Effects of dietary fatty acids on lipid metabolism in streptozotocin-induced diabetic rats

We measured the activity of liver delta9- and delta6-desaturases and examined plasma and liver microsome phospholipid fatty acid composition in control and diabetic rats fed a basal diet supplemented with 5% (by weight) olive oil (OO), sunflower oil (SO), or fish oil (FO), respectively. Plasma glucose, cholesterol, triacylglyceride, and phospholipid levels were also measured. An increase in plasma and liver microsome oleic acid and a decrease in arachidonic acid were found in diabetes. In the liver, docosahexaenoic acid levels were higher in diabetic versus control rats. Diabetes increased liver delta9-desaturase in OO-fed rats and did not modify delta6-desaturase activity in OO- or SO-fed rats. Both enzymatic activities were decreased in diabetic rats fed the FO diet. As a main conclusion, it appears that diet-induced alterations in membrane composition provide a mechanism for improving the diabetic condition in animals and overcoming the effect of insulin deficiency on desaturase activities. Plasma cholesterol was not modified either by diabetes or by diet. In diabetes, OO-fed rats showed the lowest levels of triglycerides. Plasma phospholipids were significantly higher in OO-fed versus FO-fed rats. These findings suggest that OO contributes to a better control of the hypertriglyceridemia accompanying diabetes as compared with the other two diets in this rat model.     

姜黄素对酒精诱导的大鼠脂质过氧化反应的影响

目的:观察姜黄素对酒精性肝病大鼠肝脏氧化应激指标SOD,MDA和NO及血清ALT,AST和ALP水平的影响,探讨姜黄素对酒精诱导的大鼠脂质过氧化反应的影响.方法:将40只SD大鼠随机分为对照组、模型组、姜黄素治疗Ⅰ组(40 mg/kg)、姜黄素治疗Ⅱ组(80 mg/kg)和姜黄素治疗Ⅲ组(160mg/kg),每组8只.除对照组用等量生理盐水灌胃外,其他组均采用56度白酒6.72 g/(kg·d)灌胃的方法制作酒精性肝病大鼠模型,6 wk后姜黄素治疗Ⅰ、Ⅱ、Ⅲ组分别加用姜黄素ig,至12 wk末,处死大鼠,抽取血标本测定血清ALT、AST及ALP水平;留取肝组织标本测定SOD活性、MDA及NO含量,常规HE染色观察肝脏病理变化.结果:与对照组相比,模型组大鼠血清ALT、AST及ALP水平显著升高(86.4±7.5 vs 33.5±10.3;201.0±16.8 vs 116.5±12.0;205.1±20.0 vs 104.6±9.4:均P<0.01);肝组织SOD活性明显下降(80.21±4.55 vs 180.24±27.53,P<0.01),MDA及NO含量显著升高(3.29±0.34vs 1.35±0.12;4.37±0.21 vs 2.72±0.13:均P<0.01).与模型组相比,各姜黄素治疗组血清ALT、AST及ALP水平(Ⅰ组:66.5±9.6,171.4±10.8,176.4±13.7:Ⅱ组:52.4±12.0,145.8±11.9,146.9±13.8:Ⅲ组:40.9±7.9,135.0±11.8,127.1±12.6)明显降低(P<0.05或P<0.01),肝组织MDA及NO含量(Ⅰ组:2.84±0.27,4.01±0.17;Ⅱ组:1.95±0.23,3.60±0.16;Ⅲ组:1.65±0.08,3.22±0.13)均显著降低(P<0.05或P<0.01),而SOD活性(92.36±6.47,117.69±21.96,146.70±27.361明显提高(P<0.05或P<0.01),其中以Ⅱ、Ⅲ治疗组较为显著.模型组大鼠肝细胞出现不同程度的脂肪变性,伴有点、灶状坏死,炎性细胞浸润,各姜黄素治疗组肝脏病理变化不同程度的轻于模型组.结论:姜黄素能抑制脂质过氧化,减轻或防治酒精诱导的肝损伤.     

