Evaluation of testis hormonal and histopathological alterations in type I and type II diabetic rats

2019 ◽  
Vol 120 (10) ◽  
pp. 16775-16785 ◽  
Author(s):  
Saber Barsiah ◽  
Morteza Behnam‐Rassouli ◽  
Fahimeh Shahabipour ◽  
Sareh Rostami ◽  
Mohammad A. Sabbaghi ◽  
...  
Keyword(s):  
Diabetic Rats ◽  
Type I ◽  
Type Ii ◽  
Histopathological Alterations

Tetracyclines Inhibit Protein Glycation in Experimental Diabetes

1998 ◽  
Vol 12 (1) ◽  
pp. 152-158 ◽  
Author(s):  
M.E. Ryan ◽  
N.S. Ramamurthy ◽  
L.M. Golub
Keyword(s):  
Diabetic Rats ◽  
Protein Glycation ◽  
Type I ◽  
Type Ii ◽  
Tissue Samples ◽  
Glycated Proteins ◽  
Uncontrolled Diabetes ◽  
Skin Collagen ◽  
Micro Organisms

Glycation of proteins, which is accelerated in the diabetic state, has been implicated in many of the long-term complications of diabetes. This process can be inhibited by members of the tetracycline family of compounds. This novel finding is supported by studies conducted on drug (streptozotocin)induced Type I and genetic (ZDF/Gmi- fa/fa) Type II diabetic rats. These animals were orally gavaged daily with 5 mg of doxycycline and a variety of non-antimicrobial chemically modified tetracycline derivatives for time periods of 3 weeks to 11 months, while control untreated diabetic and nondiabetic animals were gavaged with vehicle alone (2% CMC). Blood and tissue samples were collected and analyzed for glucose and glycated proteins. None of the treatments had any effect on the severity of hyperglycemia or the intracellular glycation of hemoglobin of either Type I or II diabetic animals. However, the tetracycline analogues did affect the extracellular glycation of several proteins such as those found in the serum as well as skin collagen. In the Type II (ZDF) animals, initial mortality (3-5 months) was seen only in the doxycycline-treated animals, associated with infection by tetracycline-resistant micro-organisms, which was eventually surpassed by mortality rates in the untreated diabetics (6-9 months). CMT treatment not only decreased mortality but also increased longevity in the Type II diabetic animals, most likely by preventing the development of a number of long-term complications of uncontrolled diabetes, including glycation of proteins, that eventually lead to the demise of untreated diabetic animals.

T1810 Hepatic Electrical Stimulation Reduces Blood Glucose in Both Type-I and Type-II Diabetic Rats

2009 ◽  
Vol 136 (5) ◽  
pp. A-584-A-585 ◽  
Author(s):  
Jie Chen ◽  
Jieyun Yin ◽  
Lin Lin ◽  
Pankaj J. Pasricha ◽  
Jiande Chen
Keyword(s):  
Electrical Stimulation ◽  
Blood Glucose ◽  
Diabetic Rats ◽  
Type I ◽  
Type Ii

Effects of Type II diabetes on capillary hemodynamics in skeletal muscle

2006 ◽  
Vol 291 (5) ◽  
pp. H2439-H2444 ◽  
Author(s):  
Danielle J. Padilla ◽  
Paul McDonough ◽  
Brad J. Behnke ◽  
Yutaka Kano ◽  
K. Sue Hageman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Type Ii Diabetes ◽  
Capillary Tube ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Diabetic Patients ◽  
Type I ◽  
Type Ii ◽  
Gk Rats

Microcirculatory red blood cell (RBC) hemodynamics are impaired within skeletal muscle of Type I diabetic rats (Kindig CA, Sexton WL, Fedde MR, and Poole DC. Respir Physiol 111: 163–175, 1998). Whether muscle microcirculatory dysfunction occurs in Type II diabetes, the more prevalent form of the disease, is unknown. We hypothesized that Type II diabetes would reduce the proportion of capillaries supporting continuous RBC flow and RBC hemodynamics within the spinotrapezius muscle of the Goto-Kakizaki Type II diabetic rat (GK). With the use of intravital microscopy, muscle capillary diameter ( dc), capillary lineal density, capillary tube hematocrit (Hctcap), RBC flux ( FRBC), and velocity ( VRBC) were measured in healthy male Wistar (control: n = 5, blood glucose, 105 ± 5 mg/dl) and male GK ( n = 7, blood glucose, 263 ± 34 mg/dl) rats under resting conditions. Mean arterial pressure did not differ between groups ( P > 0.05). Sarcomere length was set to a physiological length (∼2.7 μm) to ensure that muscle stretching did not alter capillary hemodynamics; dc was not different between control and GK rats ( P > 0.05), but the percentage of RBC-perfused capillaries (control: 93 ± 3; GK: 66 ± 5 %), Hctcap, VRBC, FRBC, and O2 delivery per unit of muscle were all decreased in GK rats ( P < 0.05). This study indicates that Type II diabetes reduces both convective O2 delivery and diffusive O2 transport properties within muscle microcirculation. If these microcirculatory deficits are present during exercise, it may provide a basis for the reduced O2 exchange characteristic of Type II diabetic patients.

