钙激活蛋白酶抑制剂对高糖诱导乳鼠心肌细胞凋亡的作用机制

目的 探讨钙激活蛋白酶(Calpain)抑制剂对高糖诱导的乳鼠心肌细胞凋亡的作用机制.方法 分离培养SD乳鼠心肌细胞,实验分为3组:(1)对照组;(2)高糖(35 mmol/L)组,刺激72 h;(3)高糖(35 mmol/L)+ ALLN(25 mol/L)组.MTT测定各组心肌细胞的生长活力,激光共聚焦显微镜观察和检测心肌细胞线粒体通透性和膜电位,Western blot法检测激活型caspase-3蛋白的表达.结果 MTT结果分析显示高糖刺激72 h后,心肌细胞生存率下降(55％±11％),ALLN预处理组生存率为(70％±15％),与高糖组比较差异具有统计学意义(P＜0.05).高糖可以刺激心肌细胞线粒体通透性增加,mPTP孔开放,降低心肌细胞线粒体膜电位,而ALLN预处理可以抑制高糖对心肌细胞的这种作用(相对荧光强度:30％±15％ vs 60％±11％,P＜0.05).高糖刺激可以导致心肌细胞激活型caspase-3的表达增加,加入ALLN预处理后可以抑制激活型caspase-3的表达,差异有统计学意义(0.42 ±0.11 vs 0.21±0.12,P＜0.05).结论 Calpain抑制剂对高糖诱导的乳鼠心肌细胞凋亡的作用存在保护效应.     

脑源性神经营养因子对高糖培养的大鼠海马神经元的保护作用

目的 探讨脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)对高糖培养的大鼠海马神经元存活的保护作用.方法 无血清体外培养的方法获得新生SD乳鼠海马神经元,分为正常组,高糖组及高糖BDNF组.用免疫荧光细胞化学的方法标记微管相关蛋白(Map2)检测培养的海马神经元的纯度和形态,用PI/Hoechest33342染色的方法检测神经元的存活率.结果 大鼠海马神经元在高糖培养条件下存活率下降,易坏死或凋亡,存活率正常组:(96.11±1.63)％;高糖BDNF组:(93.47±2.43)％;高糖组:(76.29±6.74)％.高糖导致的大鼠海马神经元凋亡可以被BDNF抑制.结论 BDNF对高糖导致的大鼠海马神经元坏死或凋亡具有保护作用.     

全反式维甲酸诱导人膀胱癌EJ细胞凋亡的研究

目的 探讨全反式维甲酸(ATRA)诱导人膀胱癌EJ细胞凋亡的可能性,并进一步研究其作用机制.方法 体外培养人膀胱癌EJ细胞,以不同浓度ATRA处理后,用MTT法测定细胞生长抑制情况;流式细胞术检测细胞凋亡率;分光光度法检测caspase-3活性;逆转录-聚合酶链反应(RT-PCR)法检测bcl-2 mRNA表达.结果 ATRA能显著抑制EJ细胞的生长,并在一定浓度和时间范围内呈现出时间、剂量依赖关系;细胞的凋亡率随着ATRA浓度的增大而增高;ATRA作用后bcl-2 mRNA表达随着ATRA浓度的增大而降低;caspase-3基因的活性随着ATRA浓度的增大而升高.结论 ATRA对人膀胱癌EJ细胞生长的抑制在一定浓度范围内呈时间和剂量依赖性.ATRA通过抑制bcl-2 mRNA表达,激活caspase-3基因而诱导凋亡,这为其诱导凋亡的作用机制之一.     

血管紧张素Ⅱ诱导新生鼠心肌细胞凋亡及c-fos、PCNA表达意义

目的研究血管紧张素Ⅱ(angiotensinⅡ AngⅡ)对新生鼠原代培养心肌细胞凋亡及c-fos、PCNA蛋白表达变化的影响。方法采用体外心肌细胞培养技术,培养Wistar新生鼠原代心肌细胞,将培养96h的心肌细胞随机分为两组,对照组:无血清培养2、6、12、24h。AngⅡ组:以10-7mol/LAngⅡ刺激2、6、12、24h,用TUNEL(terminal deoxynucleotidyl transferse-mediated dUTP nick-end labeling assay)方法检测凋亡细胞数,免疫组化方法观察c-fos、PCNA(proliterating cell nuclear angiten)蛋白染色。结果随着时间的延长AngⅡ组TUNEL染色凋亡心肌细胞数量与对照组相比显著增高;同时伴有早期c-fos、PCNA蛋白表达增加。结论AngⅡ可以诱导乳鼠心肌细胞凋亡,AngⅡ诱导心肌细胞凋亡早期可见c-fos、PCNA表达增强。     

