Human Intestinal Disaccharidase Activities

Heitlinger, Leo A.; Rossi, Thomas M.; Lee, Ping-Cheung; Lebenthal, Emanuel

doi:10.1097/00005176-199102000-00011

Cited by 49 publications

(32 citation statements)

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“…This finding does not appear to be the result of a sampling error since it is in agreement with disaccharidase determinations in intestinal resection specimens (53,87). Most endoscopic small-bowel biop sy specime ns are obta ined fro m the duodenum ; how eve r, much of the pu blished no rmative data fo r intestinal d isaccharidases comes from tissue obtained from th e jejunum with a Cro sby capsule (88,89).…”

Section: Intestinal Disaccharidasessupporting

confidence: 73%

Congenital Sucrase‐Isomaltase Deficiency

Treem

1995

J. pediatr. gastroenterol. nutr.

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Section: Intestinal Disaccharidasessupporting

confidence: 73%

Congenital Sucrase‐Isomaltase Deficiency

Treem

1995

J. pediatr. gastroenterol. nutr.

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“…Lactase-and sucrase-specific activities were determined in the gastrointestinal laboratory of the Buffalo Children's Hospital by the method of Dahlqvist (32,33). Tissue was homogenized at 48C in maleate buffer, incubated with the appropriate substrate at 378C for 60 minutes, and immersed in a boiling water bath for 5 minutes.…”

Section: Disaccharidase Activitymentioning

confidence: 99%

Functional Significance of Single Nucleotide Polymorphisms in the Lactase Gene in Diverse US Patients and Evidence for a Novel Lactase Persistence Allele at −13909 in Those of European Ancestry

Baffour-Awuah

Fleet

Montgomery

et al. 2015

J. pediatr. gastroenterol. nutr.

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Objectives Recent data from mainly homogeneous European and African populations implicate a 140 bp region 5′ to the transcriptional start site of LCT (the lactase gene) as a regulatory site for lactase persistence and non-persistence. As there are no studies of United States non-homogeneous populations, we performed genotype/phenotype analysis of the -13910 and -22018 LCT SNPs in New England children, mostly of European ancestry. Methods Duodenal biopsies were processed for disaccharidase activities, RNA quantification by RT-PCR, allelic expression ratios by PCR, and genotyping and SNP analysis. Results were compared to clinical information. Results Lactase activity and mRNA levels, as well as sucrase-to-lactase ratios of enzyme activity and mRNA, showed robust correlations with genotype. None of the other LCT SNPs showed as strong a correlation with enzyme or mRNA activities as did -13910. Data were consistent with the -13910 being the causal sequence variant rather than -22018. Four individuals heterozygous for -13910T/C had allelic expression patterns similar to individuals with -13910C/C genotypes; of these, 2 showed equal LCT expression from the 2 alleles and a novel variant (-13909C>A) associated with lactase persistence. Conclusion The identification of -13910C/C genotype is very likely to predict lactase non-persistence, consistent with prior published studies. A -13910T/T genotype will frequently, but not perfectly, predict lactase persistence in this mixed European-ancestry population; a -13910T/C genotype will not predict the phenotype. A long, rare haplotype in 2 individuals with -13910T/C genotype but equal allele-specific expression contains a novel lactase persistence allele present at -13909.

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“…In a review done on seven studies of adult patients with celiac disease, they found decreased disaccharidase levels in patients with more severe inflammation when compared to those with celiac without inflammation. Mean sucrase levels were 18.3 mmol/min/g of protein and 45.14 mmol/min/g of protein, respectively [17]. This was also true for lactase and maltase levels.…”

Section: Disaccharidase Deficiencies Can Coexist With Organic Disementioning

confidence: 94%

The Role of Disaccharidase Deficiencies in Functional Abdominal Pain Disorders—A Narrative Review

Puertolas

Fifi

2018

Nutrients

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Disaccharidase deficiencies are reportedly underdiagnosed in pediatric populations. Though typically thought to cause diarrheal disease, they can also be a cause of abdominal pain and dyspepsia, and patients diagnosed with these functional disorders may actually have associated enzyme deficiencies. While the effects of lactose deficiency have been widely studied, sucrase, maltase, and isomaltase are less frequently considered when approaching a patient with an apparent functional abdominal pain disorder. This review seeks to provide an up-to-date narrative on the current scientific literature on the possible role of sucrase, maltase, and isomaltase deficiency in pediatric functional gastrointestinal disorders.

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Human Intestinal Disaccharidase Activities

Cited by 49 publications

References 0 publications

Congenital Sucrase‐Isomaltase Deficiency

Congenital Sucrase‐Isomaltase Deficiency

Functional Significance of Single Nucleotide Polymorphisms in the Lactase Gene in Diverse US Patients and Evidence for a Novel Lactase Persistence Allele at −13909 in Those of European Ancestry

The Role of Disaccharidase Deficiencies in Functional Abdominal Pain Disorders—A Narrative Review

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