Die Wirkung der Hypophysektomie auf das Zellbild der Inseln bei Ratten und Meerschweinchen

Ferner, Helmut; Tonutti, E

doi:10.1007/bf00334876

Cited by 28 publications

(3 citation statements)

References 9 publications

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“…In addition hyperglueagonaemia might be due to a defect of the ventromedial nucleus of the hypothalamus in diabetic mice as described for hyperphagia and hyperinsulinism [5]. Hypophysectomy in dogs [6] and in rats [8] ultimately results in hyperplasia of alpha cells. In agreement with Samols et al…”

Section: H Laube Et Al : I-iyperglueagonemia Of the Isolated Perfusmentioning

confidence: 99%

Hyperglucagonemia of the isolated perfused pancreas of diabetic mice (db/db)

et al. 1973

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Summary. Diabetes mellitus is held to be accompanied by inappropriately high levels of plasma glueagon relative to blood glucose concentrations. This has been interpreted as indicating lack of insulin. To establish ghcagon release in presence of high levels of endogenous insulin, the effects of both glucose and arginine were studied in the isolated perfused pancreas of genetically diabetic mice (db/db). Stimulation with glucose 2.75 mM or glucose plus arginine 8.25 mM exhibited a pronounced hyperglueagonemia. Following glucose 8.25 raM, however, there was no depression of glucagon secretion. Despite excessive high levels of endogenous insulin, there was a pattern of rather non-suppressible glueagon release. Lack of insulin per se, therefore, is unlikely to be the sole cause of hyperglucagonemia in this type of genetic animal diabetes mellitus.Key words : Diabetic mice, isolated perfused pancreas, high insulin levels, hyperglucagonemia.Patients with inherited diabetes mellitus are said to demonstrate increased pancreatic glueagon release relative to blood sugar levels [25,16]. Extremely high levels of glueagon have also been reported in alloxan treated dogs [17], streptozotoein diabetic rats [13] and in patients with severe ketoacidosis [1]. This has been interpreted as a state of decreased suppressibility of the alpha cell in the diabetics, probably on the base of lack of insulin. Infusion of insulin in animals with artificially achieved diabetes corrected instantly the state of hyperglucagonemia.Recent studies-in diabetic patients, however, exhibited only a slow and modest decline of glueagon after infusion of high insulin dosages. It was, therefore, concluded that mere lack of insulin may not adequately explain the alpha cell abnormality in diabetes mellitus [26]. Most of these patients, however, were receiving tolbutamide, and exhibited a markedly decreased insulin release following a carbohydrate meal compared to non diabetic controls.The present report deals with the alpha cell function in diabetic mice. The isolated perfused mouse pancreas was examined. Due to the hyperinsulinism in these obese animals the effect of high endogenous insulin release on pancreatic glueagon secretion was examined. Material and MethodsFor the present experiments diabetic mutant mice (C 57 BL/Ks-db/db ; Jackson Laboratory, Bar Harbour, Maine, USA), weighing 50--60 g, approximately 2--3 months old, and lean litter controls were used. Each group consisted of 5 animals.The mice were operated on after a 6 h fast. The pancreas was dissected under sodium pentobarbital anesthesia in a way similar to that already described for rats [23]. Arterial flow was achieved by cannulation * Supported by Deutsche Forschungsgemeinsehaft, Bad Godesberg. of the thoracic aorta. The perfusion medium consisted of an Umbreit buffer supplemented with 1% albumin (Fa. Behring Werke, Marburg) and equilibrated with 95% O2: 5% C02. The FFA content of the albumin buffer was < 50/~Lva]/1. A constant flow rate of 1 ml/ min was achieved by a pressure of about 40 m...

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Section: H Laube Et Al : I-iyperglueagonemia Of the Isolated Perfusmentioning

confidence: 99%

Hyperglucagonemia of the isolated perfused pancreas of diabetic mice (db/db)

et al. 1973

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“…This operation indeed, when performed on adult animals, stops islet as well as body growth, the islet/body weight ratio thus being unaffected, while the acinar tissue undergoes severe atrophy. No atrophy either of the islet tissue as a whole or of alpha cells, as claimed by Ferner and Tonutti [1953], was found.…”

Section: Discussionmentioning

confidence: 70%

Anterior Pituitary and Morphology of the Pancreatic Islets in the Rat

Mosca

1957

Exp Physiol

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In the pancreas of adult normal rats the ratio of the surface areas of islets to acinar tissue is below 1/100. The alpha/beta cell ratio is about 25/75. With colchicine treatment very few mitoses are demonstrable in the islets and these are proportionally distributed in the alpha and beta cells. GH (growth hormone) seems to increase the number of mitoses in beta cells. ACTH on the other hand diminishes the number of mitoses in both alpha and beta cells. Combined treatment with GH and ACTH, however, increases the number of mitoses in both types of cells. After hypophysectomy the body weight falls, as also the acinar tissue, while the islets cease to increase with age. However, there are no changes in the ratio of islet to body weight nor in the ratio of alpha to beta cells. Treatment with GH, after hypophysectomy, results in a rise of body weight and a partial recovery of the acinar tissue, even when the amount of food supplied is the same. The islets and the alpha/beta ratio are unaffected.In young normal rats the ratio of islets to acinar tissue is about the same as in adult animals. The islet/body weight ratio is also equal in the young and adult. The alpha/beta cell ratio, however, is about 35/65 for the first 60--70 days of life and then decreases. Injection of colchicine reveals increased mitoses in beta cells during the decrease of the ratio. GH is without effect on the normal decline in the alpha/beta ratio and does not alter the number of mitoses as revealed by colchicine. ACTH, however, diminishes the number of colchicine mitoses. Hypophysectomy diminishes the rate of body growth and causes atrophy of the acini. The islets, however, in spite of constancy of food intake, continue to increase after hypophysectomy so that the ratio of islets to body weight becomes much higher than normal. Moreover, the alpha/beta cell ratio remains at the high juvenile level with advancing age. Treatment with GH, given some weeks after hypophysectomy, also causes in young rats an increase in body weight and a partial recovery of the acini. As with adult rats neither the surface area of islet tissue nor the alpha/beta ratio is affected by this treatment. Combined injections of GH and ACTH cause a gain in body weight and a recovery of the size of the adrenals, then a large number of mitoses in beta cells of the islets is detectable, and finally the typical fall of alpha to beta cell ratio from the high juvenile to the lower adult level takes place.

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“…The relative increase of alpha cells which predominated in the islets when beta cells were damaged by anterior pituitary extracts 67 " 69 was believed not to play an active role in the development of metahypophyseal diabetes. Ferner 46 and Ferner and Tonutti, 70 however, observed a decrease in the number of alpha cells after hypophysectomy in rats and guinea pigs, which caused Ferner 46 to speak of an "alphacytotropic factor of the anterior pituitary." Although growth hormone is said to increase the mitotic activity of alpha cells in rats, 71 others have not noted any influence on alpha cells after hypophysectomy or growth hormone injection.…”

Section: Influence Of Various Experimental Procedures On the Alpha Cellsmentioning

confidence: 95%