Influence of dietary capsaicin and onion on the metabolic abnormalities associated with streptozotocin induced diabetes mellitus

Effect of feeding 15 mg% capsaicin diet or 3% freeze dried onion powder containing diet were examined in albino rats rendered diabetic with streptozotocin injection. Diabetic rats maintained on onion diet for 8 weeks excreted comparatively less amounts of albumin, urea, creatinine and inorganic phosphorus. Dietary onion also partially reversed the abnormalities in plasma albumin, urea, creatinine and inorganic phosphorus in diabetic animals. Onion also produced a significant reduction in hyperglycemic status of diabetic animals. Diabetic rats maintained on onion diet had a lowered relative liver weight at the end of the study compared to diabetic control group. Diabetic rats fed onion diet also exhibited lowered lipid peroxides in circulation and in urine when compared to diabetic control group. Blood cholesterol was lowered significantly by dietary onion in diabetic animals. Cholesterol decrease was exclusively from LDL-VLDL fraction. Significant decrease in blood phospholipids and tr iglycerides also brought about by dietary onion. Hepatic cholesterol, triglycerides, phospholipids which were elevated under diabetic condition were countered significantly by dietary onion. Dietary capsaicin did not have any significant influence on any of the parameters tested in diabetic rats. Thus, the study reveals that onion feeding improves the metabolic status in diabetic condition, probably because of its hypoglycemic as well as hypocholesterolemic effect. (Mol Cell Biochem 175: 49–57, 1997)     

Protective effect of dietary curcumin and capsaicin on induced oxidation of low-density lipoprotein, iron-induced hepatotoxicity and carrageenan-induced inflammation in experimental rats

The beneficial influence of dietary curcumin, capsaicin and their combination on the susceptibility of low-density lipoprotein (LDL) to oxidation was examined in an animal study. Individually, both dietary curcumin and capsaicin significantly inhibited the in vivo iron-induced LDL oxidation, as well as copper-induced oxidation of LDL in vitro. The protective effect of the combination of curcumin and capsaicin on LDL oxidation was greater than that of individual compounds. This protective influence of spice principles was also indicated by the relative anodic electrophoretic mobility of oxidized LDL on agarose gel. In another study, rats injected with iron showed hepatic toxicity as measured by an increase in lipid peroxides and elevated serum enzymes, alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase. Dietary curcumin, capsaicin and their combination reduced the activities of these enzymes, and lowered the liver lipid peroxide level, indicating amelioration of the severity of iron-induced hepatotoxicity. In yet another study, a comparison of the extent of carrageenan-induced paw inflammation showed that both dietary curcumin and capsaicin moderately lowered inflammation, while the spice principles in combination were more effective. Dietary curcumin and capsaicin significantly decreased the activity of 5'-lipoxygenase activity in the polymorphonuclear lymphocytes in carrageenan-injected rats, the decrease being even higher in the case of combination of these two spice principles. Results suggest that dietary curcumin and capsaicin individually are protective to LDL oxidation both in vivo and in vitro, to iron-induced hepatotoxicity and to carrageenan-induced inflammation. This beneficial effect was higher when the two compounds were fed in combination.     

Zinc supplementation alleviates the progression of diabetic nephropathy by inhibiting the overexpression of oxidative-stress-mediated molecular markers in streptozotocin-induced experimental rats

Zinc deficiency during diabetes projects a role for zinc nutrition in the management of diabetic nephropathy. The current study explored whether zinc supplementation protects against diabetic nephropathy through modulation of kidney oxidative stress and stress-induced expression related to the inflammatory process in streptozotocin-induced diabetic rats. Groups of hyperglycemic rats were exposed to dietary interventions for 6 weeks with zinc supplementation (5 times and 10 times the normal level). Supplemental-zinc-fed diabetic groups showed a significant reversal of increased kidney weight and creatinine clearance. There was a significant reduction in hyperlipidemic condition along with improved PUFA:SFA ratio in the renal tissue. Expression of the lipid oxidative marker and expression of inflammatory markers, cytokines, fibrosis factors and apoptotic regulatory proteins observed in diabetic kidney were beneficially modulated by zinc supplementation, the ameliorative effect being concomitant with elevated antiapoptosis. There was a significant reduction in advanced glycation, expression of the receptor of the glycated products and oxidative stress markers. Zinc supplementation countered the higher activity and expression of polyol pathway enzymes in the kidney. Overexpression of the glucose transporters, as an adaptation to the increased need for glucose transport in diabetic condition, was minimized by zinc treatment. The pathological abnormalities in the renal architecture of diabetic animals were corrected by zinc intervention. Thus, dietary zinc supplementation has a significant beneficial effect in the control of diabetic nephropathy. This was exerted through a protective influence on oxidative-stress-induced cytokines, inflammatory proliferation and consequent renal injury.     