洛铂对卵巢癌细胞SKOV3增值抑制及对bax、bcl-2凋亡基因表达的影响

目的:研究洛泊作用于浆液性卵巢癌细胞SKOV3后其对凋亡基因bcl-2和bax表达的影响。方法:体外培养卵巢癌细胞SKOV3,用MTT比色法检测洛铂对SKOV3细胞株的增殖抑制作用,流式细胞仪检测凋亡相关蛋白bax、bcl-2的表达。结果:体外培养的卵巢癌SKOV3细胞经不同浓度的洛泊处理后细胞生长明显受到抑制,洛泊作用于卵巢癌SKOV3细胞可诱导细胞的凋亡,同时随着洛铂浓度的增加,bax基因的表达增加,而bcl-2表达减少。结论:卵巢癌SKOV3细胞对洛泊具有药物敏感性,洛泊可诱导卵巢癌细胞的凋亡,bax蛋白的表达增加和bcl-2蛋白表达的减少可能是洛泊诱导卵巢癌细胞的凋亡机制之一。     

维生素E及叶酸对高血糖孕鼠子代心肌细胞凋亡的影响

目的探讨维生素E(Ve)及叶酸对高血糖诱导的乳鼠心肌细胞凋亡蛋白caspase-3表达的影响。方法将50只清洁级成年SD孕鼠随机分为5组,分别为正常对照组(A组)、妊娠糖尿病组(B组)、叶酸组(C组)、维生素E组(D组)和Ve+叶酸组(E组)。除对照组外,其余大鼠于妊娠d 1腹腔注射链脲佐菌素(STZ)35 mg/kg制备妊娠糖尿病动物模型,对照组给予等量0.1 mmol/L(p H 4.5)柠檬酸钠—柠檬酸缓冲液。孕d 5,D、E 2组予50 mg/kg维生素E灌胃,C、E组予0.4 mg/kg叶酸灌胃,A、B组予等量的生理盐水灌胃,持续7 d。取自然分娩的乳鼠心肌组织于光镜下观察心肌结构的改变,应用免疫组织化学法检测各组乳鼠心肌细胞caspase-3抗原的表达。蛋白免疫印迹(western-blot)检测各组乳鼠心肌细胞caspase-3的表达。结果 (1)造模前各组血糖值比较差异无统计学意义(P>0.05);造模后,B、C、D、E组血糖值明显高于A组,差异有统计学意义(P<0.01);B、C、D、E 4组间比较差异无统计学意义(P>0.05)。(2)光镜下观察B、C、D、E组乳鼠心肌组织呈现不同程度损伤,表现为细胞坏死、水肿、轮廓不清,心肌纤维排列疏松紊乱、炎性细胞浸润。(3)5组乳鼠心肌细胞凋亡蛋白caspase-3的表达不同,差异有统计学意义(P<0.01)。结论妊娠糖尿病孕鼠对子代心肌细胞凋亡影响明显,孕期补充维生素E、叶酸对乳鼠心肌细胞凋亡有明显改善作用,且叶酸抑制凋亡的作用优于维生素E,同时补充维生素E和叶酸的效果优于单独补充一种。     

α-硫辛酸对高糖诱导下乳鼠心肌细胞作用

目的 探讨α-硫辛酸对高糖诱导的乳鼠心肌细胞肥大保护作用及其机制.方法 取出生1～3d乳鼠心尖部心肌细胞原代培养,用低糖培养基培养48 h后分为对照组、高糖组(25.5 mmol/L)、α-硫辛酸组(高糖+50、100、200、300 mg/L)、蛋白激酶C(PKC)抑制剂组(高糖+PKC抑制剂50 nmol/L)、核转录因子-κB(NF-κB)抑制剂组(高糖+ NF-κB抑制剂5 mmol/L);细胞培养48 h,检测细胞表面积以及蛋白含量,Wesrtern blot法检测PKC-α、NF-κB、肿瘤坏死因子-α(TNF-α)、立早基因c-fos蛋白表达.结果 与对照组比较,高糖组乳鼠心肌细胞肥大、细胞表面积增大、蛋白含量增多,心肌细胞内PKC-α(0.89±0.03)、NF-κB(0.88±0.14)、c-fos(0.62±0.14)、TNF-α(0.85±0.05)蛋白表达均升高(P＜0.05);α-硫辛酸能够减轻乳鼠心肌细胞肥大,使心肌细胞表面积减小、蛋白含量减少(P＜0.05),与高糖组比较,α-硫辛酸300 mg/L组细胞内PKC-α(0.44±0.07)、NF-κB(0.24±0.03)、TNF-α(0.39 ±0.05)、c-fos(0.15 ±0.06)蛋白表达均下降(P＜0.05).结论 α-硫辛酸可抑制高糖诱导的乳鼠心肌细胞肥大,其机制可能与抑制PKC/NF-κB/TNF-α/c-fos的信号转导通路有关.     

