Lindley, Keith James; (1994) The influence of vitamin E deficiency and of dietary polyunsaturated fats upon the structure and function of the rat proximal small intestine. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

A vicious cycle of malabsorption and malnutrition has been implicated in the pathogenesis of protracted diarrhoeal disease (PDD) in infancy. Impaired antioxidant defences are common in malnourished children, and it is hypothesised that increased fluxes of free radicals and compromised antioxidant defences might have an influence in perpetuating PDD. Vitamin E (α tocopherol) is an important lipid soluble antioxidant, and polyunsaturated fatty acids (PUFA) a major substrate for oxidative attack in biological membranes. High PUFA diets are sometimes used in the nutritional rehabilitation of infants with PDD. In order to study the effects of impaired antioxidant defences and of high PUFA diets a rat model was established. Four groups of rats were fed diets which were vitamin E sufficient or deficient and contained high or low PUFA, and jejunal structure and function studied after 24 weeks. Electrogenic secretion and absorption were measured in Ussing chambers and the maximal secretory responses (δIscmax) and the concentration of secretogogue producing a half maximal response (EC₅₀) determined. Malondialdehyde (MDA) and thiobarbituric reactive substances (TBARS) were measured in mucosal scrapings as indices of lipid peroxidation, and the fatty composition of the apical membrane by gas chromatography. A high PUFA diet resulted in a change in the fatty acid composition of the apical brush border membrane and was associated with a complex modulation of electrogenic secretion and absorption. Chronic vitamin E deficiency was associated with elevated indices of lipid peroxidation, net electroneutral jejunal secretion and a modified secretory response. The combination of vitamin E deficiency and a high PUFA diet resulted in an enteropathy, elevated indices of basal and secretogogue mediated secretion, and higher levels of lipid peroxidation. The combination of vitamin E deficiency and high PUFA intake appears deleterious. This may have implications for the nutritional rehabilitation of malnourished infants with PDD.

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