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61.
Insulin lispro is an insulin analogue that has the advantages of being fast-acting, convenient, and less likely to lead to hypoglycaemic episodes. Previous studies have proven its value in treating both Type 1 and Type 2 diabetes both alone and in combination with different treatment regimens.1,2 However, diabetes is heterogeneous and differs in etiology and clinical characteristics in different ethnic groups. Even with the same insulin treatment, different diets will produce different glycaemic profiles. Diet patterns differ between different ethnic groups. Traditional oriental foods are characterized by a higher proportion of carbohydrates and a lower proportion of fat compared to Caucasian diets. To date, there has been no study on the use of insulin lispro in Chinese diabetic patients. Whether the Chinese dietary pattern will affect the efficacy of insulin lispro treatment remains unknown. Therefore, we conducted this trial to assess the efficacy of insulin lispro treatment in Chinese patients. 相似文献
62.
目的鉴定参与线虫衰老的神经内分泌调控的新基因。方法鉴于神经系统在衰老调控中的重要作用,通过寿命分析和脂褐质自发荧光的检测,从编码突触蛋白的遗传位点中筛选参与衰老调控的基因。我们还进一步检查了这些遗传位点相应的突变体的永久性幼虫形成情况,探讨它们是否可能受胰岛素样信号通路的调控。结果遗传位点 unc-10,syd-2,hlb-1,dlk-1,mkk-4,scd-2,snb-1,ric-4,nrx-1,unc-13,sbt-1,unc-64 可能参与线虫衰老的调控。而且在衰老的调控中,unc-10,syd-2,hlb-1,dlk-1,mkk-4,scd-2,snb-1,ric-4,nrx-1 的功能可能与unc-13,sbt-1,unc-64相反。肠道脂褐质自发荧光的检测进一步证明了筛选出的各基因对应突变体的长寿或短寿表型,是由减慢或缩短的组织衰老所致。在筛选出的基因中,syd-2,hlb-1,mkk-4,scd-2,snb-1,ric-4,unc-64 也参与了永久性幼虫形成的调控。另外,daf-2突变增强了syd-2和hlb-1的表达,降低了mkk-4,nrx-1,ric-4,sbt-1,rpm-1,unc-10,dlk-1,unc-13 的表达。daf-16突变提高了syd-2和 hlb-1 的表达,降低了mkk-4,nrx-1,sbt-1,rpm-1,unc-10,dlk-1,unc-13 的表达. 结论突触功能可能在个体寿命和永久性幼虫形成的调控机制中具有重要的作用。 相似文献
63.
M. Wiegand A. A. Möller C. J. Lauer S. Stolz W. Schreiber M. Dose J. C. Krieg 《Journal of neurology》1991,238(4):203-208
Summary Nocturnal sleep was studied in 16 inpatients with Huntington's disease. In comparison with healthy controls, patients exhibited a disturbed sleep pattern with increased sleep onset latency, reduced sleep efficiency, frequent nocturnal awakenings, more time spent awake and less slow wave sleep. These abnormalities correlated in part with duration of illness, severity of clinical symptoms, and degree of atrophy of the caudate nucleus. Patients showed an increased density of sleep spindles. 相似文献
64.
Small injections of two highly sensitive anterograde tracers, Phaseolus vulgaris-leucoagglutinin (PHA-L) and biocytin, into the striatum and the subthalamic nucleus of squirrel monkeys (Saimiri sciureus) have revealed a high degree of convergence of striatal and subthalamic fibers upon single pallidal cells. Both afferent systems formed highly complex band-like patterns that were largely in register with one another. At single cell level, the somata of pallidal neurons were closely surrounded by subthalamic terminal varicosities, whereas the dendrites were entwined mostly by striatal fibers. Typically, a subthalamopallidal fiber coursed in a caudorostral direction and arborized according to a uniform pattern along its trajectory in the pallidum. Numerous thin and markedly varicose axon collaterals detached themselves at right angle from the main subthalamopallidal fiber. These highly branched collaterals were mostly oriented along the mediolateral plane and entwined rather loosely the dendrites but surrounded very closely the somata of pallidal neurons. In contrast, a striatopallidal fiber travelled in a rostrocaudal direction. Its initial segment made only en passant contacts with pallidal cell bodies, whereas its distal end closely entwined the dendrites of pallidal neurons, forming arrangements similar to 'woolly' type fibers. These results suggest that a single subthalamic fiber may influence a rather large collection of pallidal neurons in a similar fashion, compared to the striatal input which appears to exert a more specific control upon selected sets of the same pallidal neurons. 相似文献
65.