全反式维甲酸诱导人膀胱癌EJ细胞凋亡的研究

目的探讨全反式维甲酸（ATRA）诱导人膀胱癌EJ细胞凋亡的可能性，并进一步研究其作用机制。方法体外培养人膀胱癌脚细胞，以不同浓度ATRA处理后，用MTT法测定细胞生长抑制情况；流式细胞术检测细胞凋亡率；分光光度法检测caspase-3活性；逆转录一聚合酶链反应（RT—PCR）法检测bcl-2 mRNA表达。结果ATRA能显著抑制EJ细胞的生长，并在一定浓度和时间范围内呈现出时间、剂量依赖关系；细胞的凋亡率随着ATRA浓度的增大而增高；ATRA作用后bcl-2 mRNA表达随着ATRA浓度的增大而降低；caspase-3基因的活性随着ATRA浓度的增大而升高。结论ATRA对人膀胱癌EJ细胞生长的抑制在一定浓度范围内呈时间和剂量依赖性。ATRA通过抑制bcl—2 mRNA表达，激活caspase-3基因而诱导凋亡，这为其诱导凋亡的作用机制之一。     

阿托伐他汀对急性心肌梗死后大鼠心肌细胞凋亡的影响

目的 观察阿托伐他汀对大鼠急性心梗后心肌细胞凋亡及对caspase-3基因表达的影响.方法 取雄性SD大鼠50只,按数字表法随机分为3组:假手术组,生理盐水梗死模型对照组和阿托伐他汀组[10mg/(kg· d)].除假手术组只开胸外,其余大鼠术前连续灌胃3d,第4天结扎冠状动脉左前降支造成急性心肌梗死模型.伊文氏蓝和TTC染色法确定缺血和梗死心肌的范围.原位末端标记检测细胞凋亡,RT-PCR检测caspase-3 mRNA的表达.结果 与对照组比较,阿托伐他汀组可明显减少心肌梗死面积,明显减少心肌细胞凋亡和心肌内caspase-3 mRNA基因表达.结论 阿托伐他汀可减少大鼠急性心梗后心肌细胞凋亡及抑制caspase-3 mRNA基因.     

迷迭香酸对冠脉结扎大鼠心肌细胞凋亡及凋亡相关基因表达的影响

目的通过建立冠脉结扎大鼠心肌缺血模型,探讨迷迭香酸（Rosernarinic acid,RA）对冠脉结扎大鼠心肌缺血细胞橱亡及凋亡相关基因表达的影响。方法取60只雄性Wister大鼠随机分为假手术组、缺血模型组、硝酸异山梨酯组、RA小剂量组、RA中剂量组、RA高剂量组。以结扎冠状动脉前降支造成大鼠急性心肌缺血模型,采用TUNEL标记法检测细胞凋亡,免疫组织化学法检测心肌细胞bcl-2和bax基因的蛋白表达。结果缺血模型组与假手术组比较,凋亡的细胞明显增多（P〈0．01）,RA组凋亡细胞较缺血模型组明显减少（P〈0．01）,与假手术组比,缺血模型组bcl—2,bax蛋白表达量增加,bax表达尤其明显。RA各给药组bcl-2,bax蛋白的表达量比假手术组有所增加,但bax明显较缺血模型组低（F〈0．05或P〈0．01）。结论RA能上调心肌细胞抗凋亡因子bcl-2和下调促凋亡因子bax的表达,从而抑制心肌缺血后心肌细胞凋亡的发生,这可能是其心肌缺血保护作用的机制之一。     

