MORPHOLOGY OF EXPERIMENTAL, ORGAN-SPECIFIC INSULITIS OF THE MOUSE PANCREAS

1976 ◽  
Vol 83 (1) ◽  
pp. 133-150 ◽  
Author(s):  
Jørn Egeberg ◽  
Jørn Nerup ◽  
Ole Ortved Andersen ◽  
Gunnar Bendixen ◽  
Hans Kromann ◽  
...  

ABSTRACT The morphologic and metabolic effect of a single intracutaneous injection of homologous endocrine pancreas in Freund's complete adjuvant (CFA) was studied in 100 mice and compared with control groups which had been (1) immunized with murine insulin in CFA, (2) injected with CFA alone, or had (3) received no treatment. There were no differences between the control groups as regards the morphology of the pancreatic islets, and the glucose tolerance was normal. Mice immunized with islet homogenate exhibited morphological changes in the form of degranulation and cytoplasmic disintegration. These changes involved B-cells as well as A2-cells and were present from 7 to 18 days after the immunization. A significant reduction in glucose tolerance was observed 14 days after the immunization. Another characteristic finding in the islets from the immunized mice was the extravascular presence of mononuclear, agranular cells which on the basis of their morphological criteria appeared to represent lymphocytes.

1979 ◽  
Vol 80 (2) ◽  
pp. 175-179 ◽  
Author(s):  
F. A. VAN ASSCHE ◽  
L. AERTS ◽  
W. GEPTS

This present study has demonstrated that during normal pregnancy in the rat the number of β-cells is increased (hyperplasia) and the volume of the individual β-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 β-cells cannot replicate due to the unfavourable metabolic environment. This could reflect the complications caused by diabetes during human pregnancy.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
C. R. Silva ◽  
K. S. N. Marinho ◽  
T. D. S. Silva ◽  
D. K. S. Ferreira ◽  
G. M. Aguiar ◽  
...  

Studies about toxicological potential of usnic acid are limited. This way, the vast majority of data available in the literature are related only to biological activities. This is the first study that aimed to evaluate the oral toxicity of usnic acid during the period of organogenesis. Females rats were distributed in the control groups, treated I and II, at doses of 15 and 25 mg/kg, administered by gavage during the 6° to 15° days of pregnancy. After 20 days the fetuses were removed and analyzed. A reduction in weight gain during pregnancy, increased resorption, reduction in the number of viable fetuses, and their body weight were observed. Morphological changes in the litter were visualized as exposure of the eye and atrophy of the limbs at the dose of 25 mg/kg. Histological analysis of the liver of the fetus showed reduction in the number of megakaryocytes between experimental groups and increase in the number of hepatocytes in a dose of 25 mg/kg. The experimental model used in this study reveals teratogenic effect of usnic acid in the period of organogenesis. Since this achievement, the importance of evaluating the toxic effects of natural substances is imperative, in order to elucidate the care in their indication as drug.


1973 ◽  
Vol 72 (2) ◽  
pp. 279-286 ◽  
Author(s):  
Jørn Nerup ◽  
Christian Binder

ABSTRACT The clinical association between diabetes mellitus and auto-immune diseases of the thyroid, the adrenals and the gastric mucosa occurs more frequently than could be expected by chance. Sera from 133 patients with diabetes mellitus and 128 controls were therefore investigated for the presence of organ-specific auto-antibodies. Thyroid microsomal antibody and gastric-parietal-cell antibody were demonstrated with significantly increased frequency – 20% and 16% respectively – in sera from patients with diabetes mellitus. Antibodies reacting specifically with tissue components of the endocrine pancreas could not be demonstrated. From the data presented and from a review of the literature it is concluded that evidence is accumulating pointing to a disorder of the immunological system in patients with diabetes mellitus with regard to the formation of organ-specific humoral and cellular auto-immunity, and the occurrence of organ-specific auto-immune diseases.


2020 ◽  
Vol 245 (2) ◽  
pp. 315-326 ◽  
Author(s):  
Sandra K Szlapinski ◽  
Anthony A Botros ◽  
Sarah Donegan ◽  
Renee T King ◽  
Gabrielle Retta ◽  
...  

Gestational diabetes mellitus increases the risk of dysglycemia postpartum, in part, due to pancreatic β-cell dysfunction. However, no histological evidence exists comparing endocrine pancreas after healthy and glucose-intolerant pregnancies. This study sought to address this knowledge gap, in addition to exploring the contribution of an inflammatory environment to changes in endocrine pancreas after parturition. We used a previously established mouse model of gestational glucose intolerance induced by dietary low protein insult from conception until weaning. Pancreas and adipose samples were collected at 7, 30 and 90 days postpartum for histomorphometric and cytokine analyses, respectively. Glucose tolerance tests were performed prior to euthanasia and blood was collected via cardiac puncture. Pregnant female mice born to dams fed a low protein diet previously shown to develop glucose intolerance at late gestation relative to controls continued to be glucose intolerant until 1 month postpartum. However, glucose tolerance normalized by 3 months postpartum. Glucose intolerance at 7 days postpartum was associated with lower beta- and alpha-cell fractional areas and higher adipose levels of pro-inflammatory cytokine, interleukin-6. By 3 months postpartum, a compensatory increase in the number of small islets and a higher insulin to glucagon ratio likely enabled euglycemia to be attained in the previously glucose-intolerant mice. The results show that impairments in endocrine pancreas compensation in hyperglycemic pregnancy persist after parturition and contribute to prolonged glucose intolerance. These impairments may increase the susceptibility to development of future type 2 diabetes.


