lead has been researched along with Diabetes-Mellitus--Experimental* in 14 studies
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13 other study(ies) available for lead and Diabetes-Mellitus--Experimental
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Lead (Pb) exposure promotes diabetes in obese rodents.
Pb (lead) exposure occurs at elevated frequency in urban inner city populations that also have high rates of obesity and diabetes.. To determine if Pb can promote the development of diabetes in a setting of obesity, we examined the effect of Pb exposure on glucose metabolism in a rodent model of obesity.. Adult female ZDF rats were exposed to Pb in drinking water for 24 weeks. Fasting blood glucose, insulin, and glucose tolerance were measured at regular intervals. Expression of hepatic gluconeogenic genes was measured in exposed and control animals and in cultured hepatoma cells treated with Pb.. Pb exposure induced fasting hyperglycemia after 8 weeks and glucose intolerance after 12 weeks of exposure. In addition, Pb-exposed animals showed elevated hepatic triglyceride levels and increased expression of the gluconeogenic genes PEPCK and glucose-6-phosphatase. In cultured rat hepatoma cells treatment with Pb stimulated PEPCK and glucose-6-phosphatase gene expression, suggesting a possible direct effect of Pb on hepatic gluconeogenic gene expression.. In the setting of obesity, Pb exposure is prodiabetic, causing fasting hyperglycemia and glucose intolerance in rats. A contributing factor to the metabolic effects of Pb may be the direct stimulation of hepatic gluconeogenic gene expression. Topics: Animals; Cells, Cultured; Diabetes Mellitus, Experimental; Female; Glucose Intolerance; Hyperglycemia; Lead; Obesity; Rats; Rats, Zucker | 2017 |
Nephrotoxic effects of lead nitrate exposure in diabetic and nondiabetic rats: Involvement of oxidative stress and the protective role of sodium selenite.
Heavy metals are known to be toxic to organisms. The present study was undertaken to evaluate the protective effect of sodium selenite against lead nitrate (LN)-induced nephrotoxicity in diabetic and nondiabetic rats. Animals were divided into eight groups where the first was served as a control, whereas the remaining groups were treated with sodium selenite (1 mg/kg b.w.), LN (22.5 mg/kg b.w.) and a combination of LN and sodium selenite and diabetic forms of these groups. Changes in antioxidant enzyme activities, malondialdehide levels, serum urea, uric acid, creatinine levels, body, and kidney weights and histopathological changes were determined after 28 days. LN caused severe histopathological changes, increment in urea, uric acid, creatinine, and MDA levels, also decreasing in antioxidant enzyme activities, body, and kidney weights. In sodium selenite + LN group, we observed the protective effect of sodium selenite on examining parameters. Also diabetes caused alterations on these parameters compared with nondiabetic animals. We found that sodium selenite did not show protective effect on diabetes caused damages. As a result, LN caused nephrotoxicity and sodium selenite alleviated this toxicity but sodium selenite did not protect kidneys against diabetes mediated toxicity. Also, LN caused more harmfull effects in diabetic groups compared with nondiabetic groups. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1229-1240, 2016. Topics: Animals; Antioxidants; Blood Urea Nitrogen; Body Weight; Creatinine; Diabetes Mellitus, Experimental; Kidney; Lead; Male; Malondialdehyde; Nitrates; Oxidative Stress; Protective Agents; Rats; Rats, Wistar; Sodium Selenite; Uric Acid | 2016 |
Effect of melatonin on element distribution in the liver tissue of diabetic rats subjected to forced exercise.
