Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.20 (alpha-glucosidase)
 4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastrectomy or vagotomy may result in reactive hypoglycemia, which, in some cases, can reduce the plasma glucose levels to 30-40 mg/dl due to rapid digestion and absorption of food, especially carbohydrates. It also occurs sometimes in patients on hemodialysis, where it is a potentially lethal complication. Because insulin has a longer half-life due to lack of renal degradation, hypoglycemia can be induced by insulin in patients with renal failure. We treated a patient with frequent episodes of severe hypoglycemia, that were sometimes accompanied by convulsions. He had undergone total gastrectomy 8 years before and had been maintained on hemodialysis for 3 years. Hyperinsulinemia caused by oxyhyperglycemia associated with post-gastrectomy led to severe hypoglycemia in this patient because of the lack of renal insulin degradation. Since nutritional treatment did not successfully manage his reactive hypoglycemia, an alpha-glucosidase inhibitor, acarbose, was administered to treat his oxyhyperglycemia. This therapy was very effective and he has not had any recurrence of reactive hypoglycemia since the initiation of the therapy.
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PMID:Treatment with alpha-glucosidase inhibitor for severe reactive hypoglycemia: a case report. 1107 24

Postprandial reactive hypoglycemia (PRH) can be diagnosed if sympathetic and neuroglucopenic symptoms develop concurrently with low blood sugar (<3.3 mmol). Neither the oral glucose tolerance test (OGTT) nor mixed meals are suitable for this diagnosis, due to respectively false positive and false negative results. They should be replaced by ambulatory glycemic control or, as recently proposed, an hyperglucidic breakfast test. PRH patients often suffer from an associated adrenergic hormone postprandial syndrome, with potential pathologic consequences such as cardiac arrhythmia. PRH could result from (a) an exaggerated insulin response, either related to insulin resistance or to increased glucagon-like-peptide 1; (b) renal glycosuria; (c) defects in glucagon response; (d) high insulin sensitivity, probably the most frequent cause (50-70%), which is not adequately compensated by hypoinsulinemia and thus cannot be measured by indices of insulin sensitivity such as the homeostatic model assessment. Such situations are frequent in very lean people, or after massive weight reduction, or in women with moderate lower body overweight. PRH is influenced by patient's alimentary habits (high carbohydrate-low fat diet, alcohol intake). Thus, diet remains the main treatment, although alpha-glucosidase inhibitors and some other drugs may be helpful.
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PMID:Postprandial reactive hypoglycemia. 1111 13

Most of type 2. diabetic patients require medication for several concomitant diseases, most important being, hypertension, ischaemic heart disease, heart failure, dyslipidaemias, obesity. Thus the risk of drug interactions is important, particularly in elderly patients. Oral antidiabetic drugs include hypoglycaemic agents (sulphonylureas, meglitenides) and biguanides (metformin), alpha-glucosidase inhibitors, tiazolinidediones. Drug interactions with antihyperglycaemic agents can be divided into pharmacokinetic and pharmacodynamic interactions. Numerous drugs due to interactions enhance hypoglycaemic action of sulphonylureas, thus increase the risk of hypoglycaemia. Several drugs may cause impairment of glycaemic control through various mechanisms in diabetic patients treated with oral antidiabetic drugs. Currently the most controversial problem is safety of combination therapy with sulphonylurea and metformin, as several observations indicated that it can increase mortality from cardio-vascular causes.
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PMID:[Clinically important effects of oral antidiabetic drug interactions]. 1112 85

Miglitol (Bay m 1099, Bayer) is a second generation alpha-glucosidase inhibitor. It is a derivative of 1-desoxynojirimycin, and binds reversibly to the brushborder alpha-glucosidase enzymes. In contrast to its parent drug (acarbose, Bay g 5421, Bayer), miglitol is almost completely absorbed in the small intestine. It has to be taken with each main meal, and through its effect on carbohydrate digestion it blunts the postprandial blood glucose increase. Miglitol has no or a very small effect on fasting blood glucose levels. The blood-glucose lowering effects of miglitol in patients with Type 2 diabetes are lower than those of the frequently-used sulphonylurea compounds. Long-term studies show that a moderate average reduction of HbA1c of 0.3-0.7% point from baseline can be achieved. An advantage over sulphonylurea is the effect on serum insulin levels: miglitol therapy leads to slightly lower postprandial levels of serum insulin, whereas chronic sulphonylurea treatment usually increases serum insulin levels. This insulin-sparing effect may, in theory, lead to a lesser weight gain or even no weight gain and reduced risk of hypoglycaemia during chronic treatment. Long-term experience in Type 1 diabetic patients is limited. Similarly, miglitol may lead to reduced postprandial glucose excursions, slightly reduced insulin requirements and perhaps, as a consequence, a lower risk of hypoglycaemia. More long-term data are needed to fully assess to the clinical use of miglitol in these patients.
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PMID:Miglitol, a new alpha-glucosidase inhibitor. 1124 57

Currently available oral agents for the treatment of type 2 diabetes mellitus include a variety of compounds from 5 different pharmacologic classes with differing mechanisms of action, adverse effect profiles, and toxicities. The oral antidiabetic drugs can be classified as either hypoglycemic agents (sulfonylureas and benzoic acid derivatives) or antihyperglycemic agents (biguanides, alpha-glucosidase inhibitors, and thiazolidinediones). In this review, a brief discussion of the pharmacology of these agents is followed by an examination of the adverse effects, drug-drug interactions, and toxicities. Finally, treatment of sulfonylurea-induced hypoglycemia is described, including general supportive care and the management of pediatric sulfonylurea ingestions. The adjunctive roles of glucagon, diazoxide, and octreotide for refractory hypoglycemia are also discussed.
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PMID:Oral agents for the treatment of type 2 diabetes mellitus: pharmacology, toxicity, and treatment. 1142 16

