血镁水平与糖尿病患者微量白蛋白尿的相关性研究

目的：探讨糖尿病患者血清镁水平与微量白蛋白尿之间的关系。方法：纳入在我院内分泌科住院的224例2型糖尿病患者。测量身高、体重、血压,测定空腹血糖（FPG）、血脂、糖化血红蛋白（HbA1c）、超敏C反应蛋白（hs-CRP）、镁和尿白蛋白/肌酐比值（UAER）。根据血镁的下四分位数为切点将糖尿病患者分为低镁组与高镁组。微量白蛋白尿定义为：30mg/g≤UAER〈300mg/g。结果：与高镁组比较,低镁组UAER明显增加（12.52vs.10.49mg/g,P〈0.05）,其微量白蛋白尿的检出率明显升高（14.3%vs.10.7%,P〈0.05）。Spearman相关分析显示,糖尿病患者UAER与病程、SBP、FPG、低密度脂蛋白胆固醇（LDL-c）、hs-CRP和HbA1c呈正相关,而与镁呈负相关（P〈0.05）。Logistic回归分析进一步提示,低镁组发生微量白蛋白尿的风险较高镁组增加1.23倍（OR=1.23,P〈0.05）。结论：糖尿病患者低血镁与微量蛋白尿关系密切,提示血镁的降低在糖尿病早期肾脏的发生中可能起重要作用。     

急性脑血管病人血清镁含量与相关因素关系

测定８０例急性脑血管病人血清镁含量并进行相关因素分析及补镁观察。结果表明：（１）急性脑血管病人血清镁水平明显低于正常人；急性脑血管病人中，出血性脑血管病人血清镁水平高于缺血性脑血管病人。（２）急性脑血管病人血清镁水平与红细胞内镁水平呈正相关，与尿镁呈负相关，与空腹血糖呈负相关，与血浆胆固醇（ＴＣ）和低密度脂蛋白（ＬＤＬ－Ｃ）水平呈负相关；尿镁与空腹血糖、尿糖呈正相关。（３）急性脑血管病人补镁３周后，其缺血性脑血管病人血清镁由０．８１±０．２０ｍｍｏｌ／Ｌ升到１．５０±０．３１ｍｍｏｌ／Ｌ，两者差异显著（Ｐ＜０．０１）；出血性脑血管病人血清镁水平由０．９６±０．１０ｍｍｏｌ／Ｌ升到１．０４±０．２５ｍｍｏｌ／Ｌ，两者间无显著差异。     

补镁对2型糖尿病大鼠胰岛素受体表达水平的影响

目的观察补镁对2型糖尿病大鼠胰岛素受体(insulin receptor,IR)表达水平的影响。方法将高脂饲料喂养加链脲佐菌素注射方法诱发的2型糖尿病大鼠随机分为4个组,高、中、低剂量组在高脂饲料中分别加入氧化镁2000、1000、200mg/kg(以镁离子计),糖尿病对照组只喂饲高脂饲料,正常对照组喂饲普通饲料。动物自由进食,连续4周,用葡萄糖氧化酶法测定空腹尾尖血的血糖含量,腹主动脉取血用放免法测定血清胰岛素含量,用免疫组化法测定胰腺和骨骼肌组织IR表达水平。结果经Image-Pro Plus图像分析,高剂量组的胰腺和骨骼肌组织中IR表达水平分别为0.341±0.001和0.346±0.002,均较糖尿病对照组升高,而血糖水平则较糖尿病对照组降低,差异均有显著性意义(P<0.05)。结论镁补充可以提高2型糖尿病大鼠胰腺和骨骼肌组织中IR的表达水平,降低空腹血糖水平。     

老年及老年前期糖尿病患者检测尿微量蛋白对早期肾损定的临床意义

目的：分析尿白蛋白及β2微球蛋白在早期诊断糖尿病肾病的临床意义。方法：以放射免疫法检测54例老年及老年前期糖尿病病人24h尿白蛋白，β2微球蛋白及内生肌酐清除率。结果：观察到糖尿病非临床肾病时尿白蛋白及β2微球蛋白随着病程的延长而呈现增高，并与内生肌酐清除率呈负相关，与糖尿病视网膜病变呈正相关。结论：提示检测糖尿病病人尿白蛋白及β2微球蛋白有助于早期判断肾脏损害，以便尽早积极治疗。     

