Zn supplementation increased serum Zn by 15% and urinary Zn by 56%. Others have suggested that the NCV deficit derives from molecular dislocation of the myelin loops from the axolemma in the paranodal region.293 This would result in a loss of the electrical insulation between the Na+ channels in the nodal membrane and the insulated K+ channels of the juxtaparanode.354 The result of this would be inappropriate rectification of the nodal action potential and inevitable slowing of conduction. Their study revealed that the aqueous extract of M. oleifera leaves possesses potent hypoglycemic effects through the normalization of elevated hepatic pyruvate carboxylase enzyme and regeneration of damaged hepatocytes and pancreatic β-cells via its antioxidant properties. Alloxan is known to induce diabetes in experimental animals through destruction of insulin-producing 3-cells of pancreas. Glutathione peroxidase and GSH are reduced in liver; glutathione peroxidase is increased in kidney. Supplementation of Zn by subcutaneous or intraperitoneal injection, drinking water, and dietary food were all effective in preventing diabetes. intraperitoneally to induce diabetes in 8 h fasted [ 19 ] male Sprague Dawley rats weighing 180–200 g. After one hour of alloxan administration, the animals were given feed ad libitum. Alloxan-Induced Diabetes Mellitus Organosulfur Compounds as Nutraceuticals. Alloxan is known to induce diabetic renal changes as well as causing nephrotoxic alterations. Peter A.J. Zn supplementation prevents diabetes induced by single dose of STZ or alloxan, as well as preventing diabetes induced by multiple low doses of STZ. Effect of alloxan-induced diabetes on substrate kinetics of serum BChEIn view of the dramatic changes in serum BChE activity, we extended our studies and looked at the substrate kinetic Table 2 Effect of alloxan-induced diabetes on serum BChE activity (nmol/min per ml serum) in male and female rats. LLEWELYN, ... P.K. Alloxan-induced diabetes is one of he widely used model to induce Type I diabetes mellitus in the the experimental animals. Diabetes was induced by intra peritoneal injection of 120 mg/kg Alloxan. However, dietary supplementation with PB (6 g/kg extract for 4 weeks administered orally using an intragastric tube) ameliorated the alloxan‐induced diabetes in a manner comparable with that of the reference antidiabetic drug glibenclamide. Studies of glycemic control and neuropathy have also supported the glucose hypothesis.24, Vyacheslav Buko, ... Ilya Zavodnik, in Nano- and Microscale Drug Delivery Systems, 2017. Diabetes was induced in Wistar rats (n = 25) by intravenous administration of alloxan (42 mg/kg) and were analyzed at 1, 3, 6, 9 and 12 months after diabetes induction. These changes were eliminated by insulin treatment.132. This causes an insulin-dependent diabetes mellitus (called "alloxan diabetes") in these animals, with characteristics similar to type 1 diabetes in humans. Olayaki and coauthors have investigated the effect of oral administration of methanol extracts of this plant on glucose tolerance, glycogen synthesis, and lipid metabolism in rats with alloxan-induced diabetes (Olayaki et al., 2015). England, who graduated from the Bristol biochemistry department in 1965, provided sound quantitative evidence that increased glucose 6-phosphate concentration mediates inhibitory effects of fatty acid oxidation on hexokinase and hence of intracellular glucose utilization [25]. alloxan. After receiving Zn, in either group 1 or group 2, the mean fasting plasma glucose (FPG), insulin, and homeostasis model assessment for insulin resistance (HOMA-IR) decreased significantly, while BMI, waist circumference, and triglycerides (TG) did not significantly change. There were eight studies comparing the effects of Zn supplementation on lipid parameters in patients with T2D. The ability of therapeutic compounds including medicinal plants to restore glycemic balance or homeostasis in hyperglycemic condition is an index of their antidiabetic function and relevance. ), India. In addition, high-sensitivity C-reactive protein (hs-CRP) and markers of insulin resistance were decreased significantly in the Zn group but increased in the placebo group. The responses are accompanied by corresponding inverse changes in plasma insulin