Summary To define the glucose to insulin dose-response relationship before the onset of diabetes, we studied 22 nondiabetic co-twins of patients with Type 1 (insulin-dependent) diabetes mellitus and nine control subjects. All had intravenous glucose tests at 0.02, 0.1 and 0.5 g/kg and were followedup prospectively for at least 6 years. Seven twins developed diabetes a mean of 7 months later; the remaining 15 are now unlikely to develop diabetes. The seven pre-diabetic twins had higher fasting insulin levels than control subjects (4.2±2.0 vs 1.8±1.8 nmol/l; p<0.05); but lower glucose clearance (1.0±0.5 vs 1.9±0.7 %/min; p<0.05), first phase insulin response at 0.5 g/kg (21.1±23.2 vs 143±50 nmol/l; p<0.0001), and total insulin responses at 0.1 g/kg (p<0.05) and 0.5 g/kg (p<0.00005). Using a curve-fitting programme, the normal glucose to insulin relationship was lost in prediabetic twins who had lower coefficient of determination (R2) than control subjects (p<0.01). In contrast, 15 low-risk twins and their nine control subjects had similar fasting glucose and insulin levels, glucose clearance, R2 and insulin secretory responses to different glucose loads. The positive predictive values of subnormal R2 and subnormal first phase insulin response were 67 % and 58 % respectively. These observations demonstrate an altered glucose to insulin dose-response relationship and loss of maximum insulin secretory response to glucose before the onset of Type 1 diabetes. 相似文献
66.
67.
目的:探讨儿童甲亢患者糖代谢紊乱的特点。方法:用SUPER GLUCOCARD^TM血糖仪和放射免疫方法检测29例甲亢患儿餐前、餐后60min、120min血糖和餐前、餐后60min胰岛素、C肽、胰高糖素、皮质醇及T3、T4、TSH、TGA、TMA(其中10例糖耐量减低为甲亢1组,另19例糖耐量正常为甲亢2组),并与20例健康儿童进行比较。结果:(1)34.5%甲亢患儿出现糖代谢紊乱,病程大于1年和小于1年糖代谢紊乱发生率为50%,9%(P<0.05)。(2)甲亢1组餐后60min胰岛素、胰岛素/血糖、胰岛素/胰高糖素显著升高(P<0.05)。结论:甲亢儿童存在糖代谢紊乱现象,表现为葡萄糖耐量减低和胰岛素拮抗,其发生与病程有关,病程较长,发生率较高。糖代谢紊乱可能与自身免疫、胰岛β细胞功能受损及胰岛素拮抗有关。 相似文献
68.
Nitric oxide is not involved in the initiation of insulin secretion from rat islets of Langerhans 总被引:1,自引:1,他引:0
P. M. Jones S. J. Persaud T. Bjaaland J. D. Pearson S. L. Howell 《Diabetologia》1992,35(11):1020-1027
Summary The involvement of nitric oxide as an intracellular messenger in the control of insulin secretion from pancreatic Beta cells was studied in rat islets of Langerhans by measuring: (i) nitric oxide generation in response to physiological insulin secretagogues; (ii) the effects of inhibitors of nitric oxide synthesis on insulin secretory responses to physiological secretagogues, and on insulin synthesis; (iii) changes in islet cyclic guanosine monophosphate in response to secretagogues; (iv) the effects of exogenous cyclic guanosine monophosphate and dibutyryl cyclic guanosine monophosphate on insulin secretion from electrically permeabilised islets and from intact islets, respectively. These studies produced no evidence that nitric oxide generation is required for the initiation of insulin secretion by common secretagogues. However, the results of our experiments suggest that the generation of nitric oxide may be involved in long-term, glucose-dependent increases in cyclic guanosine monophosphate content of islet cells, although the physiological relevance of these changes requires further investigation. 相似文献
69.
