The Malabsorption Syndrome, with Special Reference to The Effects of Wheat Gluten

Dipeptidase deficiency and malabsorption of glycylglycine in disease states

“…enteropathy may perhaps be due to lack of a specific peptidase in the small-intestinal mucosa (Frazer, 1962). Despite increasing interest in the problem in the last few years, there are only a few reports in the literature of quantitative studies of dipeptidases of the small-intestinal mucosa in man under normal and pathological conditions (Messer, Anderson, and Townley, 1961;Lindberg, 1966a;Josefsson and Lindberg, 1967;Lindberg, Nord6n, andJosefsson, 1968;Heizer and Laster, 1969;Douglas and Peters, 1970).…”

Primary malabsorption following extreme attempts to lose weight.

“…The aetiological relationship of gluten, gliadin (the fraction of gluten soluble in alcohol), and peptides obtained by peptic-tryptic digestion of gluten and gliadin to the clinical and mucosal abnormalities has been demonstrated in several studies (Dicke, 1950;Dicke, Weijers, and Kamer, 1953;Anderson, Frazer, French, Gerrard, Sammons, and Smellie, 1952;Sheldon and Lawson, 1952;Kamer and Weijers, 1955;Schwartz, Sleisenger, Pert, Roberts, Randall, and Almy, 1957;Krainick, Debatin, Gautier, Tobler, and Velasco, 1958;Krainick and Mohn, 1959;Frazer, Fletcher, Ross, Shaw, Sammons, and Schneider, 1959; van Roon, Haex, Seeder, and Jong, 1960;Rubin, Brandborg, Flick, Phelps, Parmentier, and van Niel, 1962;Bayless, Yardley, Norton, and Hendrix, 1962;Pittman and Holub, 1965). Several authors have postulated that patients with coeliac disease have abnormal peptidase activity of the small intestinal mucosal epithelial cells which prevents the normal degradation of certain peptides derived from the intraluminal digestion of gluten or gliadin (see Frazer, 1962). These peptides are thought to enter the epithelial cells and begin the harmful chain of events which results in the flattened, infiltrated mucosa with its abnormal epithelial cell layer.…”

Coeliac Sprue: A Centennial Overview 1888-1988

“…Frazer [3] of Birmingham University, En gland [3], It was Frazer's contention that coeliac enterocytes are deficient in a pepti dase, thereby causing a build-up of damaging intermediate breakdown products of gluten in cells of the upper intestinal mucosa, the target site of damage in coeliac sprue.…”