Scavenging effect of nicorandil on free radicals and lipid peroxide in streptozotocin-induced diabetic rats

Free radicals and lipid peroxide (LPO), easily formed in the diabetic state, play an important role in the development of diabetic complications. Potentially, nicorandil may reduce the production of free radicals and LPO in various organs. In fact, increased LPO levels in the serum, kidney, and cardiac muscle of diabetic (DM) rats were reduced by nicorandil treatment (N treatment). Xanthine oxidase (XOD), which produces free radicals, was decreased in the liver and increased in the kidney of DM rats compared with control rats, and these changes were prevented by N treatment. The concentration of Cu, Zn-superoxide dismutase (SOD) decreased in the cardiac muscle and increased in the kidney of DM rats, and these changes returned to normal after N treatment. The decreased concentration of Mn-SOD in the liver, kidney, and cardiac muscle from DM rats was also reversed by N treatment. The changes in catalase and glutathione peroxidase (GSH-PX) activities in DM rats were not improved effectively by N treatment. Another K-adenosine triphosphate (K-ATP) channel opener, tilisolol hydrochloride, had an effect similar to that of nicorandil. The effects of nicorandil and tilisolol were studied only in DM rats. These data imply that N treatment, as an antioxidative therapy, may be beneficial in preventing diabetic complications due to lipoperoxidation and free radicals in DM rats.     

Effect of thalidomide and rosiglitazone on the prevention of diabetic retinopathy in streptozotocin-induced diabetic rats

Aims/hypothesis Our aim was to compare the therapeutic effect of thalidomide and rosiglitazone on the prevention of diabetic retinopathy in streptozotocin-induced diabetic rats.Methods Male Holtzman rats of 6 to 8 weeks of age and weighing 170±30 g were randomly divided into four groups: control (n=13), untreated diabetic (n=17) and diabetic rats treated with thalidomide (200 mg kg^–1 day^–1) (n=8) or rosiglitazone (1 mg kg^–1 day^–1) (n=22) for 3 months. Diabetes was induced by streptozotocin with the rats having a body weight of 70 mg/kg. After treatment, vascular endothelial growth factor (VEGF) concentrations in ocular fluid were compared between the different groups, and retinal capillary basement membrane thickness was measured by electron microscopy.Results Higher VEGF concentrations in ocular fluid and thicker basement membranes were observed in untreated diabetic rats compared to the control rats. Similar VEGF concentrations and basement membrane thickness were observed for the thalidomide-treated group compared with the control group, whereas no difference in these parameters was observed between the rosiglitazone-treated rats and the control or untreated diabetic rats.Conclusions/interpretation Our findings confirm the association between VEGF concentrations and diabetic retinopathy as suggested by other investigators. Thalidomide, but not rosiglitazone, was associated with the inhibition of basement membrane thickening and the blockade of the increase of VEGF in ocular fluid, thus representing a potential therapeutic drug for the prevention of diabetic retinopathy.Abbreviations T Thalidomide - R rosiglitazone - VEGF vascular endothelial growth factor - BM basement membrane - BMT basement membrane thickness An erratum to this article can be found at     

Elevated lipid peroxidation levels in red blood cells of streptozotocin-treated diabetic rats

This study was performed to determine whether or not hyperglycemia in diabetes results in elevated levels of lipid peroxidation products in red blood cells (RBC). Diabetes was induced in rats by treatment with streptozotocin. The level of lipid peroxidation products was examined in fresh RBC by measuring their thiobarbituric acid (TBA) reactivity after 2 and 4 months of induction of diabetes. Hyperglycemia was assessed by measuring the level of glycosylated hemoglobin and blood glucose. Results show that lipid peroxidation levels were significantly higher (50% to 84%) in RBC of diabetic rats than in controls. The increase in the level of lipid peroxidation was blocked in diabetic rats in which hyperglycemia was controlled by insulin treatment. Among phospholipid classes, relative percentage of sphingomyelin (SM) was significantly reduced in RBC at both 2 and 4 months of diabetes; whereas phosphatidylethanolamine (PE) levels were higher in RBC at 4 months of diabetes only. The level of phosphatidylcholine (PC) did not differ significantly between RBC of control and diabetic rats. This study suggests a significantly altered lipid composition and an accumulation of lipid peroxidation products in RBC of streptozotocin-treated diabetic rats.     

