胰岛素对初发2型糖尿病的疗效及影响

目的:观察胰岛素对初发2型糖尿病的疗效及不良反应,以及对血糖的影响.方法:选择2008年1月至2010年1月在我院住院的T2DM患者为观察对象.120例初发2型糖尿病患者随机分为治疗组和对照组各60例,治疗3个月后,观察治疗的疗效及对血糖控制情况.结果:治疗组的疗效优于对照组,且治疗组血糖控制效果明显优于对照组,差异有统计学意义(P＜0.05).结论:胰岛素对初发2型糖尿病疗效确切,更好地降低T2DM血糖水平,值得基层医院广泛推广和应用.     

Insulin therapy in type II diabetes

The results of conventional intensified insulin therapy (4 injections per day) in type II diabetics correspond more to those of conventional therapy (2 injections per day). Compared to a conventionally treated collective with strict dietetic regimen the intensified treated type II diabetics did not lead to an improved metabolic control. The frequency of hypoglycemic episodes did not differ in both collectives. Intensified insulin therapy is associated with subjectively increased comfort and increased life quality despite the seldom use of the advantages of the therapy. The management of the intensified therapy probably has to be learned in an earlier stage of life and requires repeated and more intensified education in elderly patients. The regression of typical late complications of diabetes mellitus as seen in the DCCT may possibly be achieved by a greater effort in therapy and empowerment of the patient.     

Insulin resistance precedes microalbuminuria in patients with insulin-dependent diabetes mellitus

BACKGROUND: Insulin resistance has been associated with hypertension and with renal complications in patients with type 1 diabetes mellitus. Causal relationships have not been fully explained. METHODS: We investigated whether insulin resistance precedes microalbuminuria by measuring insulin resistance with a euglycaemic clamp in combination with indirect calorimetry in 16 uncomplicated type 1 diabetic patients and in six healthy control subjects. The patients had over 10 year duration of diabetes, and were expected to experience either a complication-free or complicated disease course within the next few years. They have thereafter been followed for the development of microalbuminuria for 3 years. RESULTS: In a euglycaemic insulin clamp glucose disposal was lower in diabetic patients compared with control subjects (7.5 +/- 2.9 and 12.6 +/- 2.0 mg/kg LBM/min; P<0.002), mainly due to impaired glucose storage (4.3 +/- 2.3 vs 8.6 +/- 1.6 mg/kg LBM/min; P<0.001). Three years later seven IDDM patients had albumin excretion rate over 30 mg/24 h; glucose disposal (5.5 +/- 2.1 vs 9.0 +/- 2.2 mg/kg LBM/min; P<0.01) had been lower in patients who developed microalbuminuria compared with those who remained normoalbuminuric. CONCLUSIONS: Insulin resistance predicts the increment in urinary albumin excretion. Insulin resistance depends mainly on impaired glucose storage in uncomplicated IDDM.     

Insulin dependent (type 1) diabetes mellitus in advanced age

In everyday praxis diabetes mellitus diagnosed over the age of fifty years, means generally type 2 diabetes. Authors present cases where diabetes, beginning in advanced age, showed typical classical diabetic symptoms, like polyuria, polydipsia, loss of bodyweight. Apart from these signs a rapid decompensation of carbohydrate metabolism characterises this diabetes form. The most significant features are the rapid decrease of serum immunoreactive insulin and C-peptide levels, what is characteristic for the diminishing insulin secretory capacity. The patients had to be switched to insulin therapy within maximum 6 weeks. These patients can be easily differentiated both from type 2 and from the slowly progressing type 1 subtype. We suppose that the pathomechanism of this type of diabetes differs from the classical insulin-dependent form, beginning in young age.     

Family history of coronary heart disease is a stronger predictor of coronary heart disease morbidity and mortality than family history of non-insulin dependent diabetes mellitus

The aim of this study was to compare the effect of family history of non-insulin dependent diabetes mellitus (NIDDM) and coronary heart disease (CHD) as risk factors for CHD morbidity and mortality. Altogether, 394 siblings of NIDDM probands and non-diabetic probands, with and without CHD, were followed for 8 years with respect to CHD events in a prospective population-based study. The baseline study was conducted from 1983 to 1985. Age- and sex-adjusted cumulative occurrence of CHD events was higher in the siblings of the probands with CHD and with NIDDM (13.1%; P = 0.037) and in the siblings of the probands with CHD and without NIDDM (15.4%; P = 0.054), compared with the siblings of the probands without NIDDM and without CHD (4.8%). The incidence of fatal CHD events tended to be higher in a group with a family history of NIDDM and CHD, but the trend was not statistically significant. In univariate logistic regression analyses, a family history of CHD was positively associated with cumulative occurrence of CHD events (odds ratio 2.53, P = 0.009), whereas a family history of NIDDM had no significant association (odds ratio 1.39, P = 0.312). After adjustment for age, sex, family history of NIDDM and major cardiovascular risk factors, the association between family history of CHD and cumulative occurrence of CHD events remained significant (odds ratio 2.25, P = 0.048). In conclusion, the present study indicates that a family history of CHD is a stronger predictor of future CHD events than a family history of NIDDM.     