Intestinal disaccharidases and some renal enzymes in streptozotocin-induced diabetic rats fed sapogenin extract from bitter yam (Dioscorea polygonoides)

In this study, the effects of bitter yam sapogenin extract or commercial diosgenin on intestinal disaccharidases and some renal enzymes in diabetic rats were investigated. Diabetic male Wistar rats were fed diets supplemented with 1% sapogenin extract or commercial diosgenin for 3 weeks. Plasma glucose, intestinal disaccharidases and the activities of transaminases, acid phosphatase, glucose-6-phosphatase, ATP citrate lyase, glucose-6-phosphate dehydrogenase and pyruvate kinase were assessed for the level of metabolic changes in the kidney of diabetic rats. Sapogenin extract or commercial diosgenin supplementation resulted in a significant decrease in lactase and maltase activities in all three regions of the intestine compared to the diabetic control group. However, the test diets significantly reduced intestinal sucrase activity in the proximal and mid regions. Test diets supplementation resulted in a significant decrease in the activities of the transaminases compared to the normal and diabetic control groups. The activity of glucose-6-phosphatase was significantly increased while the activities of ATP citrate lyase, pyruvate kinase and glucose-6-phosphate dehydrogenase were significantly reduced in the kidney of the diabetic control rats compared to the normal group. Test diets supplementation did not significantly alter glucose-6-phosphatase, ATP citrate lyase and pyruvate kinase activities compared to the diabetic control. However, there was a significant increase in glucose-6-phosphate dehydrogenase activity toward the normal group. In conclusion, the consumption of bitter yam sapogenin extract or commercial diosgenin demonstrated hypoglycemic properties, which are beneficial in diabetes by reducing intestinal disaccharidases activities; however, bitter yam sapogenin extract may adversely affect the integrity of kidney membrane.     

Dietary fibres ameliorate decreased synthesis of heparan sulphate in streptozotocin induced diabetic rats

The role of dietary fibers in diabetes has been studied by several workers. Long term dietary treatment with increased amounts of fiber-rich low-glycaemic index natural foods improves blood glucose and reduces the number of hypoglycemic events in type I diabetic patients. On the other hand Rohrbach and Martin and Cohen and Surma described changes in the general and biochemical structure of renal tissues such as the glomerular basement membranes. One of these changes was the reduction and undersulfation of the glycoconjugate and glycosaminoglycan heparan sulfate, which plays an important role in renal structure and function. The purpose of the present study was to determine specific effects of two types of dietary fiber on the composition of kidney glycoconjugates in an animal model of diabetes type I. Streptozotocin-treated diabetic rats were fed either a control diet or diets containing 10% wheat bran (insoluble dietary fiber) or 5% guar gum (soluble dietary fiber). Effects of these fibers on glycaemic control and nephropathy were assessed using previously described methodologies. The effect of dietary fiber in the glycoconjugate composition of kidneys of control and diabetic animals was studied by estimating their total hexose content, sulfated glycosaminoglycans, hexosamines and uronic acids. The activities of enzymes that participate in the synthesis of saccharides and glycoconjugates (L-glutamine-fructose-6-phosphate aminotransferase) and their degradation (N-acetyl-beta-glucosaminidase and beta-glucuronidase) were also evaluated. Results indicated that both soluble and insoluble dietary fibers ameliorated a significant increase in the activity of GFAT. Heparan sulfate was also isolated and quantified. Results indicated that the renal content of heparan sulfate decreased in diabetic animals and that this decrement was ameliorated by the ingestion of both soluble and insoluble fiber in the diet.     

