Mg Of Acarbose Research Articles

Carbohydrate malabsorption following acarbose administration

Carbohydrate absorption was assessed during acarbose administration to investigate the actions of this drug. In 7 healthy volunteers, breath hydrogen concentration was measured at 15-min intervals after administration of 6 g of lactulose, and continued until 4 h after the breath hydrogen level exceeded its pretreatment value by ≥10 ppm, then the amount of undigested carbohydrate was calculated following administration of various doses of acarbose and Ensure Liquid. Breath hydrogen data were also obtained before and after administration of acarbose to 8 patients with Type 2 diabetes mellitus for 2 and 4 months. After administration of 50 mg of acarbose with 250 ml or 500 ml of Ensure, the mean amount of unabsorbed carbohydrate was 5.3 g and 7.7 g, respectively, while unabsorbed carbohydrate increased to 10.8 g after 100 mg of acarbose with 500 ml of Ensure. In the diabetic patients, breath hydrogen excretion decreased to 31.6 % of baseline after 2 months of acarbose administration, indicating decreased carbohydrate malabsorption. Despite this, the haemoglobin A1c level remained stable after 5 months. In conclusion, the extent of carbohydrate malabsorption depended on the acarbose dose and the carbohydrate load. Although carbohydrate malabsorption decreased with continued acarbose administration, the improvement of glycaemic control was maintained. © 1998 John Wiley & Sons, Ltd.

Analysis of the antidiabetic drug acarbose by capillary electrophoresis

This study describes the derivatization of the pseudooligosaccharide acarbose and its main metabolite, component 2, with 7-aminonaphthalene-1,3-disulfonic acid (ANDS) in human urine. Their efficient separation was possible by means of capillary zone electrophoresis, using a capillary tube of fused-silica containing 100 m M triethylammonium phosphate buffer, pH 1.5. On column laser-induced fluorescence allowed the detection of the pseudooligosaccharides in human urine in the nanomolar range. With this method, acarbose and component 2 were quantified in human urine after application of 300 mg of acarbose.

The Effect of Acarbose and Miglitol (BAY-M-1099) on Postprandial Glucose Levels Following Ingestion of Various Sources of Starch by Nondiabetic and Streptozotocin-Induced Diabetic Rats

The effect of two alpha-glucosidase inhibitors, acarbose (BAY-G-5421) and miglitol (BAY-M-1099), on postprandial glucose levels following intubation of corn, rice, spaghetti and potato (0.5 g/100 g body wt) was evaluated in nondiabetic and diabetic rats. The peak plasma glucose level and total incremental glucose were significantly decreased following ingestion of each starch source when acarbose (8 mg/100 g body wt) or BAY-M-1099 (2 mg/100 g body wt) were simultaneously intubated. The effect of both inhibitors was more pronounced in diabetic rats than in nondiabetic rats, and their effect on digestion was in a substrate-specific manner. Potato starch digestion was inhibited 58 +/- 11% by BAY-M-1099, and by acarbose, 38 +/- 9%. Rice starch digestion was inhibited by 65 +/- 2% by acarbose, and by BAY-M-1099, only 30 +/- 9%. Both drugs had a similar inhibitory effect when corn or spaghetti was ingested. BAY-M-1099 appears to be more potent than acarbose on both a weight-per-weight basis and on a molar basis. When corn or rice was used, only 2 mg of BAY-M-1099 was required to achieve a similar inhibitory effect to that of 8 mg of acarbose (9.7 X 10(-3) M) vs. 12.2 X 10(-3) M). Since both drugs blunted to varying degrees the rise in glucose level following starch ingestion, they may be a useful adjuvant in the treatment of diabetic subjects. Simultaneous use of both drugs in therapeutic treatment should be seriously considered.

Fate and effects of the α-glucosidase inhibitor acarbose in humans

Abstract The α-glucosidase inhibitor acarbose has been successfully used in diabetic patients to decrease the postprandial rise in blood glucose. The aim of the present experiments was to investigate the fate and effects of acarbose along the small intestine using a slow-marker perfusion technique. In 8 healthy volunteers, jejunal and ileal loads of acarbose, glucose, and total carbohydrates were determined following a liquid, 400-kcal formula meal containing either 200 mg of acarbose or placebo. Preprandial and postprandial plasma concentrations of glucose and several polypeptide hormones were determined. Recovery of acarbose during 4 h was 65% ± 9% (mean ± SEM) of ingested dose in the ileum but 94% ± 9% in the jejunum, indicating that the compound was neither degraded nor absorbed by the intestine to a major degree. After acarbose administration, ileal loads of glucose and total carbohydrates were considerably higher, whereas postprandial plasma concentrations of glucose, insulin, and gastric inhibitory polypeptide were lower when compared with placebo. The retardation of carbohydrate digestion to be inferred from these findings is confirmed by significantly elevated plasma concentrations of enteroglucagon after acarbose administration compared with placebo administration.