镁补充对2型糖尿病大鼠红细胞胰岛素受体亲和力的影响

目的研究镁补充对2型糖尿病大鼠红细胞胰岛素受体亲和力的影响。方法将高脂饲料喂饲加链脲佐菌素腹腔注射诱发的2型糖尿病大鼠随机分成糖尿病对照及高、中、低剂量组,饲料中分别加入氧化镁(以镁计)0、2000、1000、200mg/kg,正常对照组喂饲普通饲料,共喂养4周。检测红细胞胰岛素受体结合常数、结合容量、受体数目、空腹血糖及空腹胰岛素等指标,计算胰岛素抵抗指数与敏感指数。结果高剂量组高亲和力胰岛素受体结合常数、结合容量和受体数目分别为(1.24±0.47)×109L/mol、(1.26±0.53)×1014/L和80.23±0.47,均高于糖尿病对照组;胰岛素抵抗指数较糖尿病对照组降低而胰岛素敏感指数升高。结论镁补充能提高2型糖尿病大鼠红细胞胰岛素受体亲和力,改善胰岛素抵抗。     

补充镁对2型糖尿病大鼠胰岛素抵抗和受体亲和力的影响

目的观察镁补充对2型糖尿病大鼠胰岛素受体亲和力的影响。方法将用高脂饮食联合链脲佐菌素(STZ)方法诱发的2型糖尿病大鼠随机分为4个组,糖尿病对照组喂饲高脂饲料,高、中、低剂量组在高脂饲料中分别加入2000、1000、200mg/kg的镁(以镁离子计)。每周检测空腹血糖1次。自由饮食喂养4 w,处死动物。用放射性受体分析法测肝细胞胰岛素受体亲和力、放射免疫法测血清胰岛素(Ins)水平、比色法检测糖化血红蛋白(HbA1c)和血浆丙二醛(MDA)、葡萄糖氧化酶法测空腹血浆葡萄糖(FPG),并计算胰岛素敏感指数(ISI)和抵抗指数(IRI)。结果高剂量组的高亲和力胰岛素受体结合常数(K1)为(4.76±0.08)×108L/mol,低亲和力胰岛素受体结合常数(K2)与结合容量(R2)分别为(1.10±0.14)×106L/mol,(8.49±0.43)×1013/mg蛋白,均较糖尿病对照组显著性升高(P<0.05)。补镁第3 w开始高剂量组空腹血糖较糖尿病对照组显著性降低,高剂量组的胰岛素敏感指数较糖尿病对照组显著性升高,而胰岛素抵抗指数则显著性降低。结论镁补充可以提高2型糖尿病大鼠胰岛素受体亲和力,降低胰岛素抵抗。     

血清VEGF及sVCAM-2在2型糖尿病视网膜病变患者中的表达及意义

目的探讨血清血管内皮生长因子(VEGF)及可溶性血管内皮细胞黏附分子-2(sVCAM-2)在2型糖尿病视网膜病变患者中的表达及意义。方法选取2018年3月至2019年12月本院收治的2型糖尿病视网膜病变患者54例,根据病变程度分为增生型糖尿病视网膜病变组28例,非增生型糖尿病视网膜病变组26例;收集单纯2型糖尿病患者42例为对照组。采集空腹肘静脉血,测定血清VEGF、sVCAM-2水平以及内皮细胞和内皮祖细胞百分比。结果 3组血清VEGF及sVCAM-2水平比较差异有均统计学意义(均P0.01)。3组内皮细胞比例、内皮祖细胞比例比较差异均有统计学意义(均P0.05)。增生型糖尿病视网膜病变组和非增生型糖尿病视网膜病变组患者血清VEGF、sVCAM-2与内皮细胞水平呈正相关(均P0.01),与内皮祖细胞水平呈负相关(均P0.01)。结论血清VEGF及sVCAM-2在2型糖尿病视网膜病变患者中高表达,与微血管内皮功能水平明显相关。     

