高尿酸血症以及痛风的发病率持续升高,已经成为一个重大的公共卫生问题.肠道菌群的结构改变或失调可引起机体代谢紊乱,肠道微生态尤其与代谢性疾病的发生发展关系密切.目前研究发现高尿酸血症、痛风患者存在肠道菌群失调,降尿酸治疗后肠道菌群可发生相应改变,并且益生菌制剂具有降尿酸作用.本文概述高尿酸血症及痛风患者的肠道菌群特点,从高嘌呤及高果糖饮食对肠道菌群的影响、肠道参与嘌呤和尿酸的代谢、代谢性内毒素血症以及痛风相关炎症因子等方面探讨肠道菌群与高尿酸血症及痛风的关系,并展望肠道菌群可能成为未来诊治高尿酸血症以及痛风的一种新方法.

胰高血糖素样肽1(glucagon-like peptide-1, GLP-1)是肠道L细胞分泌的一种肽类激素,它来源于胰高血糖素原前体,是机体在响应营养摄入时释放的一类高效的肠促胰素.GLP-1是近年来2型糖尿病治疗领域研究的热点.GLP-1受体激动剂(GLP-1 receptor agonists,GLP-1RAs)及GLP-1类似物,由于其作用靶点独特、有效性及安全性俱佳而成为降糖药中最受关注的新型药物之一.本文就GLP-1的研究历程、作用特点、临床应用中的注意事项及最新研究进展等作一综述.

Ectopic adrenocorticotropic hormone (ACTH) syndrome (EAS) associated with nocardiosis is rare, and little information is available regarding its clinical characteristics. In this study, the case of a 35-year-old male patient who showed significant cushingoid features and had a cough with yellow phlegm for 1 month is described. Pulmonary computed tomography (CT) scanning and 18F-fluorodeoxyglucose positron emission tomography combined with CT identified two different lesions in the mediastinum and pulmonary region, respectively. The lesion in the mediastinum was finally diagnosed as an ACTH-secreting mediastinal paraganglioma via biopsy. The sputum culture confirmed pulmonary nocardiosis. The patient was effectively treated with complete tumor resection following the treatment of nocardiosis using trimethoprim-sulfamethoxazole. Following the present case, 11 additional cases of nocardiosis in EAS were identified in the literature and their clinical characteristics were compared and evaluated. It may be concluded that, although Nocardia remains a rare opportunistic infection pathogen in EAS, it is necessary to consider nocardiosis as a diagnosis for patients with pulmonary imaging findings of cavity, consolidation or nodule, particularly when there are brain and extra-pulmonary lesions as well as a poor response to regular treatment.

OBJECTIVE:Inflammation of the small intestine may occur in type 2 diabetes. This study aimed to investigate whether ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) were altered in chronic inflammation of the small intestine of type 2 diabetic rats.METHODS:Thirty-two male Sprague-Dawley rats were used. Eight rats in the control group were fed with regular chow, and 24 rats were fed a high-fat diet and injected with a single low dose of streptozotocin. All of the control rats and diabetic rats were bred for 10 months. Immunohistochemistry detected ABCA1 and ABCG1 in the small intestine in all the rats.RESULTS:Hematoxylin-eosin staining showed chronic inflammation in the small intestine of the diabetic rats. Immunohistochemistry staining showed that alteration of ABCA1 and ABCG1 was different in the inflammatory and epithelial cells. Quantitative analysis showed that the overall expression of ABCA1 and ABCG1 increased in the diabetic rats compared to the control rats. Both ABCA1 and ABCG1 were enriched in the inflammatory cells of the small intestine in diabetic rats. In the epithelial cells, ABCA1, but not ABCG1, was detected in significantly more diabetic rats than control rats.CONCLUSION:Both ABCA1 and ABCG1 are enriched in chronic inflammation of the small intestine of type 2 diabetic rats. ABCA1, but not ABCG1, is activated in the intestinal epithelial cells of type 2 diabetic rats.

Objective To establish type 2 diabetes rat model by high-fat diet and single low-dose streptozotocin. Methods Forty eight male SD rats (200-250 g) were randomly divided into 4 groups. Rats in group I-III were fed with three gra-dient high-fat diets, and rats in group IV were fed with regular chow. The rats in high-fat diet groups were given a single dose of streptozotocin (30mg/kg) intraperitoneal y. The rats were sacrificed at the end of the 3rd, 6th and 12th months (4 rats in each group). The weight, abdominal circumference and body length were measured, the blood glucose and lipid profile were exam-ined and the pathological changes were observed. Results The rats in the high-diet groups all presented abdominal obesity. The fasting blood glucose was >7.8mmol/L, and the rats survived without insulin treatment. The lipid profiles presented as high triglycerides, low HDL and high LDL or total cholesterol. When sacrificed after feeding with high-fat diet for 3 months, arteriolar sclerosis was found in the lungs, myocardium, kidneys, brain, skeletal muscles, eyebal s, penis and bladder in the rats of high-fat diet groups. When sacrificed after feeding with high-fat diets for 6-12 months, intimal calcification, twisting or broken elastic fiber were found in the aorta arch in the rats fed with the highest fat diet, but not in the other two high-fat groups. Conclusion Type 2 diabetes rat model can be established by high-fat diet and single low dosage of streptozotocin. Arteriolar sclerosis can be ob-served in multiple organs via inducing for 3 months. However, significant atherosclerosis in the aorta may require to be induced by diet consisting of more fat or supplemented with vascular damaging agents.

