4-苯基丁酸对高果糖喂养大鼠肝脏脂质沉积及氧化应激的影响

目的：观察内质网应激(ERS)抑制剂4-苯基丁酸(4-PBA)对高果糖饮食喂养大鼠肝脏氧化应激的影响,以探讨ERS在高果糖喂养诱导脂肪肝中的介导作用及其与氧化应激的关系。方法雄性Wistar大鼠分为对照组、高果糖组和4-PBA组[自高果糖喂养4周后给予4-PBA 0.35 g/(kg·d)],8周后处死大鼠并测定肝脏甘油三酯(TG)含量。 PCR法检测ERS标志物葡萄糖调节蛋白78(GRP78)的基因表达。测定细胞中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性及细胞中丙二醛(MDA)的含量。 Western blot法检测肝C/EBP同源蛋白( CHOP)。结果与对照组相比,高果糖组的肝脏TG含量、GRP78基因表达、CHOP蛋白表达显著增加(P<0．01),与高果糖组比较,4-PBA上述指标显著降低(P<0．01)。与对照组相比,高果糖组大鼠的SOD、GSH-Px、CAT活性下降,MDA含量升高(P均<0.01),而4-PBA组的SOD、GSH-Px、CAT活性高于高果糖组,MDA含量低于高果糖组(P均<0.01)。结论长期高果糖喂养可诱导肝脏ERS和氧化应激,ERS抑制剂4-PBA可改善高果糖饮食诱导的肝脏氧化应激。     

Adult hereditary fructose intolerance

Hereditary fructose intolerance （HFI） is an under-recognized, preventable life-threatening condition. It is an autosomal recessive disorder with subnormal activity of aldolase B in the liver, kidney and small bowel. Symptoms are present only after the ingestion of fructose, which leads to brisk hypoglycemia, and an individual with continued ingestion will exhibit vomiting,abdominal pain, failure to thrive, and renal and liver failure. A diagnosis of HFI was made in a 50-year-old woman on the basis of medical history, response to Ⅳ fructose intolerance test, demonstration of aldolase B activity reduction in duodenal biopsy, and molecular analysis of leukocyte DNA by PCR showed homozygosity for two doses of mutant gene. HFI may remain undiagnosed until adult life and may lead to disastrous complications following inadvertent fructose or sorbitol infusion. Several lethal episodes of HFI following sorbitol and fructose infusion have been reported. The diagnosis can only be suspected by taking a careful dietary history, and this can present serious complications.     

利多卡因低温湿敷对小儿输注果糖时疼痛的影响

目的 观察常温利多卡因、冷湿敷与低温利多卡因湿敷用于缓解小儿输注果糖时引起局部疼痛的效果.方法 将120例住院患儿输注果糖引起局部疼痛者,随机分为冷湿敷组、常温利多卡因组、低温利多卡因冷敷组各40例,观察3组疼痛效果.结果 应用利多卡因低温湿敷组效果明显优于其他2组.结论 小儿输注果糖引起局部疼痛可以选用低温利多卡因湿敷来减轻疼痛,效果肯定.     

磷酸肌酸钠联合果糖二磷酸钠治疗病毒性心肌炎的疗效观察

目的 探讨磷酸肌酸钠联合果糖二磷酸钠治疗病毒性心肌炎的疗效.方法 选取2010年9月至2012年8月在新疆自治区人民医院北院就诊的病毒性心肌炎患者99例,按照随机数字表法将患儿分成联合用药组（50例）和基础治疗组（49例）.两组患儿均实施常规治疗,治疗组在常规治疗的基础上加用果糖二磷酸钠,每次150剂mg/kg,每日2次,静脉滴注;联合用药组在治疗组的基础上加用磷酸肌酸钠,50 mg/kg,静脉滴注.两组疗程均为2周.结果 联合用药组治疗后的总有效率为92.0%,显著高于治疗组的67.3%（Z=2.484,P＜0.05）,联合用药组经治疗后心电图及心肌酶谱各有1例未发生变化,治疗组经治疗后心电图无变化4例,心肌酶谱无变化7例,联合用药组经治疗后心电图及心肌酶谱改变均较治疗组显著.结论 磷酸肌酸钠联合果糖二磷酸钠治疗病毒性心肌炎疗效显著,不良反应轻微,安全可行,值得临床推广.     

Dietary high calories from sunflower oil,sucrose and fructose sources alters lipogenic genes expression levels in liver and skeletal muscle in rats