Effects of dietary carbohydrate intake on antioxidant enzyme activity and copper status in the copper-deficient streptozotocin (STZ) diabetic rat

The aim of this study was to investigate how dietary lactose, compared with sucrose, in association with copper deficiency influences the antioxidant and copper status in the diabetic rat. Two groups of male rats (n = 12) were fed copper-deficient diets containing either 300 g/kg of sucrose or 300 g/kg of lactose in a pair-feeding regime for 35 days. Six rats from each group were injected with streptozotocin to induce diabetes. After a further 16 days the animals were killed and the liver, heart, and kidney removed for the measurement of copper levels and the activities of antioxidant and related enzymes. Diabetes resulted in higher hepatic and renal copper levels compared with controls. The copper content of the heart and kidney in diabetic rats consuming sucrose was also significantly higher than in those consuming lactose. Catalase activity in the liver, heart, and kidney was significantly increased in diabetic rats compared with controls. Hepatic glutathione S-transferase and glucose-6-phosphate dehydrogenase and cardiac copper zinc superoxide dismutase activities were also higher in diabetes. Sucrose, compared with lactose feeding, resulted in higher cytochrome c oxidase and glutathione peroxidase activities in the kidney while glucose-6-phosphate dehydrogenase activity was lower. The combination of lactose feeding and diabetes resulted in significantly higher activities of cardiac managanese superoxide dismutase and catalase and renal manganese superoxide dismutase and glucose-6-phosphate dehydrogenase. These results suggest that sucrose consumption compared with lactose appears to be associated with increased organ copper content and in general decreased antioxidant enzyme activities in copper-deficient diabetic rats.     

Effect of chronic ethanol consumption on postnatal development of renal (Na + K)-ATPase in the rat.

Renal (Na + K)-ATPase was studied to ascertain whether it follows the pattern of adaptation of membrane-bound enzymes that are inhibited by acute ethanol exposure and develop greater activity after chronic ethanol treatment. A colony of rats was given 20 per cent (v/v) ethanol as sole drinking solution throughout gestation, lactation and following weaning. (Na + K)-ATPase and ouabain-insensitive Ca(2+)-ATPase activities were determined; regional distribution of these enzymes was assessed in renal cortex and outer medulla. Control rats drank tap water. (Na + K)-ATPase in whole homogenate of kidney increased with age in controls and ethanol-fed rats, but the latter showed higher values at every age studied. Between 15 and 60 days of age, the control group showed 2-fold increases in cortex and 5-fold in outer medulla, whereas ethanol-fed rats reached a 3-fold increase in the enzyme activity in both renal regions. Ca(2+)-ATPase showed the same time course in developing kidney of both groups. Chronic ethanol treatment of adult rats resulted in an increase of (Na + K)-ATPase activity in cortex and outer medulla, but no change in other ATPases. Since an earlier maturational development of renal (Na + K)-ATPase was displayed by ethanol-fed rats, underlying mechanisms that may account for these results are discussed.     

Kolaviron,a biflavonoid complex of Garcinia kola seeds modulates apoptosis by suppressing oxidative stress and inflammation in diabetes-induced nephrotoxic rats

Diabetic nephropathy is a complex disease that involves increased production of free radicals which is a strong stimulus for the release of pro-inflammatory factors. We evaluated the renal protective effect of kolaviron (KV) – a Garcinia kola seed extract containing a mixture of 5 flavonoids, in diabetes-induced nephrotoxic rats. Male Wistar rats were divided into 4 groups: untreated controls (C); normal rats treated with kolaviron (C + KV); untreated diabetic rats (D); kolaviron treated diabetic rats (D + KV). A single intraperitoneal injection of streptozotocin (STZ, 50 mg/kg) was used for the induction of diabetes. Renal function parameters were estimated in a clinical chemistry analyzer. Markers of oxidative stress in the kidney homogenate were analyzed in a Multiskan Spectrum plate reader and Bio-plex Promagnetic bead-based assays was used for the analysis of inflammatory markers. The effect of kolaviron on diabetes-induced apoptosis was assessed by TUNEL assay. In the diabetic rats, alterations in antioxidant defenses such as an increase in lipid peroxidation, glutathione peroxidase (GPX) activity and a decrease in catalase (CAT) activity, glutathione (GSH) levels and oxygen radical absorbance capacity (ORAC) were observed. There was no difference in superoxide dismutase (SOD) activity. Diabetes induction increased apoptotic cell death and the levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α with no effect on IL-10. Kolaviron treatment of diabetic rats restored the activities of antioxidant enzymes, reduced lipid peroxidation and increased ORAC and GSH concentration in renal tissues. Kolaviron treatment of diabetic rats also suppressed renal IL-1β. The beneficial effects of kolaviron on diabetes-induced kidney injury may be due to its inhibitory action on oxidative stress, IL-1β production and apoptosis.     

