title: Secretion of GIP in responders to acarbose in obese Type 2(NIDDM) patients.
abstract: Acarbose has been shown to reduce postprandial hyperglycemia and to improve lipid parameters in diabetics via its inhibitory effects on intestinal alpha-glucosidases. Response to acarbose may therefore be dependent upon gastric or pancreatic hormone function. To test this hypothesis, we treated 27 mild type 2 (NIDDM) Japanese diabetics who were mildly obese with low-dose acarbose (150 mg/day) for 3 months. We then performed a responder analysis to determine specific hormonal responses that may be associated with a good response to acarbose. At the end of the treatment period, a total of 15 evaluable patients was grouped as responders (n=6) and nonresponders (n=9) based on an effective decrease in postprandial glucose levels (>30 mg/day) and glycosylated hemoglobin (HbA1c) levels (>0.5%). There were no differences between the two groups in demographic variables or mean postprandial glucose levels at baseline. There was a small but significant increase in postprandial cholecystokinin (CCK) in responders, and fasting gastric inhibitory peptide (GIP) levels were significantly increased in responders and all patients after treatment. Serum leptin levels were reduced by treatment in our mildly obese responders and this was associated with a significant decrease in body weight. These results suggest that treatment with low-dose acarbose may reduce hyperglycemia in mild type 2 Japanese patients and may improve metabolic control by regulating hormones involved in glycemic control and digestive absorption. Acarbose may provide a safe adjunct to help treat insulin resistance in type 2 patients.
authors.affiliation: Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Takei
authors.forename: K
authors.initials: K
authors.lastname: Miyamoto
authors.forename: O
authors.initials: O
authors.lastname: Funae
authors.forename: N
authors.initials: N
authors.lastname: Ohashi
authors.forename: S
authors.initials: S
authors.lastname: Meguro
authors.forename: M
authors.initials: M
authors.lastname: Tokui
authors.forename: T
authors.initials: T
authors.lastname: Saruta
mesh_terms: D020909:Acarbose / Q000627:therapeutic use*; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight / Q000187:drug effects; D003920:Diabetes Mellitus / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000378:metabolism*; D006728:Hormones / Q000097:blood; D006801:Humans; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009765:Obesity; D019518:Postprandial Period
chemical_list: D001786:Blood Glucose; D004791:Enzyme Inhibitors; D006728:Hormones; D020738:Leptin; D008055:Lipids; D005749:Gastric Inhibitory Polypeptide; D020909:Acarbose