2017 ◽  
Vol 8 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Olga V Sokolova ◽  
Ruslan A Nasyrov

A retrospective analysis of acts of forensic autopsies from the archives of St Petersburg GBOOSE BSME and histological examination of liver tissue in an amount of 152 cases (78 women and 74 men) with a statistical processing of the results for studying and evaluating the morphological changes of liver’s tissue in cases of sudden cardiac death from alcohol cardiomyopathy. Identified in the course of the study morphological changes in the endothelial lining of the microvasculature showed that in addition to direct cytotoxic effects of ethanol and its metabolites in the basis of damage to the endothelial lining of the microvasculature are the cellular responses associated with exposure to mediators, the release of which is due to irritation of reactive cells, which entails a swelling deformation and increased activity endothelial cell membranes with the expansion of intercellular spaces. The development of increased permeability of the endothelial lining of transport contributes to a violation of electrolytes and nutrients to the changes of the liver’s tissue trophism, which is a substrate for the occurrence of degenerative processes and necrobiotic major structural components of the body. In turn, a direct toxic effect of ethanol and its metabolites on the wall microvascular contributes to ischemia and necrosis of the hepatocytes with the development of severe inflammatory reactions in the surrounding liver tissue, which in turn is the direct cause of the disturbances regeneration nature and excessive proliferation connective tissue with the subsequent restructuring of the vascular bed. Identified and described the morphological criteria of changes in liver’s tissue in cases of death from alcoholic cardiomyopathy should be considered in conjunction with other visceral manifestations, being a reflection of the alcohol intoxication in chronic alcoholism.


1999 ◽  
Vol 276 (4) ◽  
pp. E689-E696 ◽  
Author(s):  
Viviane Leclercq-Meyer ◽  
Marcel M. Kadiata ◽  
Willy J. Malaisse

The effects of α- and β-2-deoxy-d-glucose tetraacetate (1.7 and 8.5 mM) on insulin, somatostatin, and glucagon secretion from isolated rat pancreases perfused in the presence of 8.3 mM d-glucose were compared with those of unesterified 2-deoxy-d-glucose tested at the same two concentrations. The unesterified glucose analog caused, in a concentration-related manner, inhibition of glucose-induced insulin and somatostatin release and augmentation of glucagon secretion. The two anomers of 2-deoxy-d-glucose tetraacetate, however, increased the secretion rate of all three hormones; this effect was also related to the concentration of the esters. No obvious anomeric specificity of the secretory response to 2-deoxy-d-glucose tetraacetate was observed. These findings indicate that the insulinotropic action of hexose esters cannot be accounted for solely by the metabolic effect of their glucidic moieties. They suggest that the A, B, and D cells of the endocrine pancreas are each equipped with a receptor system responsible for the direct recognition of monosaccharide esters as secretagogues. They further support the view that a paracrine effect of insulin on glucagon-producing cells does not represent a major component in the regulation of their secretory activity.


Blood ◽  
1984 ◽  
Vol 63 (2) ◽  
pp. 384-392 ◽  
Author(s):  
AW Boyd ◽  
JR Sullivan

Abstract A variety of chemical agents have been shown to induce differentiation in in vitro cultured neoplastic cell lines. We noted that blast cells in the peripheral blood of acute nonlymphoid leukemia patients treated with the drug Harringtonine appeared to undergo morphological changes that suggested differentiation. In view of the relatively minimal myelotoxicity of Harringtonine, we hypothesized that harringtonine was acting by differentiation-induction, which concomitantly arrested cell division. We tested this hypothesis using two different experimental approaches. First, the promyelocytic leukemic cell line, HL-60, was cultured with Harringtonine and shown to differentiate into a cell, which, by functional cell surface marker and morphological criteria, closely resembled normal monocytes. Furthermore, these changes were accompanied, and indeed slightly preceded by, loss of proliferative capacity. Second, to prove that the leukemic blasts were the cells undergoing the changes observed in vivo, freshly isolated leukemia cell populations were cultured with Harringtonine, and morphological changes paralleling those seen in the patients were observed. Thus, the antileukemic effect of Harringtonine appeared to be due to diversion of the proliferating blast cells into a differentiation pathway, which, as in normal myeloid cells, resulted in the arrest of proliferation.


2014 ◽  
Vol 1004-1005 ◽  
pp. 857-863 ◽  
Author(s):  
Yong Qiang Zhou ◽  
Tao Yan Mao

Diabetic nephropathy (DN) is a common complication of diabetes and it is related to irreversible kidney damages and chronic renal failure. Impaired glucose tolerance (IGT) is an early stage in the development of diabetes and DN. Early detection of IGT and treatment of its associated early kidney damage can effectively prevent the development of DN. In this paper, the influence of dihydromyricetin (DHM) on lowering blood glucose concentration and reducing early kidney damage in IGT rats was studied. Animal model of IGT rats was built by two week intragastric injection of D-galactose and treated with eight weeks of intragastric injection of DHM at two dose levels. The concentrations of fasting blood glucose (FBG), two-hour postprandial blood glucose (2hBG), insulin levels, contents of microalbuminuia (mAlb) and blood urea nitrogen (BUN), and activities of lactate dehydrogenase (LDH) in kidney were analysed and compared with those in control groups. Experimental results indicated that DHM treatment can significantly lower the levels of two-hour postprandial blood glucose and insulin, decrease the content of mAlb and the activities of LDH in kidney, but does not influence the level of BUN. The study suggested that DHM can effectively improve the states of IGT rats and provide a protective effect against early kidney damage.


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