Fate and effects of the α-glucosidase inhibitor acarbose in humans: An intestinal slow-marker perfusion study

The α-glucosidase inhibitor acarbose has been successfully used in diabetic patients to decrease the postprandial rise in blood glucose. The aim of the present experiments was to investigate the fate and effects of acarbose along the small intestine using a slow-marker perfusion technique. In 8 healthy volunteers, jejunal and ileal loads of acarbose, glucose, and total carbohydrates were determined following a liquid, 400-kcal formula meal containing either 200 mg of acarbose or placebo. Preprandial and postprandial plasma concentrations of glucose and several polypeptide hormones were determined. Recovery of acarbose during 4 h was 65% ± 9% (mean ± SEM) of ingested dose in the ileum but 94% ± 9% in the jejunum, indicating that the compound was neither degraded nor absorbed by the intestine to a major degree. After acarbose administration, ileal loads of glucose and total carbohydrates were considerably higher, whereas postprandial plasma concentrations of glucose, insulin, and gastric inhibitory polypeptide were lower when compared with placebo. The retardation of carbohydrate digestion to be inferred from these findings is confirmed by significantly elevated plasma concentrations of enteroglucagon after acarbose administration compared with placebo administration.

α‐GLUCOSIDASE INHIBITION IN OBESITY

Acarbose is an alpha-glucosidase inhibitor which reversibly and competitively inhibits the digestion of oligo- and disaccharides at the brush border of the small intestine. This study evaluates the preventive and therapeutic properties of acarbose in the treatment of obesity. Dose-response experiments were performed during repeated sucrose loads in man in order to investigate the effects of acarbose on plasma insulin and blood glucose levels. After titration of efficient doses, a long-term tolerance test of acarbose was undertaken in a small pilot study. Finally, the relapse preventing effect of acarbose was tested during double-blind cross-over conditions in 24 weight reduced obese women. In growing Sprague-Dawley rats, the effects of acarbose on body weight, lipid depots and adipose tissue cellularity were tested during pair-feeding and ad libitum conditions. Such effects were also studied in adult ad libitum-fed rats. Blood glucose, plasma insulin, body fat, depot lipids as well as fat cell weight and number were determined with established techniques. During a sucrose load, acarbose reduced insulin in a dose-dependent fashion. Glucose was also reduced, but not dose-dependently and only to a moderate extent. During a 200 g sucrose load, 400 mg of acarbose did not necessarily result in a maximal reduction of the insulin response while the glucose response was maximally inhibited after 100 mg. Acarbose reduced the relapse rate after weight reduction. No serious side effects were observed. Flatulence and meteorism occurred frequently. In growing rats, acarbose retarded the development of body weight and of lipid depots not only during pair-feeding conditions but also in ad libitum-fed animals eating considerably more than their controls. The spontaneous food consumption was increased by acarbose also in adult rats but in these animals neither body weight nor lipid depots were significantly reduced by acarbose. It is concluded that acarbose induces a carbohydrate malabsorption. Insulin levels are reduced not only via a decreased glycemic stimulus but also by interference with other insulin releasing mechanism(s). Acarbose is the first drug ever tested with long-term relapse reducing effects after weight reduction. Animal experiments suggest that acarbose may be of value in the prevention of obesity, particularly since the drug retards lipid accumulation also during ad libitum-feeding.

Response of serum levels of gastric inhibitory polypeptide and insulin to sucrose ingestion during long-term application of acarbose.

Sucrose (100 g) loading tests were performed in 10 healthy volunteers before and during the intake of an alpha-glucosidehydrolase inhibitor (acarbose) for 8 weeks (3 X 200 mg daily) and serum levels of glucose, immunoreactive insulin (IRI), and immunoreactive gastric inhibitory polypeptide (IR-GIP) were measured. The addition of 200 mg of acarbose to the sucrose load attenuated the sucrose-induced glycaemia and IRI response and completely abolished the IR-GIP release. The volunteers complained about meteorism and abdominal pain during the intake of the inhibitor. These side effects became less marked at the end of the study. The attenuation of complaints cannot be explained by a decreasing sucrase inhibition, since the increase of glucose, IRI, and IR-GIP after sucrose loading at the beginning and after 4 and 8 weeks was equally impaired by acarbose.