Extrapancreatic islets of Langerhans: ontogenesis and alterations in diabetic condition

1997 ◽  
Vol 153 (1) ◽  
pp. 73-80 ◽  
Author(s):  
M Bendayan ◽  
I-S Park
Keyword(s):  
Pancreatic Islets ◽  
Endocrine Cells ◽  
Adult Life ◽  
Duodenal Mucosa ◽  
Diabetic Rats ◽  
Adult Rat ◽  
Morphological Studies ◽  
Insulin Cells ◽  
Early Embryonic Stage ◽  
Different Strains

Abstract The existence of extrapancreatic islets in the duodenal mucosa of the adult rat has been established by morphological studies and the development of these islets has been followed from the early embryonic stage to neonatal and adult life. Like the pancreatic islets, glucagon cells were the first to appear at day 12 of gestation. However, in contrast to the pancreatic islets, insulin was not detected in the extrapancreatic islets until birth. At this stage, the different endocrine cells assume their classical topography, insulin cells being surrounded by non-insulin endocrine cells. In addition, the behaviour of these extrapancreatic islets in diabetic conditions was evaluated on streptozotocin-induced diabetic rats as well as on spontaneous BB Wistar diabetic rats. In both conditions, the extrapancreatic islets were found in the duodenal mucosa but were mainly composed of glucagon cells, the insulin cells having disappeared. These results demonstrate that the extrapancreatic islets are a common normal feature of the rat duodenal mucosa. They appear during fetal development, are present in different strains of rats and behave similarly to the pancreatic islets under spontaneous or chemically induced diabetic conditions. Although their exact role remains to be established, they probably react to local hyperglycaemic environment due to intestinal absorption. Journal of Endocrinology (1997) 153, 73–80

Intraportal transplantation of pancreatic islets into livers of diabetic rats. Reinnervation of islets and regulation of insulin secretion by the hepatic sympathetic nerves

Diabetes ◽  
1994 ◽  
Vol 43 (11) ◽  
pp. 1345-1352 ◽  
Author(s):  
A. Gardemann ◽  
K. Jungermann ◽  
V. Grosse ◽  
L. Cossel ◽  
F. Wohlrab ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Sympathetic Nerves ◽  
Diabetic Rats

scholarly journals Vanadyl Sulfate Treatment Stimulates Proliferation and Regeneration of Beta Cells in Pancreatic Islets

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Samira Missaoui ◽  
Khémais Ben Rhouma ◽  
Mohamed-Tahar Yacoubi ◽  
Mohsen Sakly ◽  
Olfa Tebourbi
Keyword(s):  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Control Level ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Dependent Manner ◽  
Glucose Levels ◽  
Blood Glucose Levels

We examined the effects of vanadium sulfate (VOSO4) treatment at 5 and 10 mg/kg for 30 days on endocrine pancreas activity and histology in nondiabetic and STZ-induced diabetic rats. In diabetic group, blood glucose levels significantly increased while insulinemia level markedly decreased. At the end of treatment, VOSO4at a dose of 10 mg/Kg normalized blood glucose level in diabetic group, restored insulinemia, and significantly improved insulin sensitivity. VOSO4also increased in a dose-dependent manner the number of insulin immunopositive beta cells in pancreatic islets of nondiabetic rats. Furthermore, in the STZ-diabetic group, the decrease in the number of insulin immunopositive beta cells was corrected to reach the control level mainly with the higher dose of vanadium. Therefore, VOSO4treatment normalized plasma glucose and insulin levels and improved insulin sensitivity in STZ-experimental diabetes and induced beta cells proliferation and/or regeneration in normal or diabetic rats.

Sequential Morphological Changes in Pancreatic Islets of Spontaneously Diabetic Rats

Pancreas ◽  
1990 ◽  
Vol 5 (5) ◽  
pp. 533-539 ◽  
Author(s):  
César L. A. Gómez Dumm ◽  
Maria C. Semino ◽  
Juan Jose Gagliardino
Keyword(s):  
Pancreatic Islets ◽  
Morphological Changes ◽  
Diabetic Rats ◽  
Spontaneously Diabetic Rats

scholarly journals Immunohistochemical Analysis of the Endocrine Cells in the Pancreatic Islets of Cattle

1996 ◽  
Vol 72 (6) ◽  
pp. 285-295 ◽  
Author(s):  
Takahiro HIRATSUKA ◽  
Mitsuo ABE ◽  
Kazushige TAKEHANA ◽  
Kenji IWASA ◽  
Takeo HIRAGA ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Endocrine Cells ◽  
Immunohistochemical Analysis

scholarly journals Immunocytochemical component of endocrine cells in pancreatic islets of horses.