铬、鱼油对肥胖模型大鼠血脂、血糖的影响

肥胖在全球范围内流行 ,而且严重危害身体健康。铬、鱼油参与并调节糖、脂肪代谢 ,因此 ,我们选择了铬、鱼油作为影响因素 ,观察其对饮食诱导肥胖大鼠的影响。方法 :将肥胖模型大鼠按体重随机分为 4组 ,每组 8只。分别为肥胖组 ;鱼油组 ;鱼油 +铬组和铬组 ,另设基础对照组。喂养 6周后处死动物。取睾周及肾周脂肪称重记录。测定全血血糖和血清血脂。结果 :三个实验组的血糖值、胆固醇、甘油三酯低于肥胖组 ,高密度脂蛋白胆固醇高于肥胖组。结论 :铬、鱼油能降低高血脂、高血糖 ,调节糖、脂代谢 ,这提示我们铬、鱼油能降低肥胖引起的健康危害     

母亲妊娠合并糖尿病对新生儿血糖、胰岛素、胰岛素样生长因子-1的影响

目的:研究母亲妊娠合并糖尿病对新生儿血糖、胰岛素、胰岛素样生长因子-1(IGF-1)的影响。方法:29例母亲妊娠合并糖尿病的新生儿及20例健康新生儿均于生后1h内测空腹血糖,并采脐血用放射免疫法测定胰岛素、IGF-1水平。结果:母亲妊娠合并糖尿病其新生儿生后血糖水平低于对照组(P<0.05);胰岛素、IGF-1水平高于对照组(P<0.05),血糖水平与IGF-1呈负相关(r=-0.432,P<0.05)。结论:母亲妊娠合并糖尿病会导致新生儿生后血糖水平的降低,胰岛素、IGF-1水平的升高,二者共同参与血糖的调节,对这部分新生儿应做好血糖监测,防止低血糖的发生。     

Effects of antacid or ascorbic acid on tissue accumulation and urinary excretion of chromium

Absorption of trivalent chromium is low. Unbound chromium can form insoluble complexes in the gastrointestinal tract. In this study, effects of a calcium-based antacid or ascorbic acid on ⁵¹chromium from chromium chloride were investigated. Rats were dosed with 1 mL of test substance (containing 150 mg calcium carbonate or 10 mg ascorbic acid) or 1 mL water followed by 20 uCi ⁵¹chromium chloride. Twenty-four hours after dosing, ⁵¹chromium in cumulative urine was higher (p<0.02) in the group dosed with ascorbic acid than in the groups dosed with antacid or water. Accumulation of ⁵¹chromium in the kidney, testes, and spleen was lower (p<0.05) in rats dosed with antacid than in those dosed with ascorbic acid or water. These data confirm that absorption of chromium chloride is low and suggest that antacids have a negative effect on chromium absorption from chromium chloride.     

Serum chromium does not predict glucose tolerance in late pregnancy

BACKGROUND: Chromium is an essential element in human nutrition. Serum concentrations of chromium are not well characterized during pregnancy or in gestational diabetes mellitus. OBJECTIVE: The objective of this study was to determine whether low plasma chromium concentrations (< or =3 nmol/L) are associated with altered glucose, insulin, or lipid concentrations during pregnancy. DESIGN: The study was conducted prospectively and took place at the medical obstetric clinic of a tertiary referral hospital. Seventy-nine women with abnormal results of a 50-g glucose challenge test in the third trimester of pregnancy were studied. All women had a formal 75-g oral-glucose-tolerance test, and fasting insulin, lipid, and chromium concentrations were determined. Chromium was measured by graphite furnace atomic absorption spectrometry. RESULTS: The median chromium concentration was 2 nmol/L (95% CI: 0, 12). There were no significant differences in age, plasma glucose, insulin, lipids, calculated insulin resistance, or calculated ss cell function between women with normal and those with abnormal (< or =3 nmol/L) chromium concentrations. CONCLUSIONS: Plasma chromium during pregnancy does not correlate with glucose intolerance, insulin resistance, or serum lipids. Plasma chromium concentrations may not accurately reflect tissue stores of chromium. Several trials showed a beneficial effect of chromium supplementation on glucose tolerance, insulin, and lipids. A method for assessing body chromium stores is required to allow further study.     