普罗布考对糖尿病大鼠肾组织氧化应激的影响

目的研究普罗布考（Probucol）对糖尿病大鼠肾组织氧化应激的影响。方法采用腹腔注射链脲佐菌素（STZ）建立糖尿病大鼠模型。30只Wistar大鼠分为正常对照组（NC）、糖尿病组（DM）、糖尿病普罗布考治疗组（DP）。8周末称取体重、肾重、计算肾肥大指数（肾重/体重）,检测尿白蛋白排泄率（UAER）;测定各组生化指标包括血糖（BG）、胆固醇（TC）、三酰甘油（TG）、血清肌酐（SCr）、血尿素氮（BUN）;检测肾组织中丙二醛（MDA）的含量及超氧化物歧化酶（SOD）、过氧化氢酶（CAT）与谷胱甘肽过氧化物酶（GSH-Px）活性;肾组织切片行PAS染色分析肾小球面积及肾小球体积。结果 DM组大鼠肾重、肾重/体重、UAER、TC、TG、SCr、BUN、肾小球面积、肾小球体积较NC组均明显增加,DP组上述改变较DM组均明显减轻（P〈0.05）。DP组肾组织中MDA含量明显低于DM组,SOD、CAT、GSH-Px活性明显高于DM组（P〈0.05）。结论普罗布考可能部分通过减轻肾组织氧化应激反应实现对糖尿病大鼠肾脏的保护作用。     

Renal enzymes during experimental diabetes mellitus in the rat. Role of insulin, carbohydrate metabolism, and ketoacidosis

The activities of various ammoniagenic, gluconeogenic, and glycolytic enzymes were measured in the renal cortex and also in the liver of rats made diabetic with streptozotocin. Five groups of animals were studied: normal, normoglycemic diabetic (insulin therapy), hyperglycemic, ketoacidotic, and ammonium chloride treated rats. Glutaminase I, glutamate dehydrogenase, glutamine synthetase, phosphoenolpyruvate carboxykinase (PEPCK), hexokinase, phosphofructokinase, fructose-1,6-diphosphatase, malate dehydrogenase, malic enzyme, and lactate dehydrogenase were measured. Renal glutaminase I activity rose during ketoacidosis and ammonium chloride acidosis. Glutamate dehydrogenase in the kidney rose only in ammonium chloride treated animals. Glutamine synthetase showed no particular variation. PEPCK rose in diabetic hyperglycemic animals and more so during ketoacidosis and ammonium chloride acidosis. It also rose in the liver of the diabetic animals. Hexokinase activity in the kidney rose in diabetic insulin-treated normoglycemic rats and also during ketoacidosis. The same pattern was observed in the liver of these diabetic rats. Renal and hepatic phosphofructokinase activities were elevated in all groups of experimental animals. Fructose-1,6-diphosphatase and malate dehydrogenase did not vary significantly in the kidney and the liver. Malic enzyme was lower in the kidney and liver of the hyperglycemic diabetic animals and also in the liver of the ketoacidotic rats. Lactate dehydrogenase fell slightly in the liver of diabetic hyperglycemic and NH4Cl acidotic animals. The present study indicates that glutaminase I is associated with the first step of increased renal ammoniagenesis during ketoacidosis. PEPCK activity is influenced both by hyperglycemia and ketoacidosis, acidosis playing an additional role. Insulin appears to prevent renal gluconeogenesis and to favour glycolysis. The latter would seem to remain operative in hyperglycemic and ketoacidotic diabetic animals.     

