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Query: UMLS:C0011854 (type 1 diabetes)
20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is expected that the number of patients with diabetes mellitus will increase in the near future. The high rate of microvascular and macrovascular complications developing in these patients will place an even higher burden on our healthcare systems. Several pathophysiological factors are involved in the development of complications, among which are hyperglycaemia per se, the consequent formation of advanced glycation end-products (AGEs) and the intracellular accumulation of sorbitol. In addition, hypertension and dyslipidaemia also play an important role, especially in the development of coronary heart disease and stroke. The major therapeutic goals in patients with non-insulin-dependent diabetes mellitus (NIDDM) are to reduce obesity and normalise lipid disturbances and increased blood pressure, in order to improve the well-being of the patient and reduce the risk of the development of late diabetic complications. Often, pharmacological treatment of the hyperglycaemia is necessary, in which case sulphonylureas, metformin, alpha-glucosidase inhibitors such as acarbose, or insulin may be employed. It is believed that medical interventions, by their effect on improving metabolic control, reduce the incidence and severity of diabetic complications, especially when considering the toxic effects of glucose and the accumulation of AGEs as a consequence of raised tissue glucose levels. This concept is also based on extrapolation of the finding of the Diabetes Control and Complications Trial that intensive glycaemic control in IDDM will prevent the progression of at least the microvascular complications like retinopathy and nephropathy. There are, however, no long term studies in NIDDM patients to show that treatment with oral antihyperglycaemic agents helps to postpone or prevent complications. It is expected that the UK Prospective Diabetes Study will show whether better metabolic control, either with oral antihyperglycaemics or with insulin, will indeed improve outcome. Several other studies aiming at specific risk factor intervention (hypertension, hyperlipidaemia, lipid oxidation) in NIDDM patients are currently ongoing.
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PMID:Prevention of complications in non-insulin-dependent diabetes mellitus (NIDDM). 852 59

Ultrasonographic scanning of carotid arteries allows non-invasive detection of atherosclerotic changes. This technique has been used to investigate changes in the thickness of the intimal plus medial (IM) complex, in patients with type 2 diabetes, type 1 diabetes and those in the pre-diabetic state of impaired glucose tolerance (IGT). IM thickness (IMT) increases with age, but this process was found to be considerably accelerated in patients with type 2 diabetes. In addition, IMT was significantly greater in patients with cerebral lacunar infarctions, and in those with detectable coronary artery stenosis. A study in patients with type 1 diabetes found that IMT correlates with duration of diabetes as well as age. The correlation with duration of diabetes suggests that hyperglycaemia contributes to the progression of atherosclerosis. IMT was also found to be increased in individuals with hyperinsulinaemic IGT, compared with control individuals with normal glucose tolerance. These results suggest that even relatively small increases in postprandial blood glucose levels can lead to increases in IMT and, hence, increased risk of cardiovascular disease. Further analysis revealed a correlation between hyperinsulinaemia (i.e. insulin resistance) and increased IMT. These results provide a clear rationale for the therapeutic use of alpha-glucosidase inhibitors, such as acarbose, which attenuate postprandial hyperglycaemia-induced hyperinsulinaemia.
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PMID:Asymptomatic hyperglycaemia and early atherosclerotic changes. 974 May 1

Nocturnal hypoglycemia is one of the serious complications of intensive insulin therapy in patients with insulin-dependent diabetes mellitus (IDDM; type 1 DM). We assessed the effect of voglibose (alpha-glucosidase inhibitor) administration before the evening meal on nocturnal hypoglycemia in IDDM patients with intensive insulin therapy. Ten IDDM patients received 0.3 mg voglibose just before the evening meal for 5 days. The diet and insulin regimen were not changed throughout the study. Nocturnal plasma glucose levels (10 PM, 3 AM, and 7 AM) were studied in these patients before and during voglibose administration. Blood glucose levels were measured at 3 AM before and during voglibose treatment. The mean plasma glucose level at 3 AM was 3.4+/-0.4 mmol/L before voglibose treatment and 7.3+/-1.0 mmol/L during treatment. Plasma glucose at 3 AM was elevated in 9 of 10 patients with voglibose. The decrease in plasma glucose from 10 PM to 3 AM was 6.5+/-0.8 mmol/L before voglibose administration but 3.2+/-0.9 mmol/L during treatment (P < .01). The hypoglycemia rate was 52% (17 of 33 nights) before voglibose administration but only 9.1% (3 of 33 nights) during treatment. We conclude that voglibose administration before the evening meal improves nocturnal hypoglycemia in IDDM patients with intensive insulin therapy.
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PMID:Voglibose administration before the evening meal improves nocturnal hypoglycemia in insulin-dependent diabetic patients with intensive insulin therapy. 1077 65