Insulin resistance versus insulin deficiency in non-insulin-dependent diabetes mellitus: problems and prospects

A definitive assessment of the relative roles of insulin resistance and insulin deficiency in the etiology of NIDDM is hampered by several problems. 1) Due to better methodology, data on insulin resistance are generally more accurate and consistent than data on insulin deficiency. 2) In source data, case-control studies are prone to selection bias, while epidemiological associations, whether cross-sectional or longitudinal, are liable to misinterpretation. 3) Insulin secretion and action are physiologically interconnected at multiple levels, so that an initial defect in either is likely to lead with time to a deficit in the companion function. The fact that both insulin resistance and impaired insulin release have been found to precede and predict NIDDM in prospective studies may be in part a reflection of just such relatedness. 4) Direct genetic analysis is effective in rarer forms of glucose intolerance (MODY, mitochondrial mutations, etc.) but encounters serious difficulties with typical late-onset NIDDM. Despite these uncertainties, the weight of current evidence supports the view that insulin resistance is very important in the etiology of typical NIDDM for the following reasons: 1) it is found in the majority of patients with the manifest disease; 2) it is only partially reversible by any form of treatment (117); 3) it can be traced back through earlier stages of IGT and high-risk conditions; and 4) it predicts subsequent development of the disease with remarkable consistency in both prediabetic and normoglycemic states. Of conceptual importance is also the fact that the key cellular mechanisms of skeletal muscle insulin resistance (defective stimulation of glucose transport, phosphorylation, and storage into glycogen) have been confirmed in NIDDM subjects by a variety of in vivo techniques [ranging from catheter balance (118) to multiple tracer kinetics (119) to 13C nuclear magnetic resonance spectroscopy (120)], and have been detected also in normoglycemic NIDDM offspring (121). If insulin resistance is a characteristic finding in many cases of NIDDM, insulin-sensitive NIDDM does exist. On the other hand, given the tight homeostatic control of plasma glucose levels in humans, beta-cell dysfunction, relative or absolute, is a sine qua non for the development of diabetes. If insulin deficiency must be present whereas insulin resistance may be present, is this proof that the former is etiologically primary to the latter? If so, do we have convincing evidence that the primacy of insulin deficiency is genetic in nature? The answer to both questions is negative on several accounts. The defect in insulin secretion in overt NIDDM is functionally severe but anatomically modest: beta-cell mass is reduced by 20-40% in patients with long-standing NIDDM (122). Moreover, the insulin secretory deficit is progressively worse with more severe hyperglycemia (123) and recovers considerably upon improving glycemic control (124). These observations indicate that part of the insulin deficiency is acquired (through glucose toxicity, lipotoxicity, or both). In addition, although insulin deficiency is necessary for diabetes, it may not always be sufficient to cause NIDDM. In fact, subtle defects in the beta-cell response to glucose may be widespread in the population (108, 125) and only cause frank hyperglycemia when obesity/insulin resistance stress the secretory machinery. Conceivably, there could be beta-cell dysfunction without NIDDM just as there is insulin resistance without diabetes. Incidentally, any defect in insulin secretion, whether in normoglycemic or hyperglycemic persons, could be due to other factors than primary beta-cell dysfunction: amyloid deposits in the pancreas (126), changes in insulin secretagogues (amylin, GLP-1, GIP, galanin) (127-130), early intrauterine malnutrition (131). Finally, the predictive power of early changes in insulin secretion for the development of typical NIDDM is generally lower than that of insulin     

Wound healing process differences in type I and type II diabetes mellitus

In 88 patients with purulent wounds in diabetes mellitus the course of wound healing was studied depending on the type of the disease. Clinical and morphological distinctions of the wound process in type 1 and type 2 diabetes mellitus were revealed.     

