DIABETES MELLITUS - APPROACHES TO EXPERIMENTAL MODELING AND MOLECULAR MARKER

Author(s):  
Elizaveta I. Bon ◽  
Maria A. Lychkovskaya
2018 ◽  
Vol 24 (2) ◽  
pp. 57-65
Author(s):  
S.O. Borisov ◽  
F.I. Kostev ◽  
O.V. Borisov ◽  
N.I. Molchaniuk

Programmed cell death under conditions of an infectious-inflammatory process plays a biologically exclusively positive role in the elimination of cells. Acute inflammatory process is a phenomenon capable of excessive concentration of aggressive effectors of inflammation. The aim of the work was to assess the dynamics of ultrastructural changes and early signs of apoptosis in the kidney tissues in experimental modeling of acute pyelonephritis (AP) and concomitant diabetes mellitus (DM) of type II and II when conducting complex drug correction. The work was performed on 300 adult Wistar rats, divided into 6 groups. Fragments of the kidneys were studied and photographed in the electron microscope PEM-100-01. In the kidneys of animals of the group, where traditional medical correction was used after the friendly modeling of pyelonephritis and type I diabetes, it was found that the glomerular ultrastructure was more preserved, but part of the capillaries of the glomerulus remained deformed with a narrowed lumen, there are signs of insufficient restoration of the glomerular capillary network. In the group of animals using the proposed complex drug correction, the renal structure was preserved, the capillaries of the glomerular network with unchanged architectonics. It has been established that the traditional medical correction did not sufficiently contribute to the restoration of damaged kidney tissue ultrastructure. After carrying out the complex medical correction proposed by us after a friendly simulation of an OP of DM type II, the ultrastructure of the kidney tissue in form and structure approached that of control animals, signs of a compensatory-restorative process appeared: most of the podocytes were hyperplastic and hypertrophied. The podocytes of the outer leaflet were in the active phase of activity, as evidenced by an increase in contractile function and, possibly, the release of urine from the cavity into the lumen of the proximal tubules. The structure of the tubules and interstitial tissue is close to the structure of the group of control animals, only in the cytoplasm of the podocytes of the proximal tubules there is an increased content of lysosomes. The ultrastructure of the glomeruli was normalized; the number of hypertrophic podocytes of the inner leaflet with signs of enhanced protein synthesis increased. Changes in the structures of the cortical and medulla are similar except for the state of cytotrabeculae, where their size decreased in the medulla and signs of deformation of the plasmolemma appeared. In experimental modeling of PD and DM of types I and II, pronounced ultrastructural changes in the kidney tissues were established, and manifestations of early apoptosis processes are significantly limited. The use of the complex drug correction proposed by us stimulates the development of the reparative processes of the kidney and moderately activates apoptosis. The addition of multi-vector preparations (Armadin and Nuklex) to the complex of treatment intensifies compensatory-restorative changes in the kidneys and apoptosis, which contributes to the elimination from the renal microstructures of excess damaged cells and aggressive effectors of inflammation.


2020 ◽  
Vol 6 (5) ◽  
pp. 89-96
Author(s):  
Yu. Shidakov ◽  
E. Sharova ◽  
I. Abdumalikova

Experimental modeling of diabetes mellitus, caused by exposure to alloxan, streptozotocin, dithizone in various dosages and the frequency of administration, is not entirely equivalent in etiopathogenetic mechanisms to the development of this pathology in humans. Of great interest are diet-induced modeling of the pathological process. One of the most important and affordable glucose donors is food sugar (sucrose). In order to study the development of diabetes mellitus in rats with food sugar, 2 groups of animals were formed: control (standard food) and experimental (food sugar), which were taken blood for biochemical studies after 2 weeks, and a month later histological preparations of the pancreas were selected. With the systematic intake of excessive amounts of edible sugar, after 2 weeks there was an increase in blood glucose by 25%, while at the same time, cholesterol increased by 3 times. After a month of research, carbohydrate degeneration of the pancreas is observed, combined with vacuole organ dystrophy and the development of foci of necrosis and sclerosis. Feeding rats for a month with food sugar can serve as an experimental model of carbohydrate pancreatic dystrophy.


1998 ◽  
Vol 39 (5) ◽  
pp. 663-668 ◽  
Author(s):  
Harry N. Bawden ◽  
Aidan Stokes ◽  
Carol S. Camfield ◽  
Peter R. Camfield ◽  
Sonia Salisbury

Author(s):  
Bruce R. Pachter

Diabetes mellitus is one of the commonest causes of neuropathy. Diabetic neuropathy is a heterogeneous group of neuropathic disorders to which patients with diabetes mellitus are susceptible; more than one kind of neuropathy can frequently occur in the same individual. Abnormalities are also known to occur in nearly every anatomic subdivision of the eye in diabetic patients. Oculomotor palsy appears to be common in diabetes mellitus for their occurrence in isolation to suggest diabetes. Nerves to the external ocular muscles are most commonly affected, particularly the oculomotor or third cranial nerve. The third nerve palsy of diabetes is characteristic, being of sudden onset, accompanied by orbital and retro-orbital pain, often associated with complete involvement of the external ocular muscles innervated by the nerve. While the human and experimental animal literature is replete with studies on the peripheral nerves in diabetes mellitus, there is but a paucity of reported studies dealing with the oculomotor nerves and their associated extraocular muscles (EOMs).


1971 ◽  
Vol 104 (4) ◽  
pp. 442-444 ◽  
Author(s):  
R. Tankel
Keyword(s):  

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