Effects of Aspirin and Nimesulide on tissue damage in diabetic rats

This study was designed to compare the effect of Aspirin (AS) and Nimesulide (NM) on renal failure and vascular disorder in streptozotocin (STZ)-induced diabetic rats. Rats were divided into four groups; control, diabetic rats, diabetic rats plus AS and diabetic rats plus NM, which are COX inhibitors. The renal and aorta tissues morphology were investigated by light microscopy. Trunk blood was also obtained to determine plasma lipid peroxidation product malondialdehyde (MDA) and plasma activity of antioxidant enzymes. MDA levels were increased in the diabetic rats when compared to the control group. AS and NM administration caused a significant decrease in MDA production. Morphological damage in diabetic rats was severe in the kidney and in the aorta tissue. Treatment of AS reduced these damages, but NM did not exert positive effect on these damages in diabetic rats. As a result, although both AS and NM corrected lipid peroxidation parameters such as MDA via their antioxidant properties, only AS ameliorated pathological alteration in tissues. These findings indicate that there may be another mechanism in beneficial effect of AS in diabetic rats.     

Renal Expression of FGF23 in Progressive Renal Disease of Diabetes and the Effect of Ace Inhibitor

Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone mainly produced by bone that acts in the kidney through FGF receptors and Klotho. Here we investigated whether the kidney was an additional source of FGF23 during renal disease using a model of type 2 diabetic nephropathy. Renal expression of FGF23 and Klotho was assessed in Zucker diabetic fatty (ZDF) and control lean rats at 2, 4, 6, 8 months of age. To evaluate whether the renoprotective effect of angiotensin converting enzyme (ACE) inhibitor in this model was associated with changes in FGF23 and Klotho, ZDF rats received ramipril from 4, when proteinuric, to 8 months of age. FGF23 mRNA was not detectable in the kidney of lean rats, nor of ZDF rats at 2 months of age. FGF23 became measurable in the kidney of diabetic rats at 4 months and significantly increased thereafter. FGF23 protein localized in proximal and distal tubules. Renal Klotho mRNA and protein decreased during time in ZDF rats. As renal disease progressed, serum phosphate levels increased in parallel with decline of fractional phosphorus excretion. Ramipril limited proteinuria and renal injury, attenuated renal FGF23 upregulation and ameliorated Klotho expression. Ramipril normalized serum phosphate levels and tended to increase fractional phosphorus excretion. These data indicate that during progressive renal disease the kidney is a site of FGF23 production which is limited by ACE inhibition. Interfering pharmacologically with the delicate balance of FGF23 and phosphorus in diabetes may have implications in clinics.     

Effects of dietary L-arginine supplementation on serum lipids and intestinal enzyme activities in diabetic rats

We investigated whether dietary supplementation with L-arginine, the endogenous precursor of nitric oxide, might affect serum lipid levels and activities of intestinal mucosa enzymes in animals, in which diabetes was induced by administration of streptozotocin. Control and diabetic rats were fed diets with or without 2% L-arginine supplementation for 4 weeks. Diabetic rats had significantly higher concentrations of serum triglycerides and LDL-cholesterol than control rats. These alterations were partially reduced by L-arginine supplementation. Experimental diabetes did not influence the lactase and leucine aminopeptidase activity in the intestine, but the activity of alkaline phosphatase was increased. Furthermore, activities of maltase and sucrase in the intestinal mucosa were elevated in streptozotocin-induced diabetic rats and were restored to control levels after dietary L-arginine supplementation. On the basis of the present experimental evidence, dietary L-arginine supplementation appears to affect the metabolism of lipoproteins and might alleviate some gastrointestinal dysfunctions, commonly seen in diabetes mellitus.     

Renal protection by low dose irbesartan in diabetic nephropathy is paralleled by a reduction of inflammation,not of endoplasmic reticulum stress

Diabetes can disrupt endoplasmic reticulum (ER) homeostasis which leads to ER stress. ER stress-induced renal apoptosis seems to be involved in the development of diabetic nephropathy. The present study was designed to investigate the contribution of reduced ER stress to the beneficial effects of an angiotensin receptor blocker. Insulin-dependent diabetes mellitus was induced by streptozotocin injections to hypertensive mRen2-transgenic rats. After 2 weeks animals were treated with 0.7 mg/kg/day irbesartan. Blood glucose, blood pressure and protein excretion were assessed. Expression of ER stress markers was measured by real-time PCR. Immunohistochemistry was performed to detect markers of ER stress, renal damage and infiltrating cells. Glomerulosclerosis and apoptosis were evaluated. Diabetic mRen2-transgenic rats developed renal injury with proteinuria, tubulointerstitial cell proliferation as well as glomerulosclerosis and podocyte injury. Moreover, an increase in inflammation, podocyte ER stress and apoptosis was detected. Irbesartan somewhat lowered blood pressure and reduced proteinuria, tubulointerstitial cell proliferation and glomerulosclerosis. Podocyte damage was ameliorated but markers of ER stress (calnexin, grp78) and apoptosis were not reduced by irbesartan. On the other hand, inflammatory cell infiltration in the tubulointerstitium and the glomerulus was significantly attenuated. We conclude that irbesartan reduced renal damage even in a very low dose. The beneficial effects of low dose irbesartan were paralleled by a reduction of blood pressure and inflammation but not by a reduction of ER stress and apoptosis. Thus, sustained endoplasmic reticulum stress in the kidney does not necessarily lead to increased inflammation and tubulointerstitial or glomerular injury.     