Effect of type II diabetes mellitus on cognitive function

BACKGROUND: As people with diabetes mellitus suffer from peripheral and autonomic neuropathy, we thought it possible that deficits in cognitive function might also be found. Our objective was to compare the cognitive function of elderly persons with non-insulin-dependent diabetes mellitus (NIDDM) with a matched sample of persons without NIDDM: METHODS: Ninety outpatients over 50 years of age with NIDDM and 90 matched nondiabetic patients were recruited for the study. The Modified Mini-Mental State (3MS) and the Delayed Word Recall (DWR) test were used to assess cognitive function. RESULTS: On the 3MS test, the mean score of persons with NIDDM was 75.6, and that of nondiabetic persons was 79.5 (two-tailed t = 3.04, P = .013). On the DWR, the mean score of persons with NIDDM was 3.9, and that of persons without NIDDM was 4.7 (two-tailed t = 3.52, P = .012). CONCLUSIONS: Persons with NIDDM had significantly poorer scores on two tests of cognitive function. Physicians should be aware of this association between type II diabetes and a small but definite impairment of cognitive function.     

Therapy for type 2 diabetes mellitus

Type 2 diabetes mellitus is a common, chronic disease affecting nearly 6% of the adult US population. It remains a leading cause of morbidity and mortality in Wisconsin as well as the country. Multiple lines of evidence show that controlling blood glucose in patients with type 2 diabetes can significantly decrease the development of and/or progression of microvascular complications as well as the macrovascular complications of diabetes. There are now four different classes of oral medications which are available to treat diabetes-sulfonylureas, biguanides, thiazolidinediones, and alpha-glucosidase inhibitors. Each class works differently to treat the underlying defects of diabetes which include impaired insulin secretion, insulin resistance and exaggerated postprandial hyperglycemia. This article will compare and contrast the different agents available, including appropriate use of each agent as monotherapy and in combination therapy. It will also discuss use of insulin in the patient who has failed oral therapy. Rational use of these tools, tailored for the individuals metabolic abnormalities, should allow for good glycemic control in the majority of patients with type 2 diabetes mellitus. Relaxation, massage, opium, and moderate exercise were among the recommended options for treatment of diabetes mellitus nearly 100 years ago. In the late nineteenth century, diabetes was a poorly characterized disorder, which was increasing in prevalence even at that time. Today, the underlying defects contributing to the development of type 2 diabetes are better understood, and include peripheral insulin resistance, relative pancreatic beta-cell insufficiency, increased hepatic glucose output, and an exaggerated postprandial glucose excursion. However, despite our better understanding of the disease, the prevalence of type 2 diabetes continues to increase in the US, now afflicting over 6% of the population. As our population ages and the proportion of obese people increases, we can expect to see a marked increase in the prevalence of diabetes in the future. Fortunately, our treatment options for type 2 diabetes have expanded remarkably within the last few years. Along with these new treatment options comes the exciting, although likely expensive, possibility of prevention of type 2 diabetes in at risk individuals.     

Recent advances in the treatment of type II diabetes mellitus

Diabetes mellitus needs to be managed early to prevent the onset and progression of complications. Diet and exercise may not be sufficient to achieve and maintain good glycemic control. Currently, no pharmacologic agent addresses all of the fundamental abnormalities in the pathogenesis of type II diabetes mellitus. However, the newer agents do not exacerbate the hyperinsulinemia that often occurs with type II diabetes, and they may help reduce the risk of cardiovascular disease that is associated with high insulin levels. Two of these agents, metformin and acarbose, have recently become available in the United States for the treatment of type II diabetes. With the availability of agents that differ in their mechanisms of action and side effect profiles, regimens can be individualized to address the variety of pathophysiologic abnormalities in type II diabetes. For this purpose, agents can be used alone or in combination.     

Insulin resistance in patients with familial combined hyperlipidemia and coronary artery disease

The minimum model modified by the administration of insulin provides an objective and relatively easily measured index of peripheral sensitivity to insulin which was significantly lower (p <0.02) in familial combined hyperlipidemia (FCH) with ischemic heart disease (IHD) than in FCH without IHD and in control subjects (1.2 +/- 0.6, 1.9 +/- 1.0, 2.9 +/- 1.2 x 10(-4) mU/L/ min, respectively). In patients with FCH, insulin resistance explains, at least in part, their metabolic alterations (hypertension, abnormal glucose tolerance, hyperinsulinemia) and elevated IHD.     

Depressive symptomatology and coronary heart disease in Type I diabetes mellitus: A study of possible mechanisms.