and sequential ultrastructural changes resulting in necrotic beta cell death. Modulation of NADPH oxidase subunit expression is another way of preventing ROS formation and restoring erectile function by SAC in diabetic rats; it was suggested that the poor efficacy of conventional insulin treatment for diabetic erectile dysfunction may be associated with an elevated level of ROS in penile tissue (Yang et al., 2013). First, diabetic rats develop a renal lesion (mesangial expansion) that differs from the early lesion of human nephropathy (glomerular basement membrane expansion) and do not develop end-stage renal failure. Animal models of diabetic neuropathy are also limited; however, the ability to measure nerve conduction and to perform nerve biopsies may compensate for difficulty in determining specific sensory and motor deficits. Multiple low doses of STZ induce a diabetic model that is mechanistically distinct from that induced by single high dose of STZ.48,82,100 Furthermore, Zn supplementation prevents diabetes among genetically prodiabetic models such as BB Wistar rat, NOD, and db/db or od/od mouse diabetes. Alloxan induced diabetes of 4 days duration produced metabolite changes in brain compatible with severe reduction in cerebral metabolism (phosphocreatine increased 70%), and reduced phosphofructokinase activity (fructose diphosphate levels fell 38%). Administration of alloxan (150 mg/kg body weight, i.p.) Twenty women were given 30 mg/day of supplemental Zn as Zn gluconate for 8 weeks and the remainder was given placebo. In these studies, it was found that alloxan induces very mild diabetes. As the paramutational process continues, the regulator genes involved in carbohydrate metabolism become altered in some individuals, permitting expression of diabetes in these people, despite normal parents or even a monozygotic twin. Zn supplementation significantly improved these deleterious changes in these obese children with a decrease in plasma leptin level along with other changes.63. Groups included (I) non-diabetic control, (II) thiamine (30 mg/l, IP), (III) alloxan-induced diabetic mice, (IV) diabetes + ZnO NPs (0.1 mg/kg IP), (V) diabetes + ZnO NPs (0.5 mg/kg IP), (VI) diabetes + ZnO NPs (0.1 mg/kg IP) + thiamine (30 mg/l, IP), and (VII) diabetes + ZnO NPs (0.5 mg/kg IP) + thiamine (30 mg/l, … Secondary intervention studies, that is, prevention of progress of established complications, have been much less common. have investigated how an aqueous extract from the leaves of M. oleifera exerts hypoglycemia in diabetic rats (Abd El Latif et al., 2014). The way in which the polyol pathway might act to cause the development of the conduction velocity deficit has received much attention in the past. This study evaluated the long-term effects of alloxan-induced diabetes in rat liver. In rats with STZ-induced diabetes of 6 months' duration, daily administration of the ARI ponalrestat had little effect on the conduction deficit.358 However, this study also revealed that administration of background insulin (twice-weekly doses of the long-acting preparation, heat-treated ultralente) enabled the ARI to maintain a conduction velocity significantly greater than that seen in the rats given insulin alone. Lower doses of alloxan (90-140 mg/kg, i.p.) Rats with streptozotocin-induced diabetes develop mesangial thickening with immunoglobulin deposition within 6 to 9 months of diabetes onset.12 Successful islet transplantation prevented the development of such lesions or led to stabilization and some improvement in established lesions concurrent with normalization of glucose levels.12 Studies in other animal models such as the BB/W spontaneously diabetic rat15 and the uninephrectomized, alloxan-treated dog23 support the role of glucose control in the genesis of nephropathy. These hydroxyl radicals are ultimately responsible for the death of the beta cells, which have a particularly low antioxidative defence capacity, and the ensuing state of insulin-dependent 'alloxan diabetes'. The pooled mean for total cholesterol in the Zn-supplemented group was 32.37 mg/dL lower than that in placebo groups. Methods . tathione (GSH) during the alloxan-induced diabetes melli- There were no significant differences between the control tus. I was able to show in perfused rat heart that inhibition of fatty acid oxidation with 2-bromostearate reversed the insulin resistance in cardiac muscle in alloxan diabetes [24]. Allo- 8 for each point. Complex patterns of changes in antioxidant enzymes have been described in different tissues in streptozocin diabetes.188,189 Liver and kidney have reduced catalase and SOD. It has been found that in many research studies, the dose of alloxan used to induce diabetes was suboptimal. Oxidative stress occurs in experimental diabetes induced by streptozotocin and alloxan, and in the diabetic BB Wistar rat. 's investigative team tested the hypothesis that Zn supplementation may improve insulin secretion in a genotype-dependent manner. In 1967 Chase and Tubbs reported that carnitine acyl transferase and hence fatty acid oxidation are inhibited by 2-bromostearate (see Ref. Group 1 participants received 20 mg Zn, and group 2 received placebo on a regular daily basis for 8 weeks. My interest in this general area was to be reawakened in the 1970s by Lester Reed’s discovery that the pyruvate dehydrogenase (PDH) complex is regulated by reversible phosphorylation. Second, other factors contribute to reduced MNCV with longer durations of diabetes. Alloxan diabetes and streptozotocin diabetes Figure 1 shows a schematic diagram of the tetraphasic and triphasic blood glucose responses induced by alloxan and streptozotocin, respectively, when injected [22]. The metabolic profile was confirmed by body weight, complete blood panel, intravenous glucose tolerance test (IVGTT), and meal tolerance test. Thus treatment of STZ-diabetic rats from the onset of diabetes for short periods (around 1 month) with an ARI results in an MNCV that is not significantly lower than that seen in control rats and is significantly higher than that measured in untreated diabetic littermates. z o.o. Effects of Alloxan-Induced Diabetes on Ischemia-Reperfusion Injury in Rabbit Hearts W. Mark Vogel and Carl S. Apstein Hearts from rabbits with 8-16 weeks of alloxan-diabetes were compared with hearts from normal rabbits to determine whether diabetic myocardium is more sensitive to ischemic injury. Alloxan, in t… The complexation with HPβCD enhanced the solubility of SER with the association constant for sertraline and HPβCD 6530 ± 54 M−1. Treatment of diabetic mice with a mixture of bovine brain gangliosides prevented the MNCV deficit in animals with long-term diabetes.223. Philip J. Randle, in Comprehensive Biochemistry, 2003. Alloxan-induced diabetes, a common model for evaluating the glycemic-control potential of therapeutic compounds and plants extracts in experimental studies . can result in auto-reversion to normal state. At the beginning of the study, dietary Zn averaged 7.31 mg/day and serum Zn averaged 12.98 μmol/L in the Zn group. Production and hosting by Elsevier Sp. They found that leaf extract counteracted the alloxan-induced diabetic effects in rats as it normalized the elevated serum levels of glucose, triglycerides, cholesterol, and MDA, and normalized mRNA expression of the gluconeogenic enzyme pyruvate carboxylase in hepatic tissues. However, it is certain that the male is as capable of transmitting induced glucose intolerance as is the female, thus, precluding the maternal milieu as being etiologic. However in diabetes research, among the diverse models, chemically-induced are highly preferable by investigators covering alloxan- and streptozotocin-induced rodent models. IN ALLOXAN INDUCED DIABETIC RATS HTML Full Text. In contrast, hepatic hexokinase remains stable throughout this period in the presence or absence of either starvation or diabetes mellitus. These results are summarized in Table 3. Alloxan is a toxic glucose analogue, which selectively destroys insulin-producing cells in the pancreas (that is, beta cells) when administered to rodents and many other animal species. Second, other potentially important variables that might predict or influence development of nephropathy in humans (e.g., hypertension) cannot be easily studied in animal models. osti.gov journal article: effect of alloxan-induced diabetes on magnesium metabolism in rabbits For the most part these have followed the first demonstration of a conduction deficit in diabetic rats,90 by concentrating on MNCV. 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