Effects of chromium and copper depletion on lymphocyte reactivity to mitogens in diabetes-prone BHE/cdb rats

OBJECTIVE: The purpose of this study was to measure effects of chromium (Cr) and copper (Cu) depletion on lymphocyte reactivity to mitogens in diabetes-prone BHE/cdb rats. METHODS: A 2 x 2 factorial research design was used, and 40 BHE/cdb rats were fed with Cr- and/or Cu-depleted diets or adequate Cr and/or Cu diets for 21 wk. Cr and Cu concentrations in diets and mineral concentrations of tissues of BHE/cdb rats were measured by using flame and graphite furnace atomic absorption spectrometry. Three glucose tolerance tests were performed to monitor the development of diabetes or glucose intolerance at weeks 12, 18, and 21. Splenocytes (2 x 10(6)) were incubated with phytohemagglutinin-l (PHA-L), concanavalin A (ConA), and lipopolysaccharides (LPSs), respectively, for 72 h. Four hours before the end of the incubation, splenocytes were pulsed with 3H-thymidine. The 3H-thymidine uptake by lymphocytes was used to calculate a stimulation index. RESULTS: According to glucose tolerance tests, these rats did not develop diabetes or impaired glucose tolerance throughout the study. Average Cr concentrations were 0.98 to 1.03 mg Cr/kg of diet in adequate Cr diets and 8.2 to 14 micrograms Cr/kg of diet in Cr-depletion diets. Average Cu concentrations were 3.6 to 6.4 mg Cu/kg of diet in adequate Cu diets and 1.1 to 1.3 mg Cu/kg of diet in Cu-depletion diets. Organ weights did not differ significantly among treatment groups at the end of the study. Cr or Cu depletion significantly affected iron, zinc, and magnesium concentrations in the liver. A significant interactive effect of Cr and Cu was observed on lymphocyte proliferation with PHA-L stimulation at 25 micrograms/mL (P < 0.006). However, there were no significant effects of dietary treatment on lymphocyte proliferation with 10 micrograms/mL of PHA-L, ConA, or LPS stimulations. CONCLUSIONS: When Cr and Cu were adequate in the diets, there was an enhanced effect of Cu or Cr on lymphocyte proliferation. However, when Cr was depleted in the diet, there was a suppressive effect of Cu on lymphocyte proliferation. This result indicates that adequate amounts of Cr and Cu in the diet support the immune system.     

Apple pectin affects the efficacy of epigallocatechin gallate on oral sucrose tolerance test in adult mice

Epigallocatechin gallate (EGCg), a dietary polyphenol and a major tea catechin, is a known sucrase inhibitor. Since dietary pectin is known to modulate some of the functions of the gastrointestinal tract, we investigated whether it could specifically affect the efficacy of EGCg on an oral sucrose tolerance test in mice. Male Crj:CD-1 (ICR) mice (seven weeks old) were randomly divided into two groups and fed a 5 % apple pectin (PE) or 5 % cellulose (CE) diet (control diet) for 28 days. After the experimental diet period, all mice were fasted overnight. A volume of 0.2 mL EGCg (20 mg/mL) was orally administered to all the mice by stainless steel feeding needle via injection syringe and a sucrose tolerance test was performed. The blood glucose levels were measured in blood collected from the tail vein using the OneTouch? Ultra? blood glucose monitoring system. Blood glucose levels at 30 minutes and 60 minutes after sucrose loading in the PE group were significantly higher than initial blood glucose levels. However, blood glucose levels at 30 minutes, 60 minutes, and 120 minutes after sucrose loading in the CE group were not significantly higher than initial blood glucose levels. After laparotomy, plasma lipids were also measured. Plasma triglyceride concentrations were significantly greater in the PE group than in the CE (control) group. This demonstrates that dietary pectin can affect the efficacy of EGCg on the oral sucrose tolerance test in mice.     

Maitake (Grifola frondosa) improve glucose tolerance of experimental diabetic rats

We have previously reported that rats with diabetes induced by injecting streptozotocin into neonates showed remarkably lower blood glucose, urine volume, and glucosuria after administration of Maitake (Grifola frondosa). In the present study, we investigated the effects of Maitake on insulin concentration, organ weight, serum composition, and islets of Langerhans in streptozotocin-induced diabetic rats using the same method. The diabetic rats were produced by injecting 80 mg/kg B.W. streptozotocin into 2-d-old neonates. From the age of 9 wk, the rats were given experimental diets for 100 d. The diabetes and control groups were given either diets containing 20% Maitake (DM and CM groups) or control diets (D and C groups). During administration of the experimental diets, we measured body weight, food intake, amount of feces, and serum insulin concentration at glucose loading. The glucose tolerance test was performed at the 10th week after the start of the experimental diets. The D group had an initial fasting blood glucose of 225+/-49 mg/dL, and a maximum blood glucose of 419+/-55 mg/dL at 60 min. In the DM group, however, the initial fasting blood glucose was 170+/-23 mg/dL, and the maximum blood glucose was 250+/-41 mg/dL at 15 min. Both values were markedly lower than those in the D group (p<0.05). The insulin concentration at 15 min. after glucose loading in the DM group was 41+/-16 microU/mL, which was significantly higher than that in the D group (15+/-7 microU/mL) (p<0.05). After the 100-d experimental period, blood samples were collected. The fructosamine level was significantly lower in the DM group (152+/-21 mmol/L) than in the D group (185+/-13 mmol/L). The concentration of 1.5-A.G. (1.5-anhydro glucitol) was significantly higher in the DM group (9.33+/-2.42 microg/mL) than in the D group (1.33+/-0.52 microg/mL). Observation of insulin antibody stain in the Langerhans cells of the pancreas using ABC method showed a decrease insulin antibody stain in the D group. The cells of the DM group were stained more darkly than those of the D group. From these results, we postulated that the bioactive substances present in Maitake can ameliorate the symptoms of diabetes.     