Animal models of spontaneous diabetic kidney disease

Kidney disease, characterized by proteinuria and glomerular lesions, is a common complication of spontaneous diabetes mellitus in many animal species. It occurs in animals with hypoinsulinemia, hyperinsulinemia, or impaired glucose tolerance. The renal functional and structural abnormalities in spontaneously diabetic animals resemble human diabetic nephropathy in many respects. Mesangial expansion and glomerular basement membrane thickening, two structural hallmarks of diabetic glomerulopathy in humans, are the most frequently encountered lesions in animals. In addition, a nodular form of mesangial expansion that resembles but is not identical with human nodular glomerulosclerosis or the Kimmelstiel-Wilson lesion has been observed in some animal models. Other abnormalities, such as exudative hyaline lesions and arteriolar hyalinosis, have also been noted occasionally in other models. Although diabetic animals may develop kidney disease that resembles human diabetic nephropathy, no single animal model develops renal changes identical to those seen in humans. Nonetheless, animal models with spontaneous diabetic kidney disease may be useful for investigating the mechanisms of development of diabetic nephropathy and the effects of various treatment modalities on the progression of renal disease.     

Protective effect of dietary capsaicin on induced oxidation of low-density lipoprotein in rats

An animal study was carried out to examine the beneficial influence of the known hypocholesterolemic spice principle-capsaicin on the susceptibility of low-density lipoprotein to oxidation in normal and hypercholesterolemic condition. In rats rendered hypercholeterolemic by maintaining them on a cholesterol-enriched diet for eight weeks, inclusion of capsaicin (0.015%) in the diet, produced significant hypocholesterolemic effect. Oxidation of low-density lipoprotein was induced either by copper ion in vitro after its isolation, or by ferrous ion in vivo in experimental rats under either normal or hypercholesterolemic situation and the beneficial effect of dietary capsaicin on the same was evaluated. LDL oxidation was measured by the thiobarbituric acid reactive substances (TBARS) formed and relative electrophoretic mobility of oxidized LDL. Dietary capsaicin was found to be protective to the LDL oxidation in vitro in the case of normal rats as indicated by reduction in TBARS by more than 40%. In the case of LDL isolated from hypercholesterolemic rats the extent of copper induced LDL oxidation was significantly lower than that of LDL isolated from normal rats. Dietary capsaicin did not make any difference in the extent of LDL oxidation in vitro in hypercholesterolemic rats. Ferrous ion induced in vivo oxidation of LDL was 71% lower in capsaicin fed normal rats. In high cholesterol feeding, Fe-induced in vivo oxidation of LDL was 73% lower, while the same was still marginally lower in capsaicin fed hypercholesterolemic rats. Hepatic lipid peroxidation was significantly decreased by dietary capsaicin in normal rats. While a significantly decreased level of lipid peroxidation was observed in hypercholesterolemic rats compared to normal rats, the same was not significantly altered by dietary capsaicin. Results suggest that dietary spice principle capsaicin is protective to LDL oxidation both in vivo and in vitro under normal situation, while in hypercholesterolemic situation where the extent of LDL oxidation is already lowered, capsaicin does not offer any further reduction.     

