scholarly journals Bypassed and Preserved Stomach Resulted in Superior Glucose Control in Sprague-Dawley Rats with Streptozotocin-Induced Diabetes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jason Widjaja ◽  
Ponnie Robertlee Dolo ◽  
Qiang Zhang ◽  
Libin Yao ◽  
Chao Li ◽  
...  
2018 ◽  
Vol 67 (4) ◽  
pp. 517-526 ◽  
Author(s):  
Abdulsamad Alsalahi ◽  
Mohammed A. Alshawsh ◽  
Zamri Chik ◽  
Zahurin Mohamed

Author(s):  
G.T. Frederick ◽  
R.M. Gardner ◽  
J.M. Kirkland ◽  
G.M. Stancel

Estradiol (E2)-stimulated uterine growth has been well characterized both biochemically and morphologically. Recent studies have shown that insulin plays an important role in the regulation of cellular development. This study examines the effect of streptozotocin-induced diabetes on E2-stimulated changes in the ultrastructure of the endometrium of the rat uterus.Sprague-Dawley rats were ovariectomized at 21 days of age. Diabetes, defined as blood glucose levels greater than 300mg%, was induced in half of these animals by the injection of 85mg streptozotocin/kg body weight.The remaining animals were classified as normal. Animals from both groups were injected with either 0.9% saline or 4μg E2/100gm body weight. At 18, 24, 36 and 48 hours post-injection of E2, uterine segments were collected from 8-10 animals in each experimental group and processed for electron microscopic examination. Uterine segments from saline-injected animals served as controls. Data summarized describe observations made from thin-sections and have not been extrapolated for whole cells.


2004 ◽  
Vol 286 (2) ◽  
pp. E184-E193 ◽  
Author(s):  
Theresa E. Fagan ◽  
Christie Cefaratti ◽  
Andrea Romani

Male Sprague-Dawley rats rendered diabetic by streptozotocin injection presented 10 and 20% decreases in total hepatic Mg2+ content at 4 and 8 wk, respectively, following diabetes onset. This decrease was associated with a parallel decrease in K+ and ATP content and an increase in Na+ level. In diabetic liver cells, the Mg2+ extrusion elicited by α1-adrenoceptor stimulation was markedly reduced compared with nondiabetic livers, whereas that induced by β-adrenoceptor stimulation was unaffected. In addition, diabetic hepatocytes did not accumulate Mg2+ following stimulation of protein kinase C pathway by vasopressin, diacylglycerol analogs, or phorbol 12-myristate 13-acetate derivates despite the reduced basal content in cellular Mg2+. Experiments performed in purified plasma membrane from diabetic livers located the defect at the level of the bidirectional Na+/Mg2+ exchanger operating in the basolateral domain of the hepatocyte cell membrane, which could extrude but not accumulate Mg2+ in exchange for Na+. The impairment of Mg2+ uptake mechanism, in addition to the decrease in cellular ATP level, can contribute to explaining the decrease in liver Mg2+ content observed under diabetic conditions.


BioMetals ◽  
2020 ◽  
Author(s):  
Bonisiwe Mbatha ◽  
Andile Khathi ◽  
Ntethelelo Sibiya ◽  
Irvin Booysen ◽  
Patrick Mangundu ◽  
...  

1981 ◽  
Vol 50 (3) ◽  
pp. 482-486 ◽  
Author(s):  
R. D. Murphy ◽  
A. C. Vailas ◽  
C. M. Tipton ◽  
R. D. Matthes ◽  
J. G. Edwards

Male Sprague-Dawley rats were assigned to three groups designated as diabetic, diabetic-plus-insulin, and control and tested for maximum oxygen consumption (VO2max) and maximum heart rate on three different occasions during the 6- to 8-wk experimental period. Compared with the prediabetic values and the means of the other two groups, diabetic animals had significantly higher submaximum and lower maximum VO2 values. These relationships prevailed when the groups were evaluated in terms of ml.kg-1.min-1 or ml.(kg0.79-1).min-1. In addition, the diabetic animals had significantly lower submaximum and maximum heart rates and shorter run times. Daily injections of insulin (2 U.day-1.rat-1) restored VO2max to within the limits of the control animals but did not normalize heart rates or run-time values. The linear relationship between heart rates and VO2 was repeatedly demonstrated with normal animals. However, this relationship progressively declined with the time course of diabetes. These results indicate that, in untreated diabetes, functional capacity is markedly reduced with the progression of the disease and suggest that alterations in the autonomic nervous system, tissue metabolic capacity, and decreases in lean body mass are responsible for the changes noted.


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Essam Ezzeldin ◽  
Wafaa A. H. Souror ◽  
Toqa El-Nahhas ◽  
Abdel Nasser M. M. Soudi ◽  
Abdelaaty A. Shahat

The incidence of diabetes is increasing worldwide. Chronic neuropathic pain occurs in approximately 25% of diabetic patients. Tramadol, an atypical analgesic with a unique dual mechanism of action, is used in the management of painful diabetic neuropathy. It acts on monoamine transporters to inhibit the reuptake of norepinephrine (NE), serotonin (5-HT), and dopamine (DA). The purpose of this study was to evaluate the effects of diabetes on the brain neurotransmitter alterations induced by tramadol in rats, and to study the hepatic and renal toxicities of the drug. Eighty Sprague-Dawley rats were divided randomly into two sets: the normal set and the diabetic set. Diabetes was induced in rats. Tramadol was administered orally once daily for 28 days. The levels of DA, NE, and 5-HT in cerebral cortex, thalamus/hypothalamus, midbrain, and brainstem were evaluated in rats. In addition, the renal toxicity and histopathological effects of the drug were assessed. The induction of diabetes altered neurotransmitter levels. Oral administration of tramadol significantly decreased the neurotransmitter levels. Diabetes significantly altered the effects of tramadol in all brain regions. Tramadol affected function and histology of the liver and kidney. The clinical effects of tramadol in diabetic patients should be stressed.


2021 ◽  
Vol 11 (4) ◽  
pp. 1369
Author(s):  
Khang Do Gia Hong ◽  
Yei-Jin Kang ◽  
Ji-Hyeon Oh ◽  
Seong-Gon Kim ◽  
Young-Wook Park ◽  
...  

There is an association between diabetes and impaired bone healing. The purpose of this study was to determine whether sericin had a positive effect on bone regeneration with streptozotocin-induced diabetes in a rat model. Sprague Dawley rats (n = 21) were assigned to one of three groups. A critical-sized bone defect was created on the calvaria. In the sericin group (S group, n = 7), the bone defect was filled with a sericin–gelatin combination, whereas in the gelatin group (G group, n = 7), only gelatin sponge was used. The control group (N group, n = 7) did not receive any graft. New bone formation was evaluated by micro-computerized tomogram and histological analysis. The regenerated bone volume in group S was the highest among the three groups (3.87 ± 2.51 mm3), followed by group N (1.71 ± 1.65 mm3) and group G (1.24 ± 1.05 mm3). The application of sericin in combination with a gelatin sponge enhanced the process of bone regeneration in streptozotocin-induced type I diabetes animal model.


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