2型糖尿病肾病患者血清同型半胱氨酸与尿白蛋白及胰岛素敏感性的关系

目的探讨2型糖尿病肾病(DN)患者空腹血清同型半胱氨酸(Hcy)水平与尿白蛋白及胰岛素敏感性之间的关系。方法98例2型糖尿病患者按UAER值分为正常UAER组(UAER<30mg/d为A组)、早期DN组(30mg/d≤UAER<300mg/d为B组)、临床DN组(UAER≥300mg/d为C组),以30例健康者为对照组;分别测定Hcy、空腹血糖(FPG)、空腹胰岛素(FINS)、糖化血红蛋白(HbA1c)、尿微量白蛋白排泄率(UAER),计算胰岛素敏感指数(ISI)。结果A、B、C组糖尿病病人的血浆Hcy水平,均高于对照组,有显著性差异(p<0.05);三组不同UAER值糖尿病病人间的血浆Hcy水平,也有显著性差异(p<0.05);Hcy与UAER呈显著正相关,与ISI呈显著负相关(p<0.01)。结论2型DN患者高Hcy血症与尿白蛋白呈正相关,并与胰岛素敏感性下降有关,控制尿微量白蛋白,增强胰岛素敏感性可通过调节血Hcy水平对糖尿病微血管并发症起一定预防作用。     

老年及老年前期糖尿病患者检测尿微量蛋白对早期肾损害的临床意义

目的分析尿白蛋白及β2微球蛋白在早期诊断糖尿病肾病的临床意义.方法以放射免疫法检测54例老年及老年前期糖尿病病人24h尿白蛋白、β2微球蛋白及内生肌酐清除率.结果观察到糖尿病非临床肾病时尿白蛋白及β2微球蛋白随着病程的延长而呈现增高,并与内生肌酐清除率呈负相关,与糠尿病视网膜病变呈正相关.结论提示检测糖尿病病人尿白蛋白及β2微球蛋白有助于早期判断肾脏损害,以便尽早积极治疗.     

Ⅱ型糖尿病视网膜病变的危险因素相关分析

目的探讨和分析Ⅱ型糖尿病合并视网膜病变的危险因素。方法采用眼底荧光造影法，观察Ⅱ型糖尿病患者视网膜改变。结果(1)103例Ⅱ型糖尿病病人视网膜病变发生率为28．16％。(2)年龄、病程、糖化血红蛋白、收缩压、舒张压5个因素与糖尿病视网膜病变发病有关，尿微量白蛋白排泄率与Ⅱ型糖尿病病人视网膜病变患病率密切相关。结论为防止糖尿病视网膜病变的发生，应积极控制好血糖和血压，病程长、年龄大和伴有蛋白尿患者应注意定期做眼底检查。     

Magnesium and diabetes mellitus: their relation

The aim of this review was to elaborate a synthesis about the discussions on magnesium and diabetes mellitus, in the last 14 years. The magnesium deficiency has been associated with chronic diseases, amongst them, diabetes mellitus. Epidemiological studies had shown low levels of magnesium ingestion in the general population, as well as a relation between the ingestion of food rich in magnesium and the reduction of diabetes installation and its complications. Hypomagnesemia is frequently present in diabetic patients, however there is not an exact elucidation of the mechanism of magnesium deficiency in diabetes mellitus. On the other hand, in the presence of this illness, it is observed that inadequate metabolic control can affect the corporal concentrations of magnesium, developing hypomagnesemia, which may be still directly related with some micro and macrovascular complications observed in diabetes, as cardiovascular disease, retinopathy and neuropathy. This way, the chronic complications of diabetes can appear precociously. Based on this, the supplementation with magnesium has been suggested in patients with diabetes mellitus who have proven hypomagnesemia and the presence of its complications.     

Magnesium intake is related to improved insulin homeostasis in the framingham offspring cohort

OBJECTIVE: Higher dietary intake of magnesium may protect against development of type 2 diabetes. The aim of this study was to examine the association between dietary magnesium intake and metabolic risk factors for diabetes. METHODS: We examined cross-sectional associations between magnesium intake and fasting glucose and insulin, 2-hour post-challenge plasma glucose and insulin, and insulin resistance assessed by the homeostasis model (HOMA-IR) in 1223 men and 1485 women without diabetes from the Framingham Offspring cohort. Magnesium intake was assessed by a food frequency questionnaire and magnesium intake was categorized into quintile categories. Geometric mean insulin, glucose, 2-hour post challenge plasma glucose and insulin concentrations and HOMA-IR were estimated across quintile categories of magnesium intake using Generalized Linear Models. RESULTS: After adjustment for potential confounding factors, magnesium intake was inversely associated with fasting insulin (mean: 29.9 vs 26.7 microU/mL in the lowest vs highest quintiles of magnesium intake; P trend <0.001), post-glucose challenge plasma insulin (86.4 vs 72 microU/mL; P trend <0.001), and HOMA-IR (7.0 vs 6.2; P trend <0.001). No significant association was found between magnesium intake and fasting glucose or 2-hour post challenge glucose. CONCLUSIONS: Improved insulin sensitivity may be one mechanism by which higher dietary magnesium intake may reduce the risk of developing type 2 DM.     