The objective of the present study was to investigate the effects of melatonin supplementation on elements in the liver of diabetic rats subjected to acute swimming exercise. Eighty adult male rats were equally divided into eight groups. Group 1, general control. Group 2, melatonin-supplemented control. Group 3, melatonin-supplemented diabetic control. Group 4, swimming control. Group 5, melatonin-supplemented swimming. Group 6, melatonin-supplemented diabetic swimming. Group 7, diabetic swimming. Group 8, diabetic control. Liver tissue samples were analyzed for lead, cobalt, molybdenum, chrome, sulphur, magnesium, manganese, sodium, potassium, phosphorus, copper, iron, calcium, zinc, selenium. The highest cobalt, chrome values were found in the groups 7, 8 and the groups 5, 6 respectively. Groups 3 and 7 had the highest copper values. Iron and potassium values were higher in the groups 1 and 4. Group 6 had increased magnesium value, and groups 6, 7, 8 were found to have the highest manganese levels. The highest lead values were found in the groups 5 and 6. Group 6 had the highest selenium levels. The highest zinc levels were established in 1 and 2. Groups 1, 2, 5 and 6 were found to have the highest calcium values. The results of our study indicate that melatonin supplementation in diabetes and forced exercise significantly alters the element metabolism in the liver (Tab. 3,Ref. 33). Topics: Animals; Antioxidants; Calcium; Chromium; Cobalt; Copper; Diabetes Mellitus, Experimental; Dietary Supplements; Lead; Liver; Magnesium; Male; Melatonin; Physical Conditioning, Animal; Rats; Rats, Sprague-Dawley; Selenium; Sulfur; Swimming; Tissue Distribution; Trace Elements; Zinc | 2015 |
Effects of lead nitrate and sodium selenite on DNA damage and oxidative stress in diabetic and non-diabetic rat erythrocytes and leucocytes.
The adverse effects of lead nitrate (LN) and the preventive role of sodium selenite were investigated in diabetic and non-diabetic rat blood by measuring trolox equivalent antioxidant capacity (TEAC), ferric reducing antioxidant power (FRAP), malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) also by evaluating DNA damage with comet assay. LN increased the levels of MDA, tail DNA%, mean tail length and tail moment, decreased the enzymes activities, FRAP and TEAC values. In sodium selenite+LN group, we observed the protective effect of sodium selenite on examining parameters. Diabetes caused alterations on these parameters, too. We found that sodium selenite did not protect against diabetes caused damages. As a result, LN caused toxic effects on blood cells and sodium selenite alleviated this toxicity but it did not show preventive effect against diabetes. Also, LN caused more harmfull effects in diabetic groups than non-diabetic groups. Topics: Animals; Catalase; Diabetes Mellitus, Experimental; DNA Damage; Erythrocytes; Gene Expression Regulation, Enzymologic; Glutathione Peroxidase; Glutathione Transferase; Lead; Leukocytes; Malondialdehyde; Nitrates; Oxidative Stress; Rats; Sodium Selenite; Superoxide Dismutase | 2015 |
Protective effects of sodium selenite on lead nitrate-induced hepatotoxicity in diabetic and non-diabetic rats.
In the present study, the effect of sodium selenite on lead induced toxicity was studied in Wistar rats. Sodium selenite and lead nitrate were administered orally for 28 days to streptozotocin induced diabetic and non-diabetic rats. Eight groups of rats were used in the study: control, sodium selenite, lead nitrate, lead nitrate+sodium selenite, streptozotocin-induced diabetic-control, diabetic-sodium selenite, diabetic-lead nitrate, diabetic-lead nitrate+sodium selenite groups. Serum biochemical parameters, lipid peroxidation, antioxidant enzymes and histopathological changes in liver tissues were investigated in all groups. There were statistically significant changes in liver function tests, antioxidant enzyme activities and lipid peroxidation levels in lead nitrate and sodium selenite+lead nitrate treated groups, also in diabetic and non-diabetic groups. Furthermore, histopathological alterations were demonstrated in same groups. In the present study we found that sodium selenite treatment did not show completely protective effect on diabetes mellitus caused damages, but diabetic rats are more susceptible to lead toxicity than non-diabetic rats. Topics: Animals; Antioxidants; Diabetes Mellitus, Experimental; Lead; Lipid Peroxidation; Liver; Liver Function Tests; Nitrates; Oxidative Stress; Rats; Rats, Wistar; Sodium Selenite; Streptozocin | 2015 |
Effects of zinc supplementation on the element distribution in kidney tissue of diabetic rats subjected to acute swimming.
