions no voluntary food intake occurred duringthese weeks. In the subsequent recovery period, accurate records of spontaneous feeding were made. Blood levels of glucose, insulin, and free fatty acids (FFA)were determined during the stimulation period as well as the recovery period. Duringfeeding elicited by electrical stimulation of the LH in the obese phase, there was alarge increase in the glucose level. The insulin level, very high in the intervals between the stimulation sessions, showed no change, a small decline, or a large decrease,respectively, during stimulation in the morning, the afternoon, or the night. If food was withheld during stimulation, there was a large increase in the glucose level and alarge decrease in the insulin level. The first spontaneous meal after the termination of stimulation was extremely postponed, viz, until the glucose and insulin levels returned to normal for the first time. The insulin response to the first spontaneous mealwas exaggerated. Although in the following period (about 10 days) a rapid decrease inbody weight occurred, food intake was only minimal. The insulin level was high and the glucose levelsubnormal during that period. The insulin and glucose levels were normal again only after recovery of normal body weight and food intake. It is tentatively concluded that the regulation of body energy stores (body weight) is achieved through the control of food intake by circulating insulin and glucose levels.

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PubMed1975

Rapid insulin release after ingestion of a meal in the unanesthetized rat.

Blood glucose and insulin levels were measured in undisturbed and free-moving rats. The insulin level rises already in the 1st min after the start 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 level is observed also under conditions in which either carbohydrate-free food or even "food" without any caloric value is offered. The smell of food cannot produce this early insulin response. It is concluded that in the rat other factors besides a rise in nutrient content in the blood produce insulin release in the first minutes after food ingestion.

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PubMedDate not supplied

Neuroendocrine factors regulating blood glucose, plasma FFA and insulin in the development of obesity.

A number of neurotransmitters and neuropeptides in the hypothalamus play a role in the control of food intake, metabolism, and body weight. Particularly, noradrenergic mechanisms in several areas of the hypothalamus are involved. Control of peripheral metabolism by the hypothalamus is achieved via autonomic modulation of the function of hepatocytes, adipocytes, and the endocrine cells in the islets of Langerhans. The autonomic control mechanisms ultimately lead to an appropriate shaping of blood glucose, plasma FFA, and insulin profiles to guarantee an adequate flow of nutrients under different physiological situations. Peripheral insulin and glucose can penetrate into the brain where they might affect the function of those brain structures involved in control of food intake, metabolism, and body weight.

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PubMedDate not supplied

Hepatic portal vein cannulation for infusion and blood sampling in freely moving rats.

Chronic portal vein cannulation in the rat is an important technique to study secretory rates of hormones from the endocrine pancreas. Moreover, it can be used for studying the effects of enteric hormones and pharmaca on behavioral and physiological processes. This article contains an extensive description of a cannulation technique of the portal vein that has many advantages over those reported so far in the literature, and that was very successful in several behavioral and physiological studies during the last decade.

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PubMedDate not supplied

Noradrenergic and cholinergic reinnervation of islet grafts in diabetic rats.

Grafted islets become denervated due to the islet transplantation procedure. The aim of the present study was 1) to examine whether islet grafts in the liver, the spleen, and under the kidney capsule in rats become reinnervated following the transplantation and experimental procedures used in our laboratory, 2) whether there is any difference in reinnervation at these different sites, and 3) how these results relate to previous physiological experiments. Isogeneic isolated islets were transplanted into diabetic Albino Oxford rats, resulting in normoglycaemia. After at least 5 wk, graft-receiving organs were removed and several antibodies were employed to detect insulin, neuron-specific proteins, and cholinergic and noradrenergic nerve fibers. Islets in all three receiving organs contained viable insulin-positive B-cells. Neuron-specific enolase (NSE) as well as the growth-associated protein B-50 was observed at all sites. The cholinergic marker choline acetyltransferase (ChAT) was localized in islets grafts at all sites, but with the lowest density in the spleen. Staining for the noradrenergic markers tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) was observed in islet grafts at all sites with the lowest density in grafts under the kidney capsule. All these neurochemical substances were most frequently observed in fibers associated with blood vessels, which may be the route along which nerves grow into the graft. It can be concluded that 1) islet grafts in the liver, in the spleen and under the kidney capsule become reinnervated; 2) the innervation pattern of the islet grafts differs only slightly from that in the control pancreatic islets; and 3) in combination with our previously physiological data, we can conclude that these nerve fibers are, at least partly, functionally active.

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PubMedDate not supplied

Control of insulin secretion and glucose homeostasis in exercising diabetic rats with intrasplenic or kidney subcapsular islet grafts.

This study was designed 1) to investigate mechanisms of insulin secretion during exercise after transplantation of islets in the spleen and under the kidney capsule, and 2) to compare these organs as transplantation site regarding an adequate portal or systemic delivery of insulin and glucose homeostasis during exercise. Diabetic rats were provided with 5 microL isogenic islet tissue in the spleen or under the kidney capsule, which results in normoglycemia, and were submitted to a swimming test. Portal plasma insulin levels were higher than simultaneously sampled systemic insulin levels in the control and in the intrasplenic islet grafted group, but not in the kidney subcapsular islet-grafted group. Plasma portal and systemic insulin levels decreased, and glucose levels increased during exercise in all groups. The exercise-induced increase in levels of catecholamines was larger in systemic than in portal plasma, suggesting catecholamine extraction by the lungs or intestines. The experiments were repeated after removing of adrenal medulla, resulting in nondetectable or very low plasma adrenaline levels. Despite these low adrenaline levels, insulin levels decreased during exercise. The results indicate that 1) the exercise-induced reduction of insulin secretion is not mediated by circulating adrenaline, but is probably under control of the sympathetic nervous system, which could be the result of reinnervation of the transplanted islets. 2) Although a portal-systemic insulin gradient was absent in rats with kidney subcapsular islet grafts, the absence of a difference in glucose homeostasis during exercise between the sites revealed that all investigated sites are preferential to transplant islets.

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