The effect of alpha-glucosidase inhibition on intestinal disaccharidase activity in normal and diabetic mice

Lee, Stanley M.; Bustamante, Sergio; Koldovský, Otakar

doi:10.1016/0026-0495(83)90109-9

Cited by 45 publications

(24 citation statements)

References 13 publications

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“…In this regard, enteroendocrine cell populations might be altered following bypass surgery, since anatomic and physiological plasticity of gastrointestinal mucosa is known to take place in several conditions, including bariatric surgery (21,23,26,37,42). However, to our knowledge, there are not yet any reports examining the enteroendocrine cell population after bariatric surgery.…”

mentioning

confidence: 73%

“…We found a significant increase in the K/L cell population in the jejunum anastomosed to the stomach of DJB-GK rats, although we could not attribute this to an increase in the frequency of epithelial cells coexpressing PDX1 and PAX6. Anatomic and physiological plasticity of gastrointestinal mucosa takes place in several conditions, including ileal transposition and enterogastrostomy (21,23,26,37,42). Interestingly, diet and gut microflora have been reported to influence the distribution of enteroendocrine cells in the rodent intestine (4,36,46).…”

Section: Discussionmentioning

confidence: 99%

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Duodenal-jejunal bypass protects GK rats from β-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1

Speck

Cho

Asadi

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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Speck M, Cho YM, Asadi A, Rubino F, Kieffer TJ. Duodenaljejunal bypass protects GK rats from ␤-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1. Am J Physiol Endocrinol Metab 300: E923-E932, 2011. First published February 8, 2011 doi:10.1152/ajpendo.00422.2010.-Dramatic improvement of type 2 diabetes is commonly observed after bariatric surgery. However, the mechanisms behind the alterations in glucose homeostasis are still elusive. We examined the effect of duodenal-jejunal bypass (DJB), which maintains the gastric volume intact while bypassing the entire duodenum and the proximal jejunum, on glycemic control, ␤-cell mass, islet morphology, and changes in enteroendocrine cell populations in nonobese diabetic Goto-Kakizaki (GK) rats and nondiabetic control Wistar rats. We performed DJB or sham surgery in GK and Wistar rats. Blood glucose levels and glucose tolerance were monitored, and the plasma insulin, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) levels were measured. ␤-Cell area, islet fibrosis, intestinal morphology, and the density of enteroendocrine cells expressing GLP-1 and/or GIP were quantified. Improved postprandial glycemia was observed from 3 mo after DJB in diabetic GK rats, persisting until 12 mo after surgery. Compared with the sham-GK rats, the DJB-GK rats had an increased ␤-cell area and a decreased islet fibrosis, increased insulin secretion with increased GLP-1 secretion in response to a mixed meal, and an increased population of cells coexpressing GIP and GLP-1 in the jejunum anastomosed to the stomach. In contrast, DJB impaired glucose tolerance in nondiabetic Wistar rats. In conclusion, although DJB worsens glucose homeostasis in normal nondiabetic Wistar rats, it can prevent long-term aggravation of glucose homeostasis in diabetic GK rats in association with changes in intestinal enteroendocrine cell populations, increased GLP-1 production, and reduced ␤-cell deterioration. bariatric surgery; Goto-Kakizaki rat; diabetes mellitus; glucose homeostasis; glucagon-like peptide-1; glucose-dependent insulinotropic polypeptide; K cells; L cells; pancreatic and duodenal homoeobox 1; paired box gene 6

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mentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Duodenal-jejunal bypass protects GK rats from β-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1

Speck

Cho

Asadi

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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“…Examination of glucosidase activity in the median and distal small intestine of mice has shown sucrase activity to be significantly increased after 15 days of acarbose administration, but not after 5 or 10 days (LEE et al 1983). Surprisingly, the activity of lactase, a ß-glucosidase which is not inhibited by acarbose, was dose dependently increased in normal and in diabetic mice.…”

Section: Enzyme Activity Alterations In the Small Intestinementioning

confidence: 93%

“…The wet weight of the sm all intestine was increased when acarbose was given as a food-drug mixture to normal and genetically diabetic mice for a period of 15 days (LEE et al 1983) or 10 weeks (LEE and KOLDOVSKY 1993). An increased weight of the upper, middle and lower part of the sm all intestine of rats was reported after a 3-week (PULS et al 1983) or 4-week feeding (UITENTHAL et al 1982) of acarbose.…”

Section: Weight Length and Microfloramentioning

confidence: 99%

Pharmacology of Glucosidase Inhibitors

Puls¹

1996

Oral Antidiabetics

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“…Generally, maltase activities are fivefold and more higher than sucrase activities in the small intestine of mammals (15). Disaccharidase activities in the distal part of the small intestine have been documented to be increased by long-term treatment with acarbose (16). Such increased activities are thought to be a compensatory response to the presence of undigested disaccharides and to be important for reducing the development of undesirable symptoms, such as diarrhea and flatulence.…”

Section: Antiobesity and Antidiabetic Actionsmentioning

confidence: 99%

Antiobesity and Antidiabetic Actions of a New Potent Disaccharidase Inhibitor in Genetically Obese-Diabetic Mice, KKAy.

Odaka

Shino

Ikeda

et al. 1992

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryAO-128 is a potent and structurally novel inhibitor of the intestinal disaccharidases, such as maltase and sucrase. Genetically obese-diabetic mice, KKAy, were used to examine the acute or long-term effectiveness of this compound. AO-128 decreased a postprandial rise in blood glucose after sucrose solution loading dose-dependently; the ED50 to reduce a delta increment of blood glucose by 50% was 0.22mg/kg. The intestinal sucrase and maltase activitiess were suppressed to 7 and 48% of the control levels, respectively, at a dose of 0.21mg/kg. Four-week-old female KKAy mice were kept on a laboratory diet containing 10 or 50 ppm of AO-128 for 12 weeks. The high dose of AO-128 reduced food intake and body weight gain throughout the experimental period. On the other hand, the low dose reduced body weight gain for the first 4 weeks without any effect on food intake. Development of the hyperglycemia and hyperinsulinemia characteristic of KKAy mice was moderately prevented by the low dose, and completely by the high dose. Hypertriglyceridemia tended to be suppressed by the AO-128 treatment. The high dose decreased the hemoglobin A 1 level and parametrial adipose tissue weight. Hepatomegaly and fatty liver were ameliorated by AO-128 dosedependently. Nephropathy was ameliorated by the high dose. These findings indicate that AO-128 may be useful for treating human obesity and diabetes. Key Words disaccharidase inhibitor, obesity, diabetes, KKAy mice, hy perglycemia, hyperinsulinemia, sucrase, maltase A steep rising in the postprandial blood glucose level is a therapeutic problem in carbohydrate-related disorders, such as obesity, diabetes mellitus, and hypertriglyceridemia (1, 2), because the high blood glucose level accelerates lipogenesis and fat accumulation through hypersecretion of insulin, and increases insulin require ment. Recent research indicates that alpha-glucosidase inhibitors, which delay 27

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The effect of alpha-glucosidase inhibition on intestinal disaccharidase activity in normal and diabetic mice

Cited by 45 publications

References 13 publications

Duodenal-jejunal bypass protects GK rats from β-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1

Duodenal-jejunal bypass protects GK rats from β-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1

Pharmacology of Glucosidase Inhibitors

Antiobesity and Antidiabetic Actions of a New Potent Disaccharidase Inhibitor in Genetically Obese-Diabetic Mice, KKAy.

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