The effect of hyperglycemia and insulin deficiency on the plasma level of lysosomal glycohydrolases, namely N-acetyl-beta-D-glucosaminidase, beta-D-glucuronidase, alpha-D-galactosidase, and alpha-D-glucosidase, was investigated. Two patient groups were assessed: (1) 28 children with type 1 diabetes at onset (fasting blood glucose, 444+/-154 mg/100 mL; hemoglobin A1c, 11.9%+/-2.4%; symptom duration, 15.9+/-8 days; and absence of complications), (2) 14 adult subjects undergoing an intravenous glucose tolerance test (IVGTT), consisting of 8 non-obese subjects (body mass index, 26+/-0.04 kg/m2; fasting blood glucose, 82+/-13 mg/100 mL; blood insulin, 6+/-0.04 mU/L) and 6 obese subjects (fasting blood glucose, 97+/-3.5 mg/100 mL; blood insulin, 27+/-6 mU/L, with normal oral glucose tolerance test). Enzyme activity was determined with the fluorimetric method. The mean level of all evaluated enzymes was significantly increased in patients with type 1 diabetes at diagnosis compared with normal controls. Increased enzyme levels were also detected in the group of adults undergoing an IVGTT in whom hyperglycemia was accompanied by insulin resistance (ie, obese subjects). Glycohydrolase abnormalities appear to be related to insulin deficiency rather than hyperglycemia. Lysosomal apparatus abnormalities seem to be an inherent feature of diabetes that is present at disease onset. The possible role of insulin in the regulation of plasma glycohydrolase levels is discussed.
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PMID:Plasma glycohydrolase levels in patients with type 1 diabetes at onset and in subjects undergoing an intravenous glucose tolerance test. 1107 28

In this review we present the agents that are in use in the treatment of type 2 diabetes. Sulfonylureas of the 1st and 2nd generation increase insulin secretion but can induce hyperinsulinemia and sometimes prolonged hypoglycemia. Glimepiride is a new 3rd generation sulfonylurea with some advantages over the other members of this group, such as a lower risk of hypoglycemia, no interaction with cardiovascular KATP-channels and a possibility that it may increase insulin sensitivity. There are also newer insulin secretagogues (such as neteglinide and repaglinide) with a rapid onset of action on the beta-cell, therefore inducing a more physiological profile of insulin secretion during meals. The category of insulin sensitizers includes metformin and thiazolidinediones. Metformin effectively reduces hyperglycemia, hyperlipidemia and macroangiopathy in patients with type 2 diabetes. This agent increases the sensitivity of the liver and peripheral tissues to insulin and, therefore, it could be considered as a drug of choice for the prevention of type 2 diabetes. Thiazolidinediones (rosiglitazone and pioglitazone) increase the sensitivity of the tissues to insulin. This mechanism of action makes them powerful therapeutic tools for the treatment of type 2 diabetes (and possibly other insulin resistant states) either alone or in combination with other oral agents. The category of agents that interfere with the absorption of glucose and lipids includes alpha-glucosidase inhibitors (acarbose and miglitol) and lipase inhibitors (or-listat). alpha-Glucocidase inhibitors improve the time relationship between plasma insulin and glucose increases after a meal. Therefore, these agents may be used in the treatment of patients with type 2 diabetes, either alone at a very early stage of this disease (when insulin secretion is still adequate), or in combination with insulin secretagogues. alpha-Glucosidase inhibition may also prove useful as a supplement to insulin therapy in patients with type 1 diabetes mellitus. The inhibitor of gastrointestinal lipase orlistat may prove a useful adjunct to hypocaloric diets in patients with type 2 diabetes and obesity.
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PMID:Oral hypoglycemic agents: insulin secretagogues, alpha-glucosidase inhibitors and insulin sensitizers. 1146 May 77

