The most widely used pharmacological therapies for obesity and weight management are based on inhibition of gastrointestinal lipases, resulting in a reduced energy yield of ingested foods by reducing dietary lipid absorption. Colipase-dependent pancreatic lipase is believed to be the major gastrointestinal enzyme involved in catalysis of lipid ester bonds. There is scant literature on the action of pancreatic lipase under the range of physiological conditions that occur within the human small intestine, and the literature that does exist is often contradictory. Due to the importance of pancreatic lipase activity to nutrition and weight management, the present review aims to assess the current body of knowledge with regards to the physiology behind the action of this unique gastrointestinal enzyme system. Existing data would suggest that pancreatic lipase activity is affected by intestinal pH, the presence of colipase and bile salts, but not by the physiological range of Ca ion concentration (as is commonly assumed). The control of secretion of pancreatic lipase and its associated factors appears to be driven by gastrointestinal luminal content, particularly the presence of acid or digested proteins and fats in the duodenal lumen. Secretion of colipase, bile acids and pancreatic lipase is driven by cholecystokinin and secretin release.

Mucus is a water-insoluble gel secreted by the gastrointestinal tract. It exists as a protective gel layer adherent to the epithelial surface of the stomach, small intestine and colon. The mucus gel is composed of 1–10% (w/v) mucin glycoprotein in a plasma-like fluid. Since the mucus gel is predominantly water, standard histological techniques dehydrate the mucus, making visualisation of the functional barrier difficult. Specialist techniques have been developed to enable visualisation of the intact mucus layer. A simple histological method using snap-frozen tissue, sectioned with a cryostat and stained with modified periodic acid-Schiff s/Alcian blue in mucus-preserving conditions will be described. A second powerful in vivo animal model is described which enables measurement of mucus secretion over time. The use of these two methods has allowed the characterisation of the normal mucus layer in the colon and the determination of how it is affected by disease and dietary intervention, in particular the effect of dietary fibre, and evidence that fibre deficiency results in colonic mucosal fragility is presented.

he primary structures of ispaghula husk and wheat bran were investigated in order to determine how and why these fibres are among the most beneficial dietary fibres. To this end, the polysaccharide preparations have been subjected to enzymic hydrolysis and methylation analysis. The results have shown ispaghula husk and wheat bran to be very-highly-branched arabinoxylans consisting of linear Β-D-→l(4)-linked xylopyranose →Xylp) backbones to which a-L-arabinofuranose →Araf) units are attached as side residues via α-→1(3) and a-→l(2) linkages. Other substituents identified as present in wheat bran include Β-D-glucuronic acid attached via the C→O)-2 position, and arabinose oligomers, consisting of two or more arabinofuranosyl residues linked via 1–2, 1–3, and 1–4 linkages. Ispaghula-husk arabinoxylan is more complex having additional side residues which include a-D-glucuronopyranose →GalAp)-→l→2(-linked-α-L-rhamnopyranose-(1→4)-β-D-Xylp, α-D-GalA/>-→l→3(-linked-a-L-Araf-→1)4(-p-D-Xylp, and <x-L-Araf-→1→3(-linked-p-D-Xylp-→1→4(-β-D-Xylp. The beneficial effects of increased faecal bulk and water-holding capacity are undoubtedly related to the structures of the arabinoxylans, with differences in their efficacy to treat various functional bowel disorders due to their specific structural features

The colon is subjected to a myriad of potentially damaging agents that may reside within the lumen for 1–2 d. Its first line of defence against these agents is the protective mucus bilayer that lines the entire colonic mucosa. This bilayer acts as a physical barrier to mucosal aggressors and also reduces shear stress to the mucosa. These actions are dependent on the unstimulated (‘resting’) colonic mucus thickness, and also on the rate that this layer can be replenished. The colonic mucus layer is altered in a number of colonic diseases that have been linked to a deficiency of fibre in the diet. The action of fibre intake on colonic mucus thickness and secretion is unknown. Using an in vivo rat model it has been demonstrated that: (1) fibre deficiency leads to a decreased protective potential of the mucus layer (e.g. the mean resting mucus thickness of the fibre-deficient group (429 μm) was significantly lower than its respective control (579 μm; P< 0.001), as was its total mucus secretion over 6 h (270 μm v. 541 μm; P<0.01); (2) specific fibre types in the diet alter the secretion dynamics of colonic mucus (e.g. a cellulose-based diet reduces total mucus secretion over 6 h compared with its control (175 μm v. 463 μm). Analysis of the diets suggested a necessity for both soluble and insoluble fibre types in the diet to increase mucosal protection.