Serum magnesium levels in non-diabetic offspring of patients with Type 2 diabetes mellitus

A tendency for magnesium deficiency in patients with diabetes mellitus is well established, which probably results from glycosuria-related hypermagnesiuria, nutritional factors or hyperinsulinaemia. Hypomagnesaemia is probably a secondary event but it can also lead to insulin resistance itself. The offspring of patients with Type 2 diabetes mellitus (T2DM) are at increased risk of developing diabetes and several metabolic abnormalities of the disease. The aim of this study was to determine if serum total magnesium levels in healthy offspring of T2DM patients underwent alterations and their relationship to indicators of glucose homeostasis. The sample consisted of two groups: 30 healthy offspring with at least one diabetic parent, and 30 age-matched healthy subjects with no family history of T2DM. None of the participants was on a diet. The mean serum magnesium concentration was 1.070 +/- 0.059 mmol/l in offspring and 1.075 +/- 0.084 mmol/l in controls (p=0.66). There was no statistically significant correlation between serum magnesium levels and parameters of glucose homeostasis in offspring. Our results support the conclusion that total serum magnesium probably has no relationship with the main indicators of glucose homeostasis in offspring of T2DM patients and is not likely to be a fundamental risk factor for the development of insulin resistance.     

Effect of taurine treatment on insulin secretion and action, and on serum lipid levels in overweight men with a genetic predisposition for type II diabetes mellitus

BACKGROUND: The prevalence of type 2 diabetes mellitus (T2DM) is increasing with an epidemic growth rate. Animal studies with taurine supplementation have shown increased insulin secretion and action, suggesting that taurine supplementation may have a potential to prevent T2DM. OBJECTIVE: To assess the effect of taurine treatment on insulin secretion and action, and on plasma lipid levels in overweight men with a positive history of T2DM. DESIGN: 20 nondiabetic subjects were included in a double-blinded, randomized, crossover study, receiving a daily supplementation of 1.5 g taurine or placebo for two periods of 8 weeks. The subjects were overweight first-degree relatives of T2DM patients. An intravenous glucose tolerance test (IVGTT) was used to measure first-phase insulin secretory response, and a euglycemic hyperinsulinemic clamp was used to determine peripheral insulin action. RESULTS: Mean plasma taurine concentration was 39 +/- 7 (s.d.) micromol/l after placebo and 131 +/- 62 micromol/l after taurine intervention (P < 0.0001). There was no significant difference after taurine intervention compared to placebo in incremental insulin response (Insincr.) neither during the IVGTT, nor in insulin-stimulated glucose disposal during the clamp. Insulin secretion, adjusted for insulin sensitivity, was also unchanged. There was no significant effect of taurine supplementation on blood lipid levels as well. CONCLUSION: Daily supplementation with 1.5 g taurine for 8 weeks had no effect on insulin secretion or sensitivity, or on blood lipid levels. These findings in persons with an increased risk of T2DM are in contrast to those from animal studies, and do not support the assumption that dietary supplementation with taurine can be used to prevent the development of T2DM.     

The hypoglycemic effects of hesperidin and naringin are partly mediated by hepatic glucose-regulating enzymes in C57BL/KsJ-db/db mice

Dietary antioxidant compounds such as bioflavonoids may offer some protection against the early stage of diabetes mellitus and the development of complications. We investigated the effect of citrus bioflavonoids on blood glucose level, hepatic glucose-regulating enzymes activities, hepatic glycogen concentration, and plasma insulin levels, and assessed the relations between plasma leptin and body weight, blood glucose, and plasma insulin. Male C57BL/KsJ-db/db mice (db/db mice, 5 wk old), an animal model for type 2 diabetes, were fed a nonpurified diet for 2 wk and then were fed an AIN-76 control diet or the control diet supplemented with hesperidin (0.2 g/kg diet) or naringin (0.2 g/kg diet). Hesperidin and naringin supplementation significantly reduced blood glucose compared with the control group. Hepatic glucokinase activity and glycogen concentration were both significantly elevated in the hesperidin- and the naringin-supplemented groups compared with the control group. Naringin also markedly lowered the activity of hepatic glucose-6-phosphatase and phosphoenolpyruvate carboxykinase compared with the control group. Plasma insulin, C-peptide, and leptin levels in the db/db mice from the 2 bioflavonoid-supplemented groups were significantly higher than those of the control group. Furthermore, plasma leptin was positively correlated with plasma insulin level (r = 0.578, P < 0.01) and body weight (r = 0.541, P < 0.05), and was inversely correlated with the blood glucose level (r = -0.46, P < 0.05). The current results suggest that hesperidin and naringin both play important roles in preventing the progression of hyperglycemia, partly by increasing hepatic glycolysis and glycogen concentration and/or by lowering hepatic gluconeogenesis.     