Despite the growing consensus that postprandial glucose levels provide a more accurate and valuable early marker of diabetes symptoms than fasting plasma glucose, the ability to forestall diabetic complications by managing postprandial hyperglycemia has not been proved. Patients who are not considered to have diabetes mellitus may have impaired glucose tolerance (and increased risk for developing cardiovascular disease), and targeting nonfasting glucose can reduce insulin requirements for patients with insulin-dependent diabetes mellitus (type 1 diabetes mellitus). The challenge now is to determine what fasting glucose levels merit intervention, when and how they should be determined, and who should measure them. After outlining the discrepancies and lack of consensus between measurement guidelines developed by different professional organizations, the author then reviews options for treating postprandial hyperglycemia, including prepackaged meals, alpha-glucosidase inhibitors, acarbose therapy, and fast-acting insulin preparations.
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PMID:Postprandial hyperglycemia: implications for practice. 1157 24

Summary. Many studies have shown that experimental type 1 diabetes causes morphological, functional, and metabolic alterations in the small intestine. The more frequent form of the disease, type 2 diabetes, however, has been less studied. Here the influence of diabetes on the functionality of the small intestine was studied in an experimental diabetes model, with a certain degree of residual insulin secretion, specifically in the n0-STZ model. - The diabetic rats in this model were found to have glycaemia levels higher than in the controls (8.82 +/- 0.27 and 6.18 +/- 0.18 mmol/L; p < 0.01), while their plasma insulin levels were lower than in the control rats (2.65 +/- 0.32 and 3.60 +/- 0.25 ng/ml; p < 0.05). Although there were no significant variations in body weight between the two groups, both the weight and the length of the intestine were significantly greater (p < 0.05) in the diabetic rats than in the controls. The sucrase and maltase activities were greater (p < 0.01) in the proximal intestine of the diabetic rats (94 +/- 8 and 234 +/- 12 mU/mg protein, respectively) than in the control rats (50 +/- 2 and 149 +/- 20 mU/mg protein, respectively). The 6-phosphofructo-1-kinase activity (mU/mg proteins) was less (p < 0.05) in the proximal and distal intestine of the diabetic rats (160 +/- 40 and 80 +/- 20, respectively) than in the controls (280 +/- 30 and 230 +/- 30, respectively). No significant differences were observed in the lactate dehydrogenase or active and total pyruvate dehydrogenase measured in the distal and proximal intestine of control and diabetic rats. In conclusion, our results show that experimental diabetes (n0-STZ model) similar to human type 2 diabetes produces certain morphological and enzymatic alterations which affect the digestion and absorption of carbohydrates and the intestinal metabolism of glucose. These alterations may contribute to producing the post-prandial hyperglycaemia which characterizes diabetes.
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PMID:Morphological and enzymatic changes of the small intestine in an n0-STZ diabetes rat model. 1201 71

Besides dietary approaches, various pharmacological means have been recently developed in order to better control postprandial hyperglycaemia. This objective may be obtained: 1) by slowing down the intestinal absorption of carbohydrates; 2) by insuring a better insulin priming soon after the meal; and 3) by inhibiting post-prandial glucagon secretion or action. Some hormones (amylin, glucagon-like peptide-1) can slow gastric emptying while alpha-glucosidase inhibitors (acarbose, miglitol) retard intestinal digestion and resorption of complex carbohydrates. A more physiological post-meal profile of insulin may be obtained in type 2 diabetes by using new insulin secretagogues of the glinide family (repaglinide, nateglinide) with an earlier and shorter insulinotropic action or, mainly in type 1 diabetes but also in type 2 diabetes, by using short-acting insulin analogues (lispro. Asp B28) or inhated insulin the action of which is faster than that of subcutaneous insulin. Post-prandial glucagon secretion can be inhibited by amylin. GLP-1 or insulin while other glucagon antagonists are currently in development.
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PMID:[Postprandial hyperglycemia. II. Pharmacological approaches]. 1207 90