1989 ◽  
Vol 51 (1) ◽  
pp. 35-43 ◽  
Author(s):  
Hidefumi FURUOKA ◽  
Hisao ITO ◽  
Miyuki HAMADA ◽  
Takahiko SUWA ◽  
Hiroshi SATOH ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Endocrine Cells

Modulation of transmembrane potential of isolated cardiac myocytes by insulin and isoproterenol

1990 ◽  
Vol 259 (2) ◽  
pp. H554-H559
Author(s):  
J. Eckel ◽  
H. Reinauer
Keyword(s):  
Cardiac Myocytes ◽  
Insulin Action ◽  
Transmembrane Potential ◽  
Cardiac Myocyte ◽  
Potassium Conductance ◽  
Diabetic Rats ◽  
Maximal Effect ◽  
Physiological Concentration ◽  
Adult Rat ◽  
Hormonal Modulation

Isolated muscle cells from adult rat heart have been used to study the effects of insulin and catecholamines on transmembrane potential by following triphenylmethylphosphonium cation uptake. Insulin was found to hyperpolarize the cells with a maximal effect of 3.2 +/- 0.7 mV (n = 4) at an insulin concentration of 3 x 10(-9) mol/l. This insulin action was fully antagonized by isoproterenol (10(-5) mol/l), which depolarized the cardiocytes in a dose-dependent fashion with a maximal effect of 9.5 +/- 2.2 mV. Treatment of cardiocytes with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid or CsCl resulted in a total loss of insulin action, whereas isoproterenol action was not affected. Cardiac myocytes from streptozotocin diabetic rats exhibited an unaltered hyperpolarization by insulin within the physiological concentration range. Isoproterenol now induced a biphasic response with a significant hyperpolarization at low doses and a decreased depolarization at maximal concentrations. In conclusion, 1) hormonal modulation of cardiac myocyte membrane potentials involves hyperpolarization by insulin and depolarization by beta-agonists, 2) insulin action appears to be related to an increased potassium conductance and may be antagonized by beta-stimulation, and 3) membrane potential modulation may be profoundly altered in the diabetic state.

scholarly journals Species and tissue distribution of the regulatory protein of glucokinase

1993 ◽  
Vol 294 (2) ◽  
pp. 551-556 ◽  
Author(s):  
A Vandercammen ◽  
E Van Schaftingen
Keyword(s):  
Guinea Pig ◽  
Rat Liver ◽  
Human Liver ◽  
Regulatory Protein ◽  
Control Level ◽  
Streptozotocin Diabetes ◽  
Diabetic Rats ◽  
Rat Tissues ◽  
Adult Rat ◽  
Toad Bufo

Rat liver is known to contain a regulatory protein that inhibits glucokinase (hexokinase IV or D) competitively versus glucose. This inhibition is greatly reinforced by the presence of fructose 6-phosphate and antagonized by fructose 1-phosphate and by KCl. This protein was now measured in various rat tissues and in the livers of various species by the inhibition it exerts on rat liver glucokinase. Rat, mouse, rabbit, guinea-pig and pig liver, all of which contain glucokinase, also contained between 60 and 200 units/g of tissue of a regulatory protein displaying the properties mentioned above. By contrast, this protein could not be detected in cat, goat, chicken or trout liver, or in rat brain, heart, skeletal muscle, kidney and spleen, all tissues from which glucokinase is missing. Fructose 1-phosphate stimulated glucokinase in extracts of human liver, indicating the presence of regulatory protein. In addition, antibodies raised against rat regulatory protein allowed the detection of an approximately 60 kDa polypeptide in rat, guinea pig, rabbit and human liver. The livers of the toad Bufo marinus, of Xenopus laevis and of the turtle Pseudemys scripta elegans contained a regulatory protein similar to that of the rat, with, however, the major difference that it was not sensitive to fructose 6-phosphate or fructose 1-phosphate. In rat liver, the regulatory protein was detectable 4 days before birth. Its concentration increased afterwards to reach the adult level at day 30 of extrauterine life, whereas glucokinase only appeared after day 15. In the liver of the adult rat, starvation and streptozotocin-diabetes caused a 50-60% decrease in the concentration of regulatory protein after 7 days, whereas glucokinase activity fell to about 20% of its initial level. When 4-day-starved rats were refed, or when diabetic rats were treated with insulin, the concentration of regulatory protein slowly increased to reach about 85% of the control level after 3 days, whereas the glucokinase activity was normalized after the same delay. The fact that there appears to be no situation in which glucokinase is expressed without regulatory protein is in agreement with the notion that the regulatory protein forms a functional entity with this enzyme.

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