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

Type 2 diabetes results from the abnormal resistance of peripheral tissues to insulin and from the progressive insulin secretory failure of the pancreatic beta-cells. Treatment of type 2 diabetes has greatly improved due to the availability of new classes of oral antidiabetic drugs (OADs) and new insulin analogs. Three types of oral medications exert their antidiabetic action without directly stimulating insulin release: alpha-glucosidase inhibitors (e.g., acarbose) interfere with the digestion of dietary glucose precursors and the absorption of glucose; biguanides (e.g., metformin) inhibit hepatic gluconeogenesis, thereby lowering fasting blood glucose concentrations and increasing peripheral insulin sensitivity; and thiazolidinediones (e.g., rosiglitazone) improve the sensitivity of tissues to insulin-stimulated glucose disposal. In contrast, two classes of OADs stimulate insulin release from pancreatic beta-cells. Sulfonylureas (e.g., glyburide) have been used successfully for many years to treat type 2 diabetes, but their prolonged action may result in hypoglycemia. The third-generation sulfonylurea glimepiride is associated with a reduced risk of hypoglycemia and less weight gain than other sulfonylureas. Finally, the meglitinides (e.g., repaglinide) and D-phenylalanine derivatives (e.g., nateglinide) are powerful prandial insulin secretagogues. If the pancreatic beta-cells deteriorate to such an extent that insulin secretion is significantly impaired, treatment with additional exogenous insulin may be required.
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PMID:The pathophysiologic basis of efficacy and clinical experience with the new oral antidiabetic agents. 1187 80

The dumping syndrome consists of early postprandial abdominal and vasomotor symptoms, resulting from osmotic fluid shifts and release of vasoactive neurotransmitters, and late symptoms secondary to reactive hypoglycemia. Effective relief of symptoms of dumping syndrome can be achieved with dietary modifications to minimize ingestion of simple carbohydrates and to exclude fluid intake during ingestion of the solid portion of the meal. More severely affected individuals may respond to agents such as pectin and guar, which increase the viscosity of intraluminal contents, or to drugs such as the alpha-glucosidase inhibitor acarbose, which blunts the rapid absorption of glucose, and the somatostatin analog octreotide, which alters gut transit and impairs release of vasoactive mediators into the bloodstream.
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PMID:Dumping Syndrome. 1187 94

Type 2 diabetes mellitus is now regarded a worldwide epidemic with diabetes-related complications exacting a heavy toll on those with poor metabolic control. Although there is no cure currently, the therapeutic armamentarium has expanded over the last few years to five classes of oral agents--sulfonylureas, biguanides, meglitinides, thiazolidinediones and alpha-glucosidase inhibitors. Sulfonylureas continue to be the mainstay oral hypoglycaemic agents for type 2 diabetics because they are potent insulin secretagogues and cost-effective. Metformin exerts its main effect by reducing hepatic glucose output and is proven to particularly benefit obese type 2 diabetics. Meglitinides are rapid-acting insulin secretagogues targeting a postprandial hyperglycaemia and this class of drug is useful for those who are at risk of hypoglycaemia with longer-acting sulfonylurea drugs. Thiazolidinediones constitute a new class of insulin sensitizers that work predominantly in improving glucose uptake by the adipose tissues and skeletal muscles. Alpha-glucosidase inhibitors delay the digestion and absorption of polysaccharides, thus attenuating postprandial hyperglycaemia. This review article briefly examines the nature of these oral agents, including the role of combination therapy and insulin where clinically indicated.
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PMID:Current therapeutic strategies for type 2 diabetes mellitus. 1252 Aug 25

Dumping syndrome is a sequel of gastric surgery in adults and Nissen fundoplication in children. The syndrome is characterized by various gastrointestinal symptoms as well as irritability, diaphoresis and lethargy. Shortly after a meal, symptoms are associated with hyperglycemia (early dumping), followed by late dumping symptoms associated with reactive hypoglycemia. Several therapeutic and dietary manipulations failed to control these symptoms in previous reports as well as in an infant we have followed after Nissen fundoplication. Acarbose, an alpha-glucosidase inhibitor, has been used sporadically in adults after gastric surgery, but only once in children. In most of these studies, the effect of acarbose (on reactive hypoglycemia) was evaluated over several hours postprandially or after oral glucose load. In our study, we recorded glucose dynamics by a continuous glucose monitor system over 2 to 3 days before and during acarbose treatment, while the patient was on a well-controlled diet. These measurements (720 before and 832 on therapy) suggested that both early and late dumping symptoms are causally related to the rate of glucose elevation and decline, rather than to glucose peak and nadir, respectively. Acarbose attenuated both postprandial glucose hyperglycemia and reactive hypoglycemia, which subsequently led to a significant reduction in dumping symptoms. In a follow-up of 14 months, acarbose was well tolerated and the frequency of dumping symptoms was remarkably reduced.
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PMID:Acarbose treatment of infant dumping syndrome: extensive study of glucose dynamics and long-term follow-up. 1294 6


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