Effects of aminoguanidine on lipid and protein oxidation in diabetic rat kidneys

Nonenzymatic glycation of tissue and plasma proteins may stimulate the production of oxidant and carbonyl stress in diabetes. The aim of this study was to evaluate the effects of aminoguanidine (AG) on lipid peroxidation, protein oxidation and nitric oxide (NO) release in diabetic rat kidneys. After induction of diabetes with streptozotocin, female Wistar rats were divided into 2 groups. Group DAG (n=9) rats were given AG hydrogen carbonate (1 g/L) in drinking water and group D (n=8) was diabetic control rats given only tap water. Group H (n=8) was followed as healthy controls. At the end of an 8 week period, NO release, lipid and protein oxidation were determined in kidney tissues. NO release was significantly lower in diabetic rats compared with healthy controls (p<0.05). Lipid peroxidation was significantly high in group D (3.9 +/- 0.3 nmol MDA/g tissue) compared with the group DAG (2.6 0.1 nmol MDA/g tissue, p<0.01) and group H (2.4 +/- 0.2 nmol MDA/g tissue). Protein oxidation was significantly higher in diabetics than healthy controls (563.8 +/- 23.9, 655.8 +/- 7.2, 431.5 +/- 8.8 mmol carbonyl / g tissue for group DAG, D and H, respectively, p< 0.05). A positive correlation between albuminuria and thiobarbituric acid reactive substance (TBARS) levels (r= 0.54,p<0.005) and carbonyl content (r=0.70, p<0.0005) in kidney homogenate were observed. Although AG treatment had no effect on NO release, it significantly decreased lipid peroxidation in diabetic rat cortices. Consequently increased lipid peroxidation -as well as- protein oxidation could be involved in the pathogenesis of diabetic albuminuria.     

Inhibitory effect of troglitazone on diabetic neuropathy in streptozotocin-induced diabetic rats

Summary Free-radical scavengers and inhibitors of tumour necrosis factor-α (TNF-α) such as N-acetylcysteine and pentoxifylline have been shown to inhibit the development of peripheral neuropathy in streptozotocin(STZ)-induced diabetic rats. In this study we examined the effect of troglitazone, an anti-diabetic thiazolidinedione, on diabetic neuropathy, since it also is a free-radical scavenger and a TNF-α inhibitor. Rats were fed powder chow mixed with troglitazone at 0.5 % and 0.125 % ad libitum. Although blood glucose concentrations were remarkably higher and body weight lower in diabetic than in nondiabetic rats, troglitazone had no effect on these throughout the 24-week experiment. Serum lipoperoxide concentrations, tibial nerve lipoperoxide content and serum TNF-α activity induced by lipopolysaccharide was increased in diabetic rats, but inhibited in troglitazone-treated rats. Motor nerve conduction velocity (MNCV) of the tibial nerve slowed in diabetic rats, compared with that in nondiabetic rats. On the other hand, the slowed MNCV was (p < 0.05–0.01) inhibited after weeks 12 and 16 of the experiment in diabetic rats treated with high and low doses of troglitazone, respectively. Morphometric analysis showed that troglitazone suppressed the decrease of the myelinated fibre area (p < 0.05), axon/myelin ratio (p < 0.01) and fascicular area (p < 0.05) and suppressed the increase of myelinated fibre density (p < 0.001) in diabetic rats. These results indicate that troglitazone has a beneficial effect on peripheral neuropathy in STZ-induced diabetic rats irrespective of blood glucose concentrations. [Diabetologia (1998) 41: 1321–1326] Received: 16 March 1998 and in revised form: 8 June 1998     

大豆低聚糖对高脂大鼠脂质过氧化的影响

大豆低聚糖对实验性大鼠高脂血症的防治研究结果证明：能降低血清总胆固醇（ＴＣ）（Ｐ＜０．０５），提高血清高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）（Ｐ＜０．００１），提高ＨＤＬ－Ｃ／ＴＣ比值（Ｐ＜０．００１），降低血清甘油三酯（ＴＧ）水平（Ｐ＜０．００１）；降低心肌组织过氧化脂质（ＬＰＯ）水平（Ｐ＜０．０１），提高心肌组织超氧化物歧化酶（ＳＯＤ）活性（Ｐ＜０．０１），有抑制脑组织过氧化损伤的趋势。结果提示：大豆低聚糖具有降低高脂大鼠血脂水平，拮抗过氧化损伤的作用。     

Melatonin inhibits lipid peroxidation and stimulates the antioxidant status of diabetic rats