Effect of chromium supplementation on blood glucose and lipid levels in type 2 diabetes mellitus elderly patients

Intervention trials have shown the beneficial effects of chromium supplementation in type 2 diabetes (non-insulin-dependent diabetes mellitus). This study investigated the effects of chromium picolinate on elderly diabetic patients within a rehabilitation program. Thirty-nine diabetic subjects, average age 73 years (18 males and 21 females), undergoing rehabilitation following stroke or hip fracture, were recruited to participate in this study. An additional 39 diabetic patients constituted the control group. Along with standard treatment for diabetes, the study group received 200 microg of chromium twice a day for a three-week period. Blood samples, dietary intake, and anthropometric data were collected prior to and post-intervention. Throughout the study period, participants received a diet of approximately 1500 kcal/day. Significant differences in the fasting blood level of glucose compared to the baseline (190 mg/dL vs 150 mg/dL, p < 0.001) were found at the end of the study. HbA1c also improved from 8.2% to 7.6% (p < 0.01). Total cholesterol was also reduced from 235 mg/dL to 213 mg/dL (p < 0.02). A trend towards lowered triglyceride levels was also observed (152 mg/dL vs 136 mg/dL). We conclude that, in this population of elderly, diabetic patients undergoing rehabilitation, dietary supplementation with chromium is beneficial in moderating glucose intolerance. In addition, chromium intake appears to lower plasma lipid levels.     

葡萄糖酸铬、鱼油对肥胖大鼠胰岛素抵抗和瘦素抵抗的影响

为探讨在大鼠肥胖形成的过程中 ,葡萄糖酸铬、鱼油对胰岛素抵抗和瘦素抵抗的影响。选取雄性Wistar大鼠 5 0只按体重随机分为 5组。基础对照组 :喂基础饲料同时灌胃水 5ml kgBW。高脂对照组 :喂高脂饲料同时灌胃豆油 5ml kgBW。高脂加鱼油组 :喂高脂饲料同时灌胃鱼油 5ml kgBW。高脂加铬组 :喂高脂饲料同时灌胃葡萄糖酸铬 3mg kgBW(以铬计 )。高脂加鱼油加铬组 :喂含铬高脂饲料同时灌胃鱼油 5ml kgBW。喂养五周 ,于每周末称重、采尾血测定血糖、胰岛素和瘦素。结果高脂饲料诱导的肥胖组体重、血糖、胰岛素和瘦素均高于基础对照组 ,提示铬和鱼油有降血糖、降低胰岛素、瘦素的作用 ,而且能改善胰岛素抵抗和瘦素抵抗作用。     

Supplemental-chromium effects on glucose, insulin, glucagon, and urinary chromium losses in subjects consuming controlled low-chromium diets

The effects of low-chromium diets containing chromium in the lowest quartile of normal intake on glucose tolerance and related variables in 11 females and 6 male subjects were evaluated. Subjects with glucose concentration greater than 5.56 mmol/L but less than 11.1 mmol/L 90 min after an oral-glucose challenge were designated as the hyperglycemic group and the remainder, the control group. Glucose tolerance and circulating insulin and glucagon of the hyperglycemic group all improved during chromium supplementation (200 micrograms/d) whereas those of the control group were unchanged. Glucose and insulin concentrations 60 min after the oral-glucose challenge and the sum of the 0-90 min and 0-240 min glucose values were all significantly lower after chromium supplementation in the hyperglycemic group. These data demonstrate that consumption of diets in the lowest 25% of normal chromium intake lead to detrimental effects on glucose tolerance, insulin, and glucagon in subjects with mildly impaired glucose tolerance.