Recent evidence has suggested that depressive symptomatology is a risk factor for the development of coronary heart disease (CHD) in patients with diabetes mellitus, although little is understood about mechanisms that may explain this association. The Pittsburgh Epidemiology of Diabetes Complications (EDC) Study is a natural history study of 658 men and women with childhood-onset Type I diabetes. Participants from the EDC Study who reported the fewest depressive symptoms on the Beck Depression Inventory at baseline examination were least likely to develop CHD over 10 years. Differences in insulin resistance, autonomic dysregulation, inflammation, smoking, and complications associated with Type I diabetes appear to help explain this relationship. Future research should clarify causal pathways between depressive symptomatology, behavioral and physiological processes, and CHD. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Risk factors for coronary heart disease mortality among persons with diabetes

Although synovial lining cells (SLC) have been implicated in the production of hyaluronan (HA), which is found at particularly high concentrations in synovial fluid, the degree to which individual cells within the synovium are adapted to this particular function remains to be elucidated. Uridine diphosphoglucose dehydrogenase (UDPGD) activity is the irreversible, rate-limiting step in the production of UDP-glucuronate, an essential monosaccharide in the synthesis of HA. We have assessed the UDPGD activity, microdensitometrically, in individual lining cells of normal and rheumatoid (RA) synovium, using a modified quantitative cytochemical method. In normal synovium, high activity was confined to the cells of the lining with negligible activity in the deeper subintima. The mean UDPGD activity/cell in lining cells of rheumatoid synovium was significantly lower than the activity in normal SLC. In some samples of RA and normal synovium, a bimodal distribution of cells was evident in the lining on the basis of UDPGD activity, a zone of cells in the basal layers with high UDPGD activity and a separate population of cells in more superficial layers with relatively low UDPGD activity. The results suggest that a particular population of cells is present, consistently in normal and more variably in RA synovial lining, which have high UDPGD activity/cell and may be involved in the production of HA. Furthermore, in RA synovium both the UDPGD activity/cell and the relative proportion of these cells within the lining appear to be decreased.     

Diabetes mellitus: 2. Managing type II disease

For a large and growing number of people in the United States, too much fatty food, too little activity, and an inherited tendency toward insulin resistance add up to type II diabetes. Improved diet and regular exercise are the ideal therapy. But most patients also require pharmacologic intervention to keep the disorder in check and to ward off microvascular and macrovascular and complications.     

Insulin resistance in patients with a recent diagnosis of coronary artery disease

Insulin increases limb blood flow in a time- and dose-dependent manner. This effect can be blocked by inhibiting nitric oxide synthesis. These data raise the possibility that insulin resistance is associated with endothelial dysfunction. To examine whether endothelial function and insulin sensitivity are interrelated we quantitated in vivo insulin-stimulated rates of whole body and forearm glucose uptake at a physiological insulin concentration (euglycaemic hyperinsulinaemic clamp, 1 mU.kg-1.min-1 insulin infusion for 2 h) and on another occasion, in vivo endothelial function (blood flow response to intrabrachial infusions of sodium nitroprusside, acetylcholine, and N-monomethyl-L-arginine) in 30 normal male subjects. Subjects were divided into an insulin-resistant (IR) and an insulin-sensitive (IS) group based on the median rate of whole body glucose uptake (31 +/- 2 vs 48 +/- 1 mumol.kg-1.min-1, p < 0.001). The IR and IS groups were matched for age, but the IR group had a slightly higher body mass index, percentage of body fat and blood pressure compared to the IS group. The IR group also had diminished insulin-stimulated glucose extraction (p < 0.05) compared to the IS group, while basal and insulin-stimulated forearm blood flow rates were identical. There was no difference between the IR and IS groups in the forearm blood flow response to endothelium-dependent (acetylcholine and N-monomethyl-L-arginine) or -independent (sodium nitroprusside) vasoactive drugs. In conclusion, the ability of insulin to stimulate glucose uptake at physiological insulin concentrations and endothelium-dependent vasodilatation are distinct phenomena and do not necessarily coexist.     

Appraisal and implications of predictive testing for insulin-dependent diabetes mellitus

A patient with systemic lupus erythematosus (SLE) developed reactive hemophagocytosis. This case did not show any underlying diseases such as infection or malignancy other than SLE itself. The mechanisms inducing hemophagocytosis in SLE seem to be heterogeneous and remain to be elucidated. Although an immune complex-mediated mechanism in cases with acute lupus hemophagocytic syndrome has been proposed, we suggest the possible involvement of IL-1beta as the pathogenesis of our case.