Although melatonin has been established as a free radical scavenger and antioxidant, its effects in diabetes have not been thoroughly investigated. The purpose of this study, therefore, was to investigate the effects of melatonin administration on lipid peroxidation and antioxidant status in streptozotocin (STZ)-induced diabetes in rats. Concentrations of malondialdehyde (MDA) and reduced glutathione (GSH) in erythrocytes and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were compared in 3 groups of 10 rats each [control non-diabetic rats (group I), untreated diabetic rats (group II) and diabetic rats treated with melatonin (group III)]. In the study groups, diabetes developed 3 days after intraperitoneal (i.p.) administration of a single 60-mg/kg dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10-mg/kg i.p. dose of melatonin per day. After 6 wk, the rats in groups II and III had significantly lower body weights and significantly higher blood glucose levels than the rats of group I (P<0.001 and P<0.001, respectively). There were no significant differences in body weight or blood glucose levels between groups II and III. MDA levels in untreated diabetic rats were higher than those in control group rats and in diabetic rats treated with melatonin (P<0.01 and P<0.05, respectively). However, MDA levels in diabetic rats treated with melatonin were not different from those of the control group. The GSH, GSH-Px and SOD levels of untreated diabetic rats were significantly lower than those of the control group (P<0.02, P<0.002 and P<0.05, respectively). In group III, however, melatonin prevented decreases in the thiol antioxidant and the associated enzymes, and so these levels were not significantly different from those in the control group. These results confirm the presence of oxidative stress in STZ-induced experimental diabetes and indicate the beneficial free radical-scavenging and antioxidant properties of melatonin.     

The effects of Yucca schidigera and Quillaja saponaria on DNA damage, protein oxidation, lipid peroxidation, and some biochemical parameters in streptozotocin-induced diabetic rats

The aim of this study was to examine the effects of Yucca schidigera, Quillaja saponaria, and a mixture of both plants on streptozotocin-induced diabetic rats. Animals were allocated into five groups with 10 rats each. The control (C) and diabetic control group (D) were fed with standard rat feed (SRF). The other diabetic groups, the Y. schidigera group (DY), the Q. saponaria group (DQ), and the mix group (DQY), were fed ad libitum using SRF+100 ppm Y. schidigera powder (Sarsaponin 30), SRF+100 ppm Q. saponaria powder (Nutrafito), and SRF+100 ppm Y. schidigera-Q. saponaria powder (Nutrafito Plus), respectively, for 3 weeks. The blood glucose level was found to be significantly lower in the DY and DQ groups than in the D and DQY groups (P<.001). The insulin levels increased in the DY and DQY groups (P<.05). Plasma cholesterol and triglyceride levels in the DY, DQ, and DQY groups significantly decreased compared to those of the D group (P<.01, P<.001, respectively). HDL in the diabetic groups significantly increased in the DQ and DQY groups (P<.05), while LDL did not show any significant change. Mononuclear leukocyte DNA damage, plasma malondialdehyde, and plasma protein carbonyl levels were found to be significantly lower (P<.001, P<.001, P<.05, respectively) in the DY, DQ, and DQY groups according to the D group. The low level of nitric oxide in diabetic rats increased in the DQ group (P<.01). Total antioxidant capacity between groups did not differ. Our results thus suggested that Q. saponaria and Y. schidigera powders could help in the treatment of the disease owing to their hypoglycemic, hypocholesterolemic, and antioxidant effects.     

Remodelling of zero-stress state of small intestine in streptozotocin-induced diabetic rats. Effect of gliclazide