Pancreas transplantation using type I and type II spontaneously diabetic rats—Our experimental experience

Microsurgery ◽  
2007 ◽  
Vol 27 (4) ◽  
pp. 305-311 ◽  
Author(s):  
Toshinori Ito ◽  
Kazunori Shimada ◽  
Miao Gang ◽  
Fumihiro Uchikoshi ◽  
Masayuki Tori ◽  
...  
Keyword(s):  
Pancreas Transplantation ◽  
Diabetic Rats ◽  
Type I ◽  
Type Ii ◽  
Spontaneously Diabetic Rats

Diminished levels of prostaglandin E in type I diabetic oocyte - cumulus complexes. Influence of nitric oxide and superoxide dismutase

1999 ◽  
Vol 11 (2) ◽  
pp. 105 ◽  
Author(s):  
Pustrovh Carolina ◽  
Alicia Jawerbaum ◽  
Sinner Debora ◽  
Perotti Christian ◽  
Martha A. F. Gimeno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Type I Diabetes ◽  
Diabetic Rats ◽  
Nitric Oxide Donor ◽  
Diabetic Rat ◽  
Prostaglandin E ◽  
Type I ◽  
Free Oxygen Radicals ◽  
Type Ii

In the present work the prostaglandin E (PGE) production by ovulated, immature and in vitromatured oocyte–cumulus complexes (OCC) was evaluated in a rat model of type I diabetes induced by streptozotocin (60 mg kg–1). A diminished number of ovulated OCC were found in the type I diabetic rat. In contrast to the increment in PGE generation found previously in OCC and embryos from type II diabetic rats, it was found that PGE production by type I diabetic OCC was diminished in comparison with the controls. Nitric oxide synthase (NOS) activity is enhanced in proestrous ovaries from type I diabetic rats, but cGMP levels are diminished. SIN-1 (300 µМ), a nitric oxide donor, significantly enhanced PGE generation by control OCC, but was unable to modify the PGE levels in type I diabetic OCC. L-NMMA, a nitric oxide inhibitor that diminished PGE values in type II diabetic OCC, did not modify PGE generation in either control and type I diabetic OCC. Superoxide dismutase (SOD, 1000 U mL–1), and SOD (1000 U mL–1) plus SIN-1 (300 µМ), enhanced PGE generation by both control and diabetic OCC. The present results suggest that even when nitric oxide (NO) is overproduced in diabetic ovaries, the NO–PGE pathway is impaired in type I diabetic OCC. As SOD additions are able to increase PGE generation by diabetic OCC, high concentrations of free oxygen radicals might be quenching the NO, impairing its physiological functions.

The biomimetic [Cr3O(O2CCH2CH3)6(H2O)3]+ decreases plasma insulin, cholesterol, and triglycerides in healthy and type II diabetic rats but not type I diabetic rats

2002 ◽  
Vol 7 (7-8) ◽  
pp. 852-862 ◽  
Author(s):  
Yanjie Sun ◽  
Buffie J. Clodfelder ◽  
Amanda A. Shute ◽  
Turkessa Irvin ◽  
John B. Vincent
Keyword(s):  
Plasma Insulin ◽  
Diabetic Rats ◽  
Type I ◽  
Type Ii

scholarly journals Effect of alloxan-diabetes on multiple forms of hexokinase in adipose tissue and lung

1967 ◽  
Vol 105 (3) ◽  
pp. 1301-1305 ◽  
Author(s):  
Patricia McLean ◽  
J. Brown ◽  
Eileen Walters ◽  
K. Greenslade
Keyword(s):  
Adipose Tissue ◽  
Gel Electrophoresis ◽  
Alloxan Diabetes ◽  
Diabetic Rats ◽  
Type I ◽  
Starch Gel Electrophoresis ◽  
Type Ii ◽  
Multiple Forms ◽  
Starch Gel ◽  
Hexokinase Type I