Clinical efficacy of magnesium supplementation in patients with type 2 diabetes

Effects of magnesium (Mg) supplementation on nine mild type 2 diabetic patients with stable glycemic control were investigated. Water from a salt lake with a high natural Mg content (7.1%) (MAG21) was used for supplementation after dilution with distilled water to 100mg/100mL; 300mL/day was given for 30 days. Fasting serum immunoreactive insulin level decreased significantly, as did HOMA squareR (both p < 0.05). There was also a marked decrease of the mean triglyceride level after supplementation. The patients with hypertension showed significant reduction of systolic (p < 0.01), diastolic (p = 0.0038), and mean (p < 0.01) blood pressure. The salt lake water supplement, MAG21, exerted clinical benefit as a Mg supplement in patients with mild type 2 diabetes mellitus.     

Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients

In vitro and in vivo animal studies have reported strong insulin-like or insulin-potentiating effects after cinnamon administration. Recently, a human intervention study showed that cinnamon supplementation (1 g/d) strongly reduced fasting blood glucose concentration (30%) and improved the blood lipid profile in patients with type 2 diabetes. The objective of this study was to investigate the effects of cinnamon supplementation on insulin sensitivity and/or glucose tolerance and blood lipid profile in patients with type 2 diabetes. Therefore, a total of 25 postmenopausal patients with type 2 diabetes (aged 62.9 +/- 1.5 y, BMI 30.4 +/- 0.9 kg/m2) participated in a 6-wk intervention during which they were supplemented with either cinnamon (Cinnamomum cassia, 1.5 g/d) or a placebo. Before and after 2 and 6 wk of supplementation, arterialized blood samples were obtained and oral glucose tolerance tests were performed. Blood lipid profiles and multiple indices of whole-body insulin sensitivity were determined. There were no time x treatment interactions for whole-body insulin sensitivity or oral glucose tolerance. The blood lipid profile of fasting subjects did not change after cinnamon supplementation. We conclude that cinnamon supplementation (1.5 g/d) does not improve whole-body insulin sensitivity or oral glucose tolerance and does not modulate blood lipid profile in postmenopausal patients with type 2 diabetes. More research on the proposed health benefits of cinnamon supplementation is warranted before health claims should be made.     

Chromium and polyphenols from cinnamon improve insulin sensitivity

Naturally-occurring compounds that have been shown to improve insulin sensitivity include Cr and polyphenols found in cinnamon (Cinnamomon cassia). These compounds also have similar effects on insulin signalling and glucose control. The signs of Cr deficiency are similar to those for the metabolic syndrome and supplemental Cr has been shown to improve all these signs in human subjects. In a double-blind placebo-controlled study it has been demonstrated that glucose, insulin, cholesterol and HbA1c are all improved in patients with type 2 diabetes following Cr supplementation. It has also been shown that cinnamon polyphenols improve insulin sensitivity in in vitro, animal and human studies. Cinnamon reduces mean fasting serum glucose (18-29%), TAG (23-30%), total cholesterol (12-26%) and LDL-cholesterol (7-27%) in subjects with type 2 diabetes after 40 d of daily consumption of 1-6 g cinnamon. Subjects with the metabolic syndrome who consume an aqueous extract of cinnamon have been shown to have improved fasting blood glucose, systolic blood pressure, percentage body fat and increased lean body mass compared with the placebo group. Studies utilizing an aqueous extract of cinnamon, high in type A polyphenols, have also demonstrated improvements in fasting glucose, glucose tolerance and insulin sensitivity in women with insulin resistance associated with the polycystic ovary syndrome. For both supplemental Cr and cinnamon not all studies have reported beneficial effects and the responses are related to the duration of the study, form of Cr or cinnamon used and the extent of obesity and glucose intolerance of the subjects.