BACKGROUND: Biomechanical properties in terms of residual strains in diabetic small intestine have not been studied. Furthermore, no data have been reported on affect of gliclazide on gastrointestinal complications of diabetes. AIMS: To determine remodelling of zero-stress state of small intestine in streptozotocin-induced diabetic rats and effect of gliclazide treatment. MATERIALS: Morphological properties and residual strains were studied in duodenum, jejunum and ileum obtained from diabetic rats, gliclazide-treated diabetic rats and normal rats (n = 8 each group). METHODS: Diabetes was induced by single intraperitoneal injection of 65 mg/kg streptozotocin. Gliclazide (10 mg kg(-1) day(-1) was injected directly into stomach lumen by intragastric gavage twice daily. Experimental period was 35 days. To approach no-load state; intestinal segments were surgically excised and cut transversely into short ring-shaped segments. Each ring was cut radially to obtain geometry of zero-stress state. Circumferential length, the wall thickness and opening angle were measured from digital images of each specimen and residual strains were computed. RESULTS: Blood glucose level of diabetic group (approximately 20 mmol/l) was consistently higher than that in normal group (approximately 4 mmol/l) after induction of diabetes (p < 0.001). Gliclazide lowered average blood glucose level to between 10 and 15 mmol/l (p < 0.001). Plasma insulin levels of both diabetic groups (average between 10 and 15 pmol/l) were significantly lower than those in normal group (average approximately 18 pmol/l, p < 0.05). Wet weight per unit length and wall thickness of duodenum, jejunum and ileum were significantly higher in Diabetes group than those in Normal group (p < 0.05). Opening angle and absolute value of residual strain were significantly smaller in duodenum and larger in jejunum and ileum in Diabetes group than in Normal group (p < 0.001). Gliclazide treatment partly restored these changes (p < 0.05). CONCLUSIONS: Diabetes induced morphometric and biomechanical remodelling in intestine. Gliclazide partly restored these changes.     

Left ventricular dysfunction and remodeling in streptozotocin-induced diabetic rats.

BACKGROUND: It is not fully clarified how diabetes mellitus (DM)-induced cardiac dysfunction is associated with histopathological changes of the heart in a long lasting period of DM. METHODS AND RESULTS: Eighteen weeks after a streptozotocin injection was given to Wistar - Kyoto rats (D rats), echocardiography and hemodynamic studies including the dobutamine infusion test were performed. After perfusion fixation, immunofluorescent staining and histopathology of the heart were analyzed, and analysis with electron microscopy was also conducted. Systolic blood pressure in the conscious state and left ventricular (LV) ejection fraction by 2-dimensional echocardiography were reduced in D rats. LV mechanical responses to dobutamine assessed by maximal LV pressure derivative (+LVdP/dt) also decreased with higher dobutamine doses in D rats. Although LV and right ventricular (RV) wall thickness were smaller in D rats, there were increased RV volumes, indicating LV and RV dilatational remodeling in D rats. The cardiomyocyte transverse diameter and actin staining in cardiomyocytes in both the LV and RV were significantly reduced, and capillary tortuosity and type IV collagen were increased, indicating microangiopathy in D rats. CONCLUSIONS: Advanced insulin-dependent DM incurred not only RV remodeling but also overt resting LV systolic dysfunction and decreased LV responsiveness to beta adrenergic stimulation with dilatational remodeling, accompanied by pathological changes of capillaries and cardiomyocytes including actin filaments.     

Improvement of lipid profile by amaranth (Amaranthus esculantus) supplementation in streptozotocin-induced diabetic rats

BACKGROUND/AIMS: Lipid disorders may exacerbate some complications of diabetes. Amaranth has been reported to exhibit a cholesterol-lowering effect in hyperlipidemic animals. The present study was designed to investigate the effect of amaranth on serum glucose and the lipid profile in diabetic rats. METHODS: Male Sprague-Dawley rats were assigned to normal control, diabetic control, diabetic amaranth-grain (AG)-supplemented (500 g/kg diet) and diabetic amaranth-oil (AO)-supplemented (90 g/kg diet) groups and fed experimental diets for 3 weeks. Effects were monitored on glucose tolerance, serum and liver lipids, and fecal excretions of lipids and bile acids. RESULTS: Fasting serum glucose levels and the glucose tolerance of diabetic rats were improved by AG and AO supplementation. Serum and liver lipids such as total cholesterol, triglyceride (TG) and very-low-density lipoprotein cholesterol concentrations were also lowered in diabetic animals by AG and AO consumption. Fecal excretions of cholesterol, TG and bile acid were markedly reduced in diabetic rats, and these parameters were dramatically increased by AG and AO supplementation. CONCLUSION: AG and AO supplementation improve the glucose and lipid metabolism in streptozotocin-induced diabetic rats.     

Hypothalamic regulation of impaired growth hormone secretion in diabetic rats. 1. Studies in streptozotocin-induced diabetic rats.