KBG syndrome is characterized by postnatal short stature, macrodontia, facial and hand anomalies, delayed bone age and intellectual disability. KBG syndrome is an infrequently reported autosomal dominant condition caused by a mutation or haploinsufficiency of ANKRD11 at 16q24.3. We report on a patient, who showed many manifestations of KBG syndrome and was found to harbor a de novo ANKRD11 mutation, c.362T > A (p.Met121Lys). As the patient showed additional characteristics not occurring in KBG syndrome, a CGH array was performed which showed a de novo microdeletion of 9q31.2-q33.1. The majority of findings in our patient can be explained by the combined ANKRD11 mutation and 9q31.2-33.1 deletion. The case demonstrates well the need for comparing an abnormal genotype with a detailed phenotype analysis and the need for further studies in case the phenotype is unusual for the genotype. (C) 2013 Published by Elsevier Masson SAS.

Aarskog(–Scott) syndrome (AAS) is characterized by short stature, and facial, limb, and genital anomalies. AAS can be an X‐linked condition caused by mutations in the FGD1 gene, but there is evidence that an autosomal dominant or recessive form also exists. We report on a Chinese family in whom several members have manifestations of AAS, but differ in limb anomalies and show additional characteristics. FGD1 sequencing and linkage analysis excluded FGD1 as the cause in this family. A common known submicroscopic chromosome imbalance is less likely. Both autosomal dominant and recessive patterns of inheritance remain possible. © 2010 Wiley‐Liss, Inc.

患者 男,43岁,已婚;江西籍农民.因"反复头晕、乏力2个月,伴纳差、腹胀1月余",于2008年7月23日转入我院内分泌科治疗.2个月前患者无明显诱因下出现头晕、乏力,在当地医院(具体不说)查血Na+116.7mmol/L,血Cl-86.6mmol/L,予抗炎、补液(具体不祥)治疗后上述症状减轻,但血钠未予复查.

患者,已婚女性,38岁农民,因头痛伴反复意识不清9个月余,于2003年5月19日入院.9个月余前患者受凉后出现干咳,曾有1次咳少量血丝痰,在外院口服琥乙红霉素等药后好转.

由于尿崩症患者临床相对较少见,尽管目前对尿崩症的研究日益深入,但临床上尿崩症的首诊误诊率仍较高,有的甚至因此延误了治疗.为提高对该病的认识,现将1992年2月至2002年2月我院内分泌科收治的47例尿崩症患者的临床资料分析报道如下,以供临床参考.

OBJECTIVE:To investigate the effects of sodium metavanadate (SMV) on blood sugar and glucose phosphorylation in mice, and to discuss the possible mechanism of its hypoglycemic effects.METHODS:Diabetic mice (D) and control mice (V) were randomly allocated to drink SMV (0.2 mg/ml) (CV and DV groups) or NaCl (80 mmol/L) (C and V groups) respectively. The study lasted for 5 weeks. Liver glucokinase, muscle hexokinase, blood glucose and insulin were assayed at the end of each week.RESULTS:Blood glucose was higher in the diabetic groups before the administration of SMV, and the blood glucose level of group DV decreased from (18.77 +/- 1.28) to (8.94 +/- 0.94) mmol/L (P < 0.01) after oral administration of SMV for one week. While liver glucokinase increased from (1.29 +/- 0.64) to (15.36 +/- 1.57) mIU/min/mg protein and muscle hexokinase increased from (1.93 +/- 0.50) to (18.62 +/- 1.71) mIU/min/mg protein (P < 0.01) respectively. There was no continuous change of these parameters during the later weeks. No significant change of serum insulin was observed in the diabetic mice. There was a remarkable negative correlation of blood glucose level with liver glucokinase and muscle hexokinase levels.CONCLUSION:The hypoglycemic effects of SMV was independent of insulin level. In consideration of the close relations of the activities of liver glucokinase and muscle hexokinase with diabetes, and the improving of impaired glucose phosphorylation in diabetic mice by oral sodium metavanadate, which might be the mechanism of hypoglycemic effects of SMV.

钒(vanadium)是地球上广泛分布的微量元素,其含量约占地壳构成的0.02%.钒在人体内的含量大约为25mg,在食物中通常以VO2+或HVO42-形式存在,其中在蘑菇、莳萝、欧芹及黑胡椒中含量最多,新鲜水果、蔬菜、谷物及海产品等亦是钒的主要来源. 1813年地质学家Del Rio首次发现了钒,随后钒的各项生理和药理作用逐渐得到证实.迄今为止,钒的最引人注目的作用是它的降血糖作用,这种作用不仅在1型和2型糖尿病的动物模型中得到证实,而且在有限的临床实验中也得出了类似的结论.现就钒的降血糖作用及机制综述如下.

羊栖菜本种系北太平洋西部特有的暖温性海藻,为马尾藻科植物,可食用和药用.近年来研究显示,羊栖菜具有降血压、抗肿瘤、提高机体免疫力和抗氧化等功效.本实验以四氧嘧啶诱导的糖尿病大鼠为对象,观察羊栖菜降血糖作用,实验结果报告如下. 取体重为190～200 g雄性SD大鼠50只,按体重随机分为5组,其中1组为空白对照组,其他40只大鼠按200 mg/kg剂量,皮下注射四氧嘧啶,造成实验性糖尿病.7 d后测定大鼠血糖浓度,将形成糖尿病的大鼠根据血糖浓度分组.