Summary Insulin resistance and a defective insulin activation of the enzyme glycogen synthase in skeletal muscle during euglycaemia may have important pathophysiological implications in Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia may serve to compensate for these defects in Type 2 diabetes by increasing glucose disposal through a mass action effect. In the present study, rates of whole-body glucose oxidation and glucose storage were measured during fasting hyperglycaemia and isoglycaemic insulin infusion (40 mU·m–2min–1, 3 h) in 12 patients with Type 2 diabetes. Eleven control subjects were studied during euglycaemia. Biopsies were taken from the vastus lateralis muscle. Fasting and insulin-stimulated glucose oxidation, glucose storage and muscle glycogen synthase activation were all fully compensated (normalized) during hyperglycaemia in the diabetic patients. The insulin-stimulated increase in muscle glycogen content was the same in the diabetic patients and in the control subjects. Besides hyperglycaemia, the diabetic patients had elevated muscle free glucose and glucose 6-phosphate concentrations. A positive correlation was demonstrated between intracellular free glucose concentration and muscle glycogen synthase fractional velocity insulin activation (0.1 mmol/l glucose 6-phosphate: r=0.65, p<0.02 and 0.0 mmol/l glucose 6-phosphate: r= 0.91, p<0.0001). In conclusion, this study indicates an important role for hyperglycaemia and elevated muscle free glucose and glucose 6-phosphate concentrations in compensating (normalizing) intracellular glucose metabolism and skeletal muscle glycogen synthase activation in Type 2 diabetes. 相似文献
70.
Summary Insulin binding to trophoblast plasma membranes and the placental glycogen content were measured in twelve healthy women, in eleven well-controlled gestational diabetic women who were treated either with diet alone (n=4) or with insulin (n=7) and in 18 women with well-controlled overt diabetes mellitus (six White B; four White C; eight White D). The competitive binding assay was carried out with 22 concentrations of unlabelled insulin. Binding data were analysed by a non-linear direct model fitting procedure assuming one non-cooperative binding site. Maximum specific binding was unchanged in the total collective of gestational diabetic women, but was decreased by 30% in those treated with diet (6.2±2.2%) and increased by 90% in insulin-treated women (16.4±10.2%) as compared to the control subjects (8.7±2.5%). The diet-treated women had only 40% as many and those treated with insulin had more than twice as many receptors compared to control subjects on a per mg protein basis and if expressed per total placenta. In patients with overt diabetes mellitus maximum specific binding (18.5±10.6 %) was higher (p<0.05) due to more receptors compared to control subjects but was similar to the insulin-treated gestational diabetic patients. Maximum specific binding and receptor concentrations did not correlate linearly with maternal plasma insulin levels. Receptor affinities were virtually similar in all groups (1.8·109 l/mol). The placental glycogen content was reduced (p<0.05) to about 80% of that of control subjects in the diet-treated collective, whereas it was unchanged compared to control subjects in the insulin-treated gestational diabetic women despite a 40% increase (p<0.001) of the maternal-to-cord serum glucose ratio. In overt diabetic patients the maternal-to-cord serum glucose ratio and the placental glycogen content were higher (p<0.05) than in the control subjects. We conclude that trophoblast plasma membranes from gestational diabetic women treated with diet alone express less and those from women treated with insulin express more insulin receptors than those from a healthy control group in vitro. These differences could not have been disclosed without consideration of the mode of treatment. Trophoblast plasma membranes from overt diabetic women have more insulin receptors than those from healthy control subjects. 相似文献