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

1. The effects of KAD-1229 (a novel non-sulphonylurea agent), voglibose (an alpha-glucosidase inhibitor) and nateglinide (a non-sulphonylurea antihyperglycaemic agent) on hyperglycaemia induced by a meal load were assessed in diabetic rats. 2. KAD-1229 suppressed the increase in plasma glucose levels seen after a meal load and the area under the curve for plasma glucose levels (AUCglucose) up to 5 h after the meal load. 3. Voglibose also suppressed the increase in plasma glucose levels; however, a significant decrease in AUCglucose following voglibose was not observed. 4. Nateglinide suppressed the increase in plasma glucose levels at 30 min and 1 h after the meal load; however, plasma glucose levels was above control thereafter and the AUCglucose was not decreased. 5. The results indicate that KAD-1229 has an antihyperglycaemic effect and KAD-1229 is suggested to be a suitable agent for controlling post-prandial hyperglycaemia.
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PMID:Effect of KAD-1229, a novel hypoglycaemic agent, on plasma glucose levels after meal load in type 2 diabetic rats. 1201 Jan 87

Several epidemiological studies have shown an association between postprandial hyperglycemia and mortality from cardiovascular disease. Postprandial hyperglycemia is frequently associated with visceral obesity which plays a key role in metabolic abnormalities such as dyslipidemia and hypertension. Inhibitors of alpha-glucosidase and nateglinide have beneficial effects on the metabolic syndrome associated with visceral obesity. Voglibose in combination with diet therapy reduces visceral fat deposition and ameliorates insulin resistance. Acarbose slightly reduces blood pressure of hypertensive diabetic patients. Nateglinide, a rapidly acting insulin secretagogue, lowers postprandial glucose levels without significant body weight gain. These drugs may protect pancreatic beta-cells from postprandial glucose toxicity and prevent the progression of diabetes.
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PMID:[Pharmacological treatment of postprandial hyperglycemia in hypertensive patients with type 2 diabetes mellitus]. 1287 88

Prediabetes is the subclinical impairment in fasting plasma glucose, impaired glucose tolerance or both. The degree of impairment is between euglycemia and the hyperglycemia of type 2 diabetes (T2DM). Prediabetes is not considered benign, because it is a risk factor for T2DM but is also associated with micro and macrovascular complications. Lifestyle interventions including diet and exercise are first-line treatments. Medications can also play a role, as randomized controlled trials of biguanides (metformin) alpha-glucosidase inhibitors (Acarbose), inhibitors of pancreatic lipase (Orlistat), PPAR-gamma agonists (Rosiglitazone, Pioglitazone), meglitinides (Nateglinide) and GLP-1 receptor agonists (Liraglutide) have all shown benefits. Bariatric surgery is another efficacious means of preventing T2DM in patients with prediabetes and obesity. Prediabetes in its various guises is a risk factor for the future development T2DM and diabetic complications. Importantly the prediabetic state is amenable to interventions that prevent/delay transition to overt T2DM. Knowledge gaps exist regarding how best to make prognostication highly sensitive and specific as to which patient will develop T2DM. Moreover, understanding of phenotype specific pathophysiology may add value to funding appropriate interventions for patients with prediabetes. Management of patients with prediabetes should be individualized based on the algorithms that predict phenotype specific risk and allow for the use of phenotype tailored interventions.
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PMID:Treating prediabetes: why and how should we do it? 3228 63