Introduction and ObjectivesThe objectives of this study were to investigate the underlying mechanism of PPARα, LXRα, ChREBP, and SREBP-1c at the level of gene and protein expression with high-energy diets in liver and skeletal muscle.Materials and methodsMetabolic changes with consumption of high fat (Hfat), high sucrose (Hsuc) and high fructose (Hfru) diets were assessed. Levels of mRNA and protein of PPARα, LXRα, ChREBP, and SREBP-1c were investigated. Body weight changes, histological structure of liver and plasma levels of some parameters were also examined.ResultsIn Hfru group, body weights were higher than other groups (P < 0.05). In liver, LXRα levels of Hsuc and Hfru groups were upregulated as 1.87 ± 0.30 (P < 0.05) and 2.01 ± 0.29 (P < 0.01). SREBP-1c levels were upregulated as 4.52 ± 1.25 (P < 0.05); 4.05 ± 1.11 (P < 0.05) and 3.85 ± 1.04 (P < 0.05) in Hfat, Hsuc, and Hfru groups, respectively. In skeletal muscle, LXRα and SREBP-1c were upregulated as 1.77 ± 0.30 (P < 0.05) and 2.71 ± 0.56 (P < 0.05), in the Hfru group. Protein levels of ChREBP (33.92 ± 8.84 ng/mg protein (P < 0.05)) and SREBP-1c (135.16 ± 15.57 ng/mg protein (P < 0.001)) in liver were higher in Hfru group. In skeletal muscle, LXRα, ChREBP and SREBP-1c in Hfru group were 6.67 ± 0.60, 7.11 ± 1.29 and 43.17 ± 6.37 ng/mg, respectively (P < 0.05; P < 0.01; P < 0.05). The rats in Hfru group had the most damaged livers.ConclusionBesides liver, fructose consumption significantly effects skeletal muscle and leads to weight gain, triggers lipogenesis and metabolic disorders.     

Effects of low fructose diet on glycemic control,lipid profile and systemic inflammation in patients with type 2 diabetes: A single-blind randomized controlled trial

Background and aimType 2 diabetes is one of the global epidemic disorders, which causes many side effects on the body. Fructose is a lipogenic monosaccharide. Recent studies have reported the adverse effects of this carbohydrate on diabetes. This study aimed to evaluate the clinical efficacy of a low-fructose diet on the metabolic alterations in patients with type 2 diabetes.MethodsThis study was a randomized, single-blind clinical trial on 50 patients with type 2 diabetes. Participants randomly allocated to two groups, to receive either diabetic-diet or diabetic-diet with low-fructose for 8-weeks. Anthropometric measurements, systolic blood pressure (SBP), Diastolic blood pressure (DBP) and metabolic factors were assessed at baseline and the end of the trial.ResultsAt the end of trial, reduction in body weight, waist circumference, and blood pressure were not significant except for DBP (P = 0.013). Statistical analysis showed that low-fructose diet compared to control group significantly declined fasting blood glucose (FBG), Hemoglobin A1c (HbA1c), Triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C) and high-sensitivity C-reactive protein (hs-CRP) (P = 0.015, P = 0.001, P=<0.0001, P= <0.0001 and P= <0.0001 respectively).ConclusionOur results showed that eight weeks of low-fructose diet results in a significant improvement in FBG, HbA1c, TG, HDL-C and hs-CRP in patients with type 2 diabetes.     

Dietary fructose as a natural sweetener in poorly controlled type 2 diabetes: a 12-month crossover study of effects on glucose, lipoprotein and apolipoprotein metabolism

The metabolic effects of fructose incorporated in the normal diets of 13 poorly controlled, Type 2 diabetic patients were studied in a 6-month, randomized, crossover study. Patients used 60 g day-1 of crystalline fructose in divided amounts as part of their isocaloric (1400-3900 kcal), weight-maintaining diet. During fructose supplementation, the distribution of carbohydrate-derived calories was 35% complex and 15% simple, the latter solely from fructose. This was compared with the patients' values on their usual diabetic diet (carbohydrate 50% (mostly complex), fat 38%, and protein 12%). After 6 months of taking fructose, fasting serum glucose decreased from 12.6 +/- 1.1 (+/- SE) to 9.8 +/- 1.3 mmol l-1 (p less than 0.02), while it was unchanged on normal diet (11.0 +/- 0.1 vs 11.6 +/- 0.9 mmol l-1, NS). Glycosylated haemoglobin was also reduced from 11.3 +/- 0.4 to 9.9 +/- 0.5% (p less than 0.05) on fructose, but unchanged on the control diet (10.4 +/- 0.7 vs 11.2 +/- 0.7%, NS). No significant long-term deleterious changes were observed in the fasting serum lipids, lipoproteins, and apolipoproteins A-1 and B-100. Fructose was well tolerated without significant effects on body weight, or lactic acid and uric acid levels.     

果糖液的结晶性能研究

对果糖液在结晶条件下的稳定性及其结晶性能进行了研究。结果表明：果糖在６０℃、ｐＨ４．０左右时比较稳定；对结晶有着重要影响的粘度与浓度和温度有密切关系。     

Diagnosis of fructose-1,6-bisphosphatase deficiency using leukocytes: normal leukocyte enzyme activity in three female patients

Summary In the past 5 years we have discovered 8 boys and 3 girls who suffer from fructose-1,6-bisphosphatase deficiency. Although they all showed the typical symptoms of the deficiency such as frequent vomiting, hypoglycemia, lactic acidosis, and hepatomegaly, the age at diagnosis varied from 2 months to 4 years. All the boys revealed the deficient enzyme activity in leukocytes but none of the girls. The liver biopsy was investigated in six patients to confirm the diagnosis. These results suggest the existence of tissue-specific isoenzymes for fructose-1,6-bisphosphatase possibly with a different gene origin.Abbreviations FBP fructose-1,6-bisphosphate - FBPase fructose-1,6-bisphosphatase Dedicated to Prof. Dr. N. Zöllner on the occasion of his 70th birthday