|Nichols, Buford - BAYLOR COLL MEDICINE|
|Avery, Stephen - BAYLOR COLL MEDICINE|
|Butte, Nancy - BAYLOR COLL MEDICINE|
|Opekun, Anton - BAYLOR COLL MEDICINE|
|Hahn, Dagmar - UNIV. BERN, SWITZERLAND|
|Sterchi, Erwin - UNIV. BERN, SWITZERLAND|
Submitted to: Pediatric Research
Publication Type: Abstract Only
Publication Acceptance Date: March 1, 2002
Publication Date: April 1, 2002
Citation: Nichols, B.L., Avery, S.E., Butte, N.F., Opekun, A.R., Hahn, D., Sterchi, E.E. 2002. Yeast amyloglucosidase dietary supplements increase starch digestion by maltase-glucoamylase (mga) knockout and wild-type mice. Pediatric Research. 51:145A. Interpretive Summary: Interpretive Summary not needed for this 115.
Technical Abstract: BACKGROUND: Last year, we reported that 26% of children with chronic abdominal pain have low activities of duodenal glucoamylase (Karnsakul, W, Kitagawa, S, Olive, O, Villa, X, Sterchi, EE, Hahn, D, Lugenbuehl, U, Nichols, BL. Frequency of Disaccharidase Deficiencies in Childhood Chronic Abdominal Pain Pediatric Res. 49: 118A, 2000). Dietary supplements with yeast derived enzymes are currently available for relief of lactose and sucrose intolerance symptoms but none have been proposed for glucoamylase deficiencies. Aspergillus n. amyloglucosidase (AMG), a yeast glucoamylase widely used in food manufacturing, has the same substrate specificities as brush-border MGA and is a likely candidate. OBJECTIVE: Testing of AMG dietary supplementation for enhanced in vivo starch digestion in glucoamylase deficient and sufficient mice. DESIGN/METHODS: MGA Null, Heterozygous, and Wild type (WT) mice were genotyped by Q-PCR. 48 were studied more than 25 d after weaning by Oxymax 0100-207M indirect calorimetry (Columbus Instruments, Columbus, OH). Design: 4 d of 24 hr calorimetry on ad lib 60% starch chow with amyloglucosidase (AMG 300L, Novo, DK) added to drinking water (1% w/v) on d 3. Control: isocaloric 14% starch diet. Prandial RQ (pRQ) period was 6 PM to 6 AM. Mean pRQ was analyzed for genotype, day, and treatment effects by ANOVA and GLM. RESULTS: All genotypes of mice responded to AMG supplements with increased pRQ, from combined mean 0.98 to 1.05 (p=0.000). Feeding a low starch diet blocked the AMG pRQ response. Mean Null mouse AMG pRQ was not significantly greater than WT. AMG for 4 d resulted in progressive pRQ rise of combined mean to 1.07. After AMG, a 2 d delay of pRQ return to baseline was observed. CONCLUSIONS: 24 h of AMG increased pRQ with a calculated 24% enhancement of starch digestion in all mice. These results suggest that supplemented AMG increases in vivo intestinal starch digestion and that the AMG activity is resistant to intestinal degradation. The effect of AMG response on Null MGA KO was not significantly different from WT suggesting that supplementary AMG may override brush-border MGA starch digestion. Our results in mice suggest that AMG dietary supplementation could be used to increase starch digestion in symptomatic human MGA deficiencies.