|1.||Holst, Jens J: 4 articles (11/2009 - 10/2004)|
|2.||Ney, Denise M: 3 articles (11/2009 - 02/2003)|
|3.||Murali, Sangita G: 3 articles (11/2009 - 02/2003)|
|4.||Chaves, P: 2 articles (11/2014 - 01/2002)|
|5.||Sangild, Per T: 2 articles (01/2010 - 09/2002)|
|6.||Liu, Xiaowen: 2 articles (11/2009 - 12/2008)|
|7.||Sourial, Magdy: 2 articles (01/2008 - 10/2004)|
|8.||Fuller, Peter J: 2 articles (01/2008 - 10/2004)|
|9.||Taylor, Russell G: 2 articles (01/2008 - 10/2004)|
|10.||Bhasin, D K: 2 articles (03/2006 - 10/2000)|
|1.||Body Weight (Weight, Body)
11/01/2009 - "EN induced significantly greater jejunal sucrase activity and gain of body weight, and improved feed efficiency compared with PN+GLP-2 alone. "
12/01/2008 - "Combination treatment with EN+GLP-2 induced synergistic intestinal growth in ileum, resulting in greater mucosal cellularity, sucrase segmental activity, and gain of body weight (ENxGLP-2, P < 0.04). "
01/01/2000 - "Total homogenate sucrase activity per unit body weight did not differ (P > 0.05) among the age groups studied. "
12/01/1991 - "At the end of 3 days' fasting, rats had 20% less body weight, 30% less mucosal protein and 50% less jejunal sucrase activity per unit length than those before fasting. "
06/01/1990 - "These observations demonstrate that changes in the intestinal sucrase activity of the obese mouse precede the development of excessive body weight."
09/01/1995 - "Infection with Giardia lamblia induced precocious expression of sucrase activity and impaired mucosal absorption."
01/01/1995 - "Sucrase activity was not affected by a challenge infection. "
01/01/1986 - "Small intestinal sucrase activity during experimental infections with Nippostrongylus brasiliensis and/or Eimeria nieschulzi in rats."
03/01/1995 - "The activities of alkaline phosphatase and sucrase in the duodenum of primary infection rats decreased nearly half of the controls 2 weeks after infection, whereas the activities were unchanged in the reinfection group. "
05/01/1994 - "Functional abnormalities of absorptive epithelium, indicated by D-xylose malabsorption and decreased sucrase activity, occurred before the onset of diarrhea or opportunistic enteric infections. "
07/01/1999 - "Compared with transection, resection resulted in mucosal hyperplasia with significant decreases in the specific and total activities of sucrase, lactase, and maltase. "
12/01/1992 - "In jejunal villi, adaptational hyperplasia was associated with an increase in total epithelial alkaline phosphatase, but not total sucrase, activity; alkaline phosphatase activity increased most obviously in cells at the 11-50% position (from the tip) on villi. "
02/01/2003 - "Acute IGF-I treatment induced sustained jejunal hyperplasia on the basis of significantly greater concentrations of jejunal mucosal protein and DNA without a change in histology or sucrase activity. "
07/01/1994 - "Transection alone stimulated mucosal hyperplasia, intestinal sucrase specific activity, and glucose transport at 10 days but not at 21 days. "
03/01/1990 - "Despite villus cell hyperplasia in 85% bypass rats, mucosal sucrase and alkaline phosphatase fell in jejunum and remained low in ileum, while leucine amino peptidase rose in ileum. "
10/01/1989 - "These CS-glcs provide a new generation of sucrase inhibitors which may be useful in the treatment of diabetes mellitus."
10/01/2014 - "on inhibition of sucrase related to diabetes mellitus (DM). "
02/01/1985 - "Eight weeks after subtotal pancreatectomy, the rats contracted insulin-deficient diabetes mellitus, and sucrase activity was enhanced in both the Thiry-Vella loop and in the proximal jejunum in continuity. "
01/04/1999 - "To clarify the relationship between diabetes mellitus and carbohydrate digestion, the activities of sucrase and isomaltase, which form a complex enzyme (SI complex) on the brush border membranes, were compared in the progression of diabetes mellitus in Otsuka Long-Evans Tokushima fatty (OLETF) rats, a model of human non-insulin-dependent diabetes mellitus with insulin resistance, and Long-Evans Tokushima Otsuka (LETO) rats as non-diabetic controls. "
10/01/1998 - "These results suggest that 1) hyperglycemia directly increases the activities of intestinal maltase, sucrase, and lactase; 2) hyperglycemia does not influence renal maltase activity; and 3) hyperglycemia is partly responsible for increased activities of intestinal disaccharidases in diabetes mellitus."
|5.||Inflammatory Bowel Diseases (Inflammatory Bowel Disease)
08/01/1990 - "Sucrase-isomaltase expression may be useful as a clinical marker to improve our prognostic capabilities in patients with dysplastic lesions of the colon, that is, inflammatory bowel disease."
04/01/2008 - "Furthermore, isolated reports described severe postoperative chronic diarrhoea mimicking enterocolitis in patients with sucrase-isomaltase deficiency, inflammatory bowel disease (IBD), or intestinal microvillus atrophy. "
02/01/2000 - "coli, Vibrio cholerae and human immunodeficiency virus/acquired immunodeficiency disorder, enteral feeding diarrhea, Helicobacter pylori gastroenteritis, sucrase maltase deficiency, inflammatory bowel disease, irritable bowel syndrome, small bowel bacterial overgrowth and lactose intolerance. "
01/01/1979 - "Jejunal mucosal function and structure was examined in 31 patients with ulcerative colitis and 29 patients with Crohn's disease with ileal, ileocolonic or colonic involvement; A significant reduction of the specific activity of disaccharidases (lactase, sucrase and trehalase) in jejunal mucosal homogenate occurred in patients with inflammatory bowel disease. "
|3.||gamma-Glutamyltransferase (gamma-Glutamyl Transpeptidase)
|6.||DNA (Deoxyribonucleic Acid)
|7.||Insulin-Like Growth Factor I (IGF-1)
|10.||Messenger RNA (mRNA)
|2.||Enteral Nutrition (Feeding, Tube)
|3.||Colonic Pouches (S Pouch)