Garlic ameliorates hyperlipidemia in chronic aminonucleoside nephrosis

Nephrotic syndrome (NS) is characterized by proteinuria, oxidative stress and endogenous hyperlipidemia. Hyperlipidemia and oxidative stress may be involved in coronary heart disease and the progression of renal damage in these patients. Garlic has been suggested to be beneficial in various disease states. Some of the beneficial effects of garlic may be secondary to its hypolipidemic and antioxidant properties. Therefore, the effect of a 2% garlic diet on acute and chronic experimental NS induced by puromycin aminonucleoside (PAN) was studied in this work. Acute NS was induced by a single injection of PAN to rats which were sacrificed 10 days later. Chronic NS was induced by repeated injections of PAN to rats which were sacrificed 84 days after the first injection. Garlic treatment was unable to modify proteinuria in either acute or chronic NS, and hypercholesterolemia and hypertriglyceridemia in acute NS. However, garlic treatment diminished significantly total-cholesterol, LDL-cholesterol and triglycerides, but not HDL-cholesterol in chronic NS. Garlic induced no change in the percentage of sclerotic glomeruli in chronic NS and a significative decrease on the percentage of sclerotic area of these glomeruli (33 ± 3% in NS+Garlic group vs. 47 ± 4% in NS group, p = 0.0126). The enhanced in vivo renal H2O2 production and the diminished renal Cu, Zn-SOD and catalase activities in acute NS, and the decreased renal catalase activity in chronic NS were not prevented by garlic treatment. These data indicate that garlic treatment ameliorates hyperlipidemia and renal damage in chronic NS which is unrelated to proteinuria or antioxidant enzymes.     

Trigonella foenum graecum (fenugreek) seed powder improves glucose homeostasis in alloxan diabetic rat tissues by reversing the altered glycolytic,gluconeogenic and lipogenic enzymes

Trigonella foenum graecum (fenugreek) seed powder has been suggested to have potential antidiabetic effects. The effect of oral administration of Trigonella whole seed powder (5% in the diet) for 21 days on glycolytic, gluconeogenic and NADPlinked lipogenic enzymes were studied in liver and kidney tissues of alloxan-induced diabetic Wistar rats. Diabetic rats were characterised by a 4fold higher blood glucose level and a 0.7fold lower body weight compared to normal controls. The activities of the glycolytic enzymes were significantly lower in the diabetic liver and higher in the diabetic kidney. The activities of gluconeogenic enzymes were higher in both liver and kidney during diabetes, however the activities of the lipogenic enzymes were decreased in both tissues during diabetes. Trigonella seed powder treatment to diabetic rats for 21 days brought down the elevated fasting blood glucose levels to control levels. The altered enzyme activities were significantly restored to control values in both the liver and kidney after Trigonella seed powder treatment. The therapeutic role of Trigonella seed powder in type1 diabetes as exemplified in this study can be attributed to the change of glucose and lipid metabolising enzyme activities to normal values, thus stabilizing glucose homeostasis in the liver and kidney. These biochemical effects exerted by Trigonella seeds make it a possible new therapeutic in type1 diabetes.     

Low-carbohydrate diet and oxidative stress in diabetic and nondiabetic rats

Hyperglycemia of diabetes has been implicated in increased tissue oxidative stress, with consequent development of secondary complications. Thus, stabilizing glucose levels near normal levels is of utmost importance. Because diet influences glycemic control, this study investigated whether a low-carbohydrate (5.5%) diet confers beneficial effects on the oxidative status of the heart, kidney, and liver in diabetes. Male and female normal and diabetic rats were fed standard chow (63% carbohydrates) or low-carbohydrate diet for 30 days. Elevated glucose, HbA(1c), and alanine and aspartate aminotransferases in diabetic animals were reduced or normalized by the low-carbohydrate diet. While diabetes increased cardiac activities of glutathione peroxidase and catalase, low-carbohydrate diet normalized cardiac glutathione peroxidase activity in diabetic animals, and reduced catalase activity in females. Diabetic rats fed low-carbohydrate diet had altered activities of renal glutathione reductase and superoxide dismutase, but increased renal glutathione peroxidase activity in diabetic animals was not corrected by the test diet. In the liver, diabetes was associated with a decrease in catalase activity and glutathione levels and an increase in glutathione peroxidase and gamma-glutamyltranspeptidase activities. Decreased hepatic glutathione peroxidase activity and lipid peroxidation were noted in diet-treated diabetic rats. Overall, the low-carbohydrate diet helped stabilize hyperglycemia and did not produce overtly negative effects in tissues of normal or diabetic rats.