We have developed two rodent models of diet-induced magnesium-deficiency in which histologically defined cardiac lesions can be induced within two to three weeks. During the development of these lesions, the magnesium-deficient animals exhibit circulating cytokine levels which are indicative of a generalized inflammatory state. Dramatic elevations of the macrophage-derived cytokines, IL-1, IL-6, and TNF-alpha together with significantly elevated levels of the endothelial cell-derived cytokine, endothelin, were detected in the plasma of these animals. We believe that the pathophysiological effects caused by the action of these cytokines may play a role in the promotion of cardiovascular pathology associated with magnesium deficiency.

Alterations in gastrointestinal mucin induced by dietary fiber may affect nutrient bioavailability, cytoprotection of the mucosa or other aspects of gastrointestinal function. To allow quantitative study of gastrointestinal mucin, a polyclonal antibody to the mucin of the rat small intestine was produced by injecting rabbits with a high-molecular-weight subfraction (MW 2 x 10(6)) of purified mucin glycoprotein derived from rat intestinal mucin. An enzyme-linked immunosorbent assay was developed and used for the mucin assay. Three groups of male Wistar rats consumed 5% guar gum, 5% citrus fiber or a fiber-free control diet ad libitum for 4 wk. After an overnight fast, luminal and tissue mucin antibody reactivities were determined in the rat stomach, colon and small intestine. In all groups, total (luminal and tissue) mucin reactivity was greater in the small intestine than in the colon or stomach. The group fed 5% citrus fiber had significantly greater mucin reactivity in luminal samples from stomach and intestine than did the fiber-free control group. Fiber-induced increments in gastrointestinal mucin production or availability may be responsible for several reported consequences of fiber feeding, such as more rapid transit times and delayed or impaired nutrient absorption.

Mixed micelles were prepared containing combinations of either taurocholate or taurochenodeoxycholate, monoolein, oleic acid, dioleylphosphatidylcholine (lecithin) and cholesterol. These were incubated with commercial bile-acid-sequestering resins, cholestyramine and DEAE-Sephadex, or various dietary fibers and fiber components including wheat bran, cellulose, alfalfa, lignin and 2 viscosity grades of guar gum. Binding was determined as the difference between the radioactivity of each micellar component added and that recovered in the centrifugal supernatant after incubation. In general, the extent of bile salt sequestration was characteristic and reproducible for each bile salt, and was largely unaffected by the presence of one or more additional components of the micellar mixture, including the other bile salt. Cholestyramine bound 81-92% of the bile salts and 86-99% of the phospholipid and cholesterol present in micelles. DEAE-Sephadex sequestered only 49% of the taurocholate and 84% of the taurochenodeoxycholate, but completely removed all of the phospholipid and cholesterol from micelles containing either bile salt. Among the dietary fibers, guar gum of either viscosity bound between 20-38% of each micellar component, whereas lignin, alfalfa, wheat bran and cellulose were progressively less effective