In this study, we report the effect of zinc supplementation on the distribution of elements in kidney tissue of diabetic rats subjected to acute swimming exercise. Diabetes was induced by two subcutaneous injections of 40 mg/kg of streptozotocin within a 24-h period. Zinc was given intraperitoneally at a dose of 6 mg/kg per day for a period of 4 weeks. The rats (n = 80) were equally divided into eight study groups: controls, zinc-supplemented, swimming, diabetic, zinc-supplemented diabetic, zinc-supplemented swimming, diabetic swimming, and zinc-supplemented diabetic swimming. The levels of lead, cobalt, molybdenum, chromium, boron, magnesium, iron, copper, calcium, zinc, and selenium were determined in the kidney tissue samples by ICP-AES. Higher molybdenum, calcium, zinc, and selenium values were found in both swimming and nonswimming diabetic rats. Significantly higher iron values were found in swimming, diabetic, diabetic swimming, and zinc-supplemented diabetic swimming rats (p < 0.001). Diabetic, zinc-supplemented diabetic, diabetic swimming, and zinc-supplemented diabetic swimming rats had the highest copper values. These results show that zinc supplementation normalized the higher levels of molybdenum, calcium, selenium, and iron levels seen in diabetic rats, indicating that zinc may have a regulatory effect on element metabolism in kidney tissue. Topics: Analysis of Variance; Animals; Boron; Calcium; Chromium; Cobalt; Copper; Diabetes Mellitus, Experimental; Dietary Supplements; Injections, Intraperitoneal; Iron; Kidney; Lead; Magnesium; Male; Molybdenum; Rats; Rats, Sprague-Dawley; Selenium; Streptozocin; Swimming; Trace Elements; Zinc; Zinc Sulfate | 2012 |
Effect of zinc supplementation on the distribution of various elements in the serum of diabetic rats subjected to an acute swimming exercise.
The present study aims to examine the effect of supplementation of zinc on the distribution of various elements in the sera of diabetic rats subjected to an acute swimming exercise. A total of 80 Sprague-Dawley-type adult male rats were equally allocated to one of eight groups: Group 1, general; Group 2, zinc-supplemented; Group 3, zinc-supplemented diabetic; Group 4, swimming control; Group 5, zinc-supplemented swimming; Group 6, zinc-supplemented diabetic swimming; Group 7, diabetic swimming; and Group 8, diabetes. The rats were injected with 40 mg/kg/day subcutaneous streptozotocin (STZ) twice, with a 24-h interval between two injections. Zinc was supplemented at a dose of 6 mg/kg/day (ip) for 4 weeks. Blood samples were collected at the end of the 4-week study, and serum levels of lead, cobalt, molybdenum, chrome, sulfur, magnesium, manganese, sodium, potassium, phosphorus, copper, iron, calcium, zinc, and selenium (mg/L) were determined with atomic emission. The lowest molybdenum, chrome, copper, iron, potassium, magnesium, sodium, phosphorus, lead, selenium, and zinc values were obtained in Group 7 and 8. These same parameters were higher in the swimming exercise group (Group 4), relative to all other groups. The values in zinc-supplemented groups were found lower than the values in Group 4, but higher than those in Group 6 and 7. The results obtained from the study demonstrate that acute swimming exercise and diabetes affect the distribution of various elements in the serum, while zinc supplementation can prevent the negative conditions associated with both exercise and diabetes. Topics: Animals; Calcium; Chromium; Cobalt; Copper; Diabetes Mellitus, Experimental; Dietary Supplements; Elements; Iron; Lead; Magnesium; Male; Manganese; Molybdenum; Phosphorus; Physical Conditioning, Animal; Potassium; Rats; Rats, Sprague-Dawley; Selenium; Serum; Sodium; Sulfur; Swimming; Zinc; Zinc Sulfate | 2011 |
[Effect of cadmium and lead compounds on behavior of some enzymes in peripheral blood of rats with experimental diabetes].