The development of immune-mediated diabetes in BB rats may involve a defect of the gastrointestinal tract (GI), as suggested by increased gut permeability. This study aimed at measuring invertase, maltase, lactase, and peroxidase activities in the duodenum of diabetesprone BioBreeding (BBdp) rats and control BioBreeding rats (BBc) given free access to NIH-07 diet up to the time of killing at 60 66 d of age. After washing the entire small intestine, the duodenal mucosa was scraped off in the first 5-cm segment from the pylorus and frozen in distilled water. Invertase, maltase, and lactase activities were measured by monitoring the conversion of [U-(14)C]sucrose, [U-(14)C]maltose, and [D-[1-(14)C]glucose] lactose to radioactive hexoses, which were phosphorylated in the presence of adenosine triphosphatase and yeast hexokinase and then separated from their precursor by ion-exchange chromatography. Peroxidase activity was measured by a spectrophotometric procedure. In the BBdp rats, the activity of invertase, maltase, and lactase averaged, respectively, 70.2 +/- 4.4, 81.2 +/- 4.3, and 75.7 +/- 4.1% (n = 16 and p < 0.001 in all cases) of the control values found in BBc rats of the same sex. Inversely, after exclusion of two female BBc rats with abnormally high plasma D-glucose concentration, the activity of peroxidase in the BBdp rats averaged 157.4 +/- 20.0% (n = 16; p < 0.02) of the mean control value recorded in BBc rats of the same sex (100.0 +/- 9.3%; n = 14). These findings are compatible with the view that a proinflammatory state of the GI associated with compromise function may precede the occurrence of pancreatic insulitis in BBdp rats and, possibly, human subjects with type 1 diabetes.
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PMID:Invertase, maltase, lactase, and peroxidase activities in duodenum of BB rats. 1262 29

Nursing home staff are well aware of the increasing number of residents who experience diabetes mellitus. These residents consume an inordinate amount of resources and often have major disabilities and co-morbidities. Although nonpharmacological therapies, such as consistent carbohydrate intake and increased activity levels, are always indicated in diabetes management, pharmacological therapies are often necessary to prevent the acute complications of diabetes and delay some of the long-term complications. Residents with type 2 diabetes may be managed with oral antidiabetic agents and insulin, whereas residents with type 1 diabetes will always require insulin. Oral antidiabetic agents include insulin secretagogues, which stimulate endogenous insulin secretion and are most effective in leaner persons with type 2 diabetes. Metformin is another oral antidiabetic agent; this decreases inappropriate hepatic glucose release and is most effective in obese residents with high fasting blood glucose levels. The thiazolidinediones, also called glitazones, are insulin sensitisers that enable peripheral tissues to utilise insulin more effectively. The alpha-glucosidase inhibitors delay intestinal absorption of ingested carbohydrates. In addition to oral antidiabetic agents, insulin is frequently used in diabetes management. Insulin is always indicated in type 1 diabetes and is often necessary for residents with type 2 diabetes to optimise glycaemic control. Insulin can be rapid, fast, intermediate or long acting. In addition, basal insulin is now available. These insulins can be combined with each other and, in type 2 diabetes, with oral antidiabetic agents. In order to use pharmacological therapies appropriately, the glycaemic patterns of nursing home residents should be identified, using capillary blood glucose monitoring. Once these patterns have been identified, nonpharmacological therapies can be used, usually in conjunction with the many oral antidiabetic agents and various insulins available, to optimise glycaemic control in each resident.
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PMID:Management of diabetes mellitus medications in the nursing home. 1581 54


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