Growth hormone (GH) secretion is blunted in diabetic rats. In the present experiment we observed that pituitary GH concentrations and the plasma GH response to an exogenous dose of growth hormone-releasing hormone (GHRH) is decreased in streptozotocin-induced diabetic rats (p less than 0.02) with respect to normal rats. In an attempt to determine if increased somatostatin (SRIF) secretion is responsible for the decreased GH secretion, we studied the effect of modulating SRIF tone on the GH response to GHRH in normal and streptozotocin-induced diabetic rats. Rats were pretreated with either normal sheep serum and saline (NSS+SAL), somatostatin antibodies (SRIF-Ab), or pyridostigmine (PD), an acetylcholinesterase inhibitor hypothesized to reduce hypothalamic SRIF secretion. Pretreatment of normal rats with SRIF-Ab or PD resulted in an increased GH response to exogenous GHRH in comparison to NSS+SAL-pretreated normal rats at 5 min postinjection. In contrast, pretreatment of diabetic rats with SRIF-Ab or PD did not alter the GH response to exogenous GHRH when compared to NSS+SAL-pretreated diabetic animals. These results suggest that the blunted GH response to exogenous GHRH observed in streptozotocin-induced diabetic rats may not be due to an increase of endogenous SRIF tone.     

N-乙酰半胱氨酸对糖尿病大鼠肾脏NADPH氧化酶表达的影响

目的探讨N-乙酰半胱氨酸（NAC）对糖尿病大鼠肾脏尼克酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶表达的影响。方法大鼠随机分为正常对照（NC）组、正常对照NAC治疗组（CT组）、糖尿病组（DM组）和糖尿病NAC治疗组（DT组）。8周后测定血糖、胰岛素、肌酐、游离15-F2t-异前列烷和总抗氧化物水平、24小时尿蛋白排泄量（UPro/24h）、肾系膜基质增宽指数、肾皮质p22phox、p67phox、铜-锌-超氧化物歧化酶（Cu-Zn-SOD）和结缔组织生长因子（CTGF）蛋白表达。结果糖尿病大鼠UPro/24h、血浆游离15-F2t-异前列烷水平、系膜基质增宽指数、肾脏p22phox、p67phox和CTGF蛋白表达显著增高，血浆总抗氧化物浓度和肾脏Cu-Zn-SOD蛋白表达显著降低。NAC治疗能显著逆转糖尿病大鼠上述各项指标的变化。结论NAC显著降低糖尿病大鼠肾脏氧化应激水平，减轻氧化应激对肾组织的损伤，产生肾脏保护作用。     

Reduced noradrenaline turnover in streptozotocin-induced diabetic rats

Summary To clarify whether activity of the sympathetic nervous system is decreased in streptozotocin-induced diabetic rats, noradrenaline turnover, which is a reliable indicator of sympathetic nervous system activity, was measured in the interscapular brown adipose tissue, heart and pancreas of streptozotocin diabetic rats. Results from studies using inhibition of noradrenaline biosynthesis with -methyl-p-tyrosine demonstrated significant reductions (p<0.05-0.001) in sympathetic nervous system activity in the interscapular brown adipose tissue, heart and pancreas of streptozotocin (65 mg/kg) diabetic rats, compared with measurements in streptozotocin (35 mg/kg) diabetic and saline-control rats. The daily injections of neutral protamine Hagedorn insulin to streptoz/otocin (65 mg/kg) diabetic rats prevented the decrease of noradrenaline turnover in the interscapular brown adipose tissue and heart significantly (p<0.02), but this was less marked in pancreas, compared with non-treated streptozotocin (65 mg/kg) diabetic rats. Furthermore reduced noradrenaline turnover was also observed in the control rats which showed comparable changes in body weight to the rats injected with streptozotocin (65 mg/kg). These results suggest that poorly controlled streptozotocin diabetic rats may have reduced sympathetic nervous function, and that insulin therapy might prevent this.     

链脲佐菌素诱导的糖尿病大鼠视网膜的免疫损伤

分别用免疫组化、免疫荧光方法和计算机图像分析技术研究糖尿病（DM）大鼠视网膜组织中IgA、IgG和IgM的沉积情况。与对照组相比，DM大鼠视网膜组织中IgA、IgG和IgM的沉积增加，有统计学意义（均P〈0．05），说明免疫损伤可能参与了糖尿病视网膜病变的发生发展。