Disease relevance of voglibose

• Effect of an intestinal disaccharidase inhibitor (AO-128) on obesity and diabetes [1].
• Voglibose, one of the most important alpha-glucosidase inhibitors, delays the digestion and absorption of carbohydrates, thereby inhibiting postprandial hyperglycemia and hyperinsulinemia, and is the aid in the treatment of diabetes [2].
• Four weeks after TAC, both the heart weight/body weight ratio and the lung weight/body weight ratio were lower in the voglibose group than in the TAC group [3].
• AO-128 normalized hyperglycemia and markedly reduced hypertriglyceridemia and hyperinsulinemia in fatty rats [4].
• Repeated episodes of paralytic ileus in an elderly diabetic patient treated with voglibose [5].

High impact information on voglibose

• We further investigated whether the levels of 8-OHdG and HNE-modified proteins would be modified in the pancreatic beta-cells of GK rats fed with 30% sucrose solution or 50 ppm of voglibose (alpha-glucosidase inhibitor) [6].
• OBJECTIVE; To examine the effects of diet and diet with voglibose or glyburide on abdominal adiposity and metabolic abnormalities in patients with type 2 diabetes [7].
• The efficacy of voglibose on glycemic excursions in non-insulin-treated NIDDM patients [8].
• RESULTS: After the study treatment, HbA1c and plasma glucose in the patients who had received voglibose were comparable to those of patients in the control group [9].
• Voglibose did not however alter the rate of gastric emptying [10].

Chemical compound and disease context of voglibose

• Increased flatulence was observed in 56.7 and 90% of the patients taking voglibose and acarbose, respectively, while abdominal distention was noted in 10 and 16.7% [11].
• Voglibose significantly prevented hypotension and neurotensin increment after glucose intake and had no influence on glucose or insulin increment [12].
• Symptoms related to hypoglycemia (e.g., increased appetite, palpitation, sweating, tremor) were scarcely observed with either voglibose or nateglinide treatments [13].
• The patient started prednisone treatment, but one month later treatment with voglibose, an alpha-glucosidase inhibitor (alpha-GI), was started because of prednisone-induced diabetes mellitus [14].
• Octreotide, voglibose and diet therapies failed to improve the nocturnal hypoglycemia [15].

Biological context of voglibose

• CONCLUSION: Improvement of glycemic control through voglibose therapy inhibited cardiac remodeling by decreasing myocardial oxidative stress in mice with cardiac pressure overload [3].
• Echocardiographic and invasive hemodynamic examination showed improvement of left ventricular function in voglibose-treated mice [3].
• Food intake of fatty rats treated with AO-128 was decreased throughout the experiment [4].
• The maximum concentration (Cmax) and area under the plasma concentration-time curve (AUC) of plasma IRI after meals decreased significantly with all treatments except voglibose 0.3 mg compared with placebo [16].
• Pioglitazone significantly decreased systolic and diastolic blood pressure levels at 12 weeks, but voglibose had no effect [17].

Anatomical context of voglibose

• A new disaccharidase inhibitor, AO-128, showed 190-3900-fold more potent inhibition of purified rat small intestine sucrase-isomaltase (S-1) complex and 23-33-fold more potent inhibition of semipurified porcine small intestine disaccharidases than acarbose [1].
• In addition, AO-128 decreased body weight gain, food efficiency, epididymal adipose tissue weight, carcass weight, and body fat deposition [4].
• Metabolic improvements associated with a reduction of abdominal visceral fat caused by a new alpha-glucosidase inhibitor, AO-128, in Zucker fatty rats [18].
• Administration of AO-128 (50 p.p.m./day), a new alpha-glucosidase inhibitor, caused a substantial reduction of mesenteric fat weight accompanied by a marked decrease in fat cell volume in Zucker fatty rats [18].
• The present study was designed to determine the possible significance of a therapeutic dose (0.2 mg) of AO-128 on carbohydrate absorption by measuring the breath hydrogen concentration, which is an index of the amount of unabsorbed carbohydrate in the large intestine [19].

Associations of voglibose with other chemical compounds

• RESEARCH DESIGN AND METHODS: Sixteen NIDDM patients (4 patients treated with diet therapy alone and 12 receiving a sulfonylurea) were given 0.6 mg of voglibose daily for 4 weeks [10].
• CONCLUSIONS: Voglibose modified neither the pharmacodynamics nor the pharmacokinetics of warfarin under steady-state conditions [20].
• METHODS: The small intestine 30 cm long from 2 cm caudal ward Treitz's ligament of Wistar rat was used as an in situ loop, which was randomly perfused in recircular mode with maltose (10mmol/L) with or without different dosages of voglibose and/or GA for an hour [21].
• Voglibose also decreased significantly the plasma levels of soluble intercellular adhesion molecule 1 and urinary excretion of 8-iso-prostaglandin F(2)alpha and 8-hydroxydeoxyguanosine (P<.01) and C-reactive protein (P<.05) relative to the control group [22].

Gene context of voglibose

• Voglibose treatment decreased the myocardial expression of an NADPH oxidase subunit (p47phox) [3].
• In contrast, no significant changes in plasma adiponectin or TNF-alpha levels were observed in voglibose-treated patients [17].
• CONCLUSIONS: The rate of gastric emptying affects the efficacy of voglibose therapy in NIDDM patients [10].
• Ten-week-old, male fatty rats were kept on CE-2 diet containing 10 or 25 ppm of AO-128 for 4 weeks [4].
• The first administration of 1 mg voglibose enhanced GLP-1 secretion > 80% above controls [23].

Analytical, diagnostic and therapeutic context of voglibose

• Insulin sensitivity (KITT) was improved to a statistically significant level in both the patients treated with voglibose and the patients in the control group [9].
• A statistically significant increase in AUCinsulin occurred after treatment with voglibose (2,223.5 +/- 390.6 to 1,546.7 +/- 303.4 pmol.l-1.h, P < 0.05), but no change occurred in the control group (2,364.5 +/- 315.4 to 2,464.2 +/- 269.3 pmol.l-1.h, P = 0.60) [9].
• Urinary CPR excretion decreased by 30.6% and 41.7%, respectively, in subjects who received acarbose 50 mg or 100 mg compared with the previous day when no drug was given, whereas the urinary CPR excretion did not decrease significantly with voglibose [16].
• Oral administration of voglibose prolonged the duration of normoglycaemia and reduced the incidence of hypoglycaemia attacks [24].
• Analysis of the diurnal metabolic profiles revealed a significant reduction of postprandial hyperglycemia and hyperlipidemia in the voglibose group relative to the control group (P<.05), despite the similar improvement in body mass index and hemoglobin A(1c) in both groups [22].

References