Comparison has been made of the effect of alloxan-diabetes on the multiple forms of hexokinase (EC 2.7.1.1) in adipose tissue and lung. Types I and II hexokinase were distinguished in adipose tissue by their different stabilities to heat treatment, which made it possible to determine the activity of each form spectrophotometrically; additional confirmatory evidence was obtained from starch-gel electrophoresis. Type II hexokinase was markedly depressed in adipose tissue from alloxan-diabetic rats. Lung contained types I, II and III hexokinase, type I predominating. There was no significant change in the pattern of these multiple forms of hexokinase in lung from alloxan-diabetic rats. These results are discussed in relation to current ideas that the insulin-sensitivity of a tissue may be correlated with the content of type II hexokinase.

scholarly journals The effect of anti-insulin serum and alloxan-diabetes on the distribution and multiple forms of hexokinase in lactating rat mammary gland

1968 ◽  
Vol 109 (5) ◽  
pp. 737-741 ◽  
Author(s):  
Eileen Walters ◽  
Patricia McLean
Keyword(s):  
Mammary Gland ◽  
Soluble Fraction ◽  
Diabetic Rats ◽  
Particulate Fraction ◽  
Type I ◽  
Type Ii ◽  
Multiple Forms ◽  
Hexokinase Activity ◽  
Control Value ◽  
Rat Mammary Gland

1. The distribution and multiple forms of hexokinase activity in lactating rat mammary gland were investigated in alloxan-diabetic rats and in rats treated with anti-insulin serum. It was found that 46% of the total hexokinase of mammary-gland tissue from control rats was in the particulate fraction, but this percentage was decreased in the alloxan-diabetic rats to 11% of the total hexokinase. The hexokinase activity of the soluble fraction was not significantly altered but there was a decrease in the type II/type I quotient. 2. The early changes that occurred on insulin deprivation were studied 1hr. after administration of anti-insulin serum to lactating rats, at which time the hexokinase bound to the particulate fraction had decreased to 11% of the control value and that in the soluble fraction had increased by approx. 50%. The hexokinase type II/type I quotient in the soluble fraction was significantly decreased. These results suggested that there was a release of particulate-bound hexokinase in rats treated with anti-insulin serum.

Heat-Etching with a Bullivant Type II Simple Freeze-Cleave Device

1970 ◽  
Vol 28 ◽  
pp. 106-107 ◽  
Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt
Keyword(s):  
New Zealand ◽  
General Hospital ◽  
Massachusetts General Hospital ◽  
Type I ◽  
Type Ii ◽  
Collaborative Effort ◽  
Temperature And Pressure ◽  
The University

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.

Labelling of non-A, non-B hepatitis infected chimpanzee hepatocytes with nuclease-gold conjugates

1984 ◽  
Vol 42 ◽  
pp. 250-251
Author(s):  
G. D. Gagne ◽  
M. F. Miller ◽  
D. A. Peterson
Keyword(s):  
Endoplasmic Reticulum ◽  
Experimental Infection ◽  
Uranyl Acetate ◽  
Type I ◽  
Cellular Injury ◽  
Type Ii ◽  
Tubular Structures ◽  
Type Iii ◽  
Type Iv ◽  
Infected Chimpanzee

Experimental infection of chimpanzees with non-A, non-B hepatitis (NANB) or with delta agent hepatitis results in the appearance of characteristic cytoplasmic alterations in the hepatocytes. These alterations include spongelike inclusions (Type I), attached convoluted membranes (Type II), tubular structures (Type III), and microtubular aggregates (Type IV) (Fig. 1). Type I, II and III structures are, by association, believed to be derived from endoplasmic reticulum and may be morphogenetically related. Type IV structures are generally observed free in the cytoplasm but sometimes in the vicinity of type III structures. It is not known whether these structures are somehow involved in the replication and/or assembly of the putative NANB virus or whether they are simply nonspecific responses to cellular injury. When treated with uranyl acetate, type I, II and III structures stain intensely as if they might contain nucleic acids. If these structures do correspond to intermediates in the replication of a virus, one might expect them to contain DNA or RNA and the present study was undertaken to explore this possibility.

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