The aim of these tests was to show whether in an experimental diabetes toxic compounds of the cadmium and lead would intensify changes in the enzymes activity caused by a diabetes itself. The test was carried out on the Wistar breed of rats. After inducing the experimental diabetes animals were given cadmium and lead compounds by searchers directly into their stomachs. The following enzymes the AspAT and the AlAT and the alkaline phosphatase (AP) were indicated among all tested animals. The statistic significant increase of the AspAT and the AlAT and the decrease of the alkaline phosphatase in a blood were documented in the experimental diabetes as well as among animals subjected to the cadmium and lead in comparison with the results secured from the checking group of animals. In comparison to animals with a diabetes itself, in the experimental diabetes the toxic compounds of the cadmium and lead explicitly increased the activity changes of the AlAT and the alkaline phosphatase. On the grounds of the above results it can be assumed that in the diabetic diseases the toxic metals may intensify pathological changes. Topics: Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Cadmium; Diabetes Mellitus, Experimental; Lead; Rats; Rats, Wistar | 1992 |
Studies on induction of delta-aminolevulinic acid synthase, ferrochelatase, cytochrome P-450 and cyclic AMP by phenformin. Chlorpropamide, allylisopropylacetamide and lead in hepatocytes from normal and experimental diabetic rats.
The present work demonstrates that phenformin exerted an inducing effect on delta-aminolevulinic acid synthase (ALA-S) and ferrochelatase activities and on cytochrome P-450 content in isolated hepatocytes from rats with experimental diabetes. Similar results were obtained with respect to ALA-S activity and cytochrome P-450 content when chlorpropamide was used. The inducing effect exerted by allylisopropylacetamide (AIA) on ALA-S and ferrochelatase activities in diabetic hepatic cells was markedly greater than that observed in normal hepatocytes. This stimulatory response was not enhanced by adding dibutyryl cyclic AMP (cAMP). When phenformin was added to isolated rat hepatocytes of normal rats, induction of ALA-S and ferrochelatase activities and cytochrome P-450 content was observed only in the presence of added dibutyryl cAMP. Addition of chlorpropamide to this in vitro system did not exert an inducing effect on the same enzymes even in the presence of dibutyryl cAMP. The present results add more experimental evidence about the lability of the heme pathway of diabetic hepatocytes. Topics: 5-Aminolevulinate Synthetase; Allylisopropylacetamide; Animals; Bucladesine; Chlorpropamide; Cyclic AMP; Cytochrome P-450 Enzyme System; Diabetes Mellitus, Experimental; Enzyme Induction; Ferrochelatase; In Vitro Techniques; Lead; Liver; Lyases; Male; Phenformin; Rats | 1990 |
HMP-shunt and cholesterol metabolism in experimental models involving normal and preneoplastic liver growth.
Previous studies from our laboratories have shown a stimulation of HMP-shunt, cholesterol metabolism and DNA synthesis during cell proliferation. In order to understand the co-ordinated regulation of these pathways during cell growth, the above metabolic pathways were studied in: liver regeneration after partial hepatectomy, lead-induced liver hyperplasia, liver cell proliferation induced by insulin in streptozotocin-diabetic rats, liver cell proliferation in fasted rats after refeeding and, hepatocyte nodules induced by a selection procedure. The results indeed indicate that changes in HMP-shunt and cholesterol metabolism occur at a very early stage during the process of normal as well as preneoplastic cell growth. The coordinated regulation between cell growth and changes in these metabolic pathways needs further study. Topics: Animals; Cell Division; Cholesterol; Diabetes Mellitus, Experimental; Diethylnitrosamine; Fasting; Glucosephosphate Dehydrogenase; Hepatectomy; In Vitro Techniques; Insulin; Lead; Liver; Liver Neoplasms, Experimental; Liver Regeneration; Male; Nitrates; Organ Size; Pentose Phosphate Pathway; Precancerous Conditions; Rats; Rats, Inbred Strains | 1987 |
Metabolic disorders of serum lipoproteins in endotoxin-poisoned mice: the role of high density lipoprotein (HDL) and triglyceride-rich lipoproteins.
A study was performed to clarify the role of serum lipoproteins, especially high density lipoprotein (HDL) and triglyceride-rich lipoproteins in endotoxemic or endotoxin-poisoned animals. The level of HDL-cholesterol decreased markedly in mouse serum 18-24 hr postintoxication, while the amount of low density lipoprotein (LDL)-cholesterol in the sera of poisoned mice was about 175% of that of the controls. Serum lecithin-cholesterol acyltransferase activity in the poisoned mice decreased slightly for 3-6 hr after endotoxin injection, but became markedly increased at 18-24 hr as compared with that in the controls. The amount of serum very low density lipoprotein (VLDL) showed a marked increase in the poisoned mice 8-24 hr postintoxication. The HDL fraction in the electrophoretic patterns of serum was reduced according to the dose of endotoxin 18 hr postintoxication. The HDL fraction in mice injected with lead acetate plus endotoxin was markedly lower than that in the poisoned mice. When streptozotocin-diabetic mice were injected with endotoxin, the HDL fraction was higher than that in the endotoxin-poisoned mice. In endotoxin-poisoned mice a correlation was observed between the lipid peroxide and LDL levels in the serum. In disk electrophoretic patterns, the HDL fraction in mice given vitamin E-supplemented diet showed a higher level than that in mice given a normal diet. Lipoprotein lipase (LPL) activity in poisoned mice significantly decreased to 59% of the control value 18 hr postintoxication, but hepatic triglyceride lipase activity was only slightly increased in endotoxin-poisoned mice. In analysis of HDL apoprotein peptide in serum lipoprotein, the apo C-II peptide level was clearly lower in mouse serum 18 hr postintoxication than that in the controls. These results suggest that the decrease in LPL activity in endotoxin-poisoned mice may be closely related to a decrease in the apo C-II peptide level, and also that it plays an important part in HDL and triglyceride-rich lipoprotein metabolism in the poisoned mice. Topics: Animals; Apolipoprotein C-II; Apolipoproteins; Apolipoproteins C; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Diabetes Mellitus, Experimental; Endotoxins; Lead; Lipase; Lipid Peroxides; Lipoproteins; Lipoproteins, HDL; Lipoproteins, LDL; Lipoproteins, VLDL; Liver; Male; Mice; Organometallic Compounds; Phosphatidylcholine-Sterol O-Acyltransferase; Streptozocin; Triglycerides; Vitamin E | 1982 |
[A combined carbohydrate immunocytochemical technic for localization of glycogen in the pancreatic islands of steroid diabetic rats].
Topics: Animals; Diabetes Mellitus, Experimental; Glycogen; Histocytochemistry; Immunoenzyme Techniques; Islets of Langerhans; Lead; Organometallic Compounds; Rats; Triamcinolone Acetonide | 1982 |
[Effect of lead and carbon monoxide under the condition of diabetic metabolism (author's transl)].
The NZO-Mice were used to study the influence of carbon monoxide and lead under the condition of diabetic metabolism. The animals treated with 80 ppm (COHb 10.81) showed significantly lower tolerance for glucose. Even after removing the burden of carbon monoxide for 50 days, the blood sugar level after glucose tolerance test remained in experimental animals significantly higher than in controls (20-min-value). The NZO-Mice after enteral lead exposition showed no significant changes of the condition of the diabetic metabolism after the glucose tolerance test. However, the NZO-Mice, compared to NMRI mice and rats, reached significantly higher level of blood sugar. Topics: Animals; Blood Glucose; Carbon Monoxide; Diabetes Mellitus, Experimental; Glucose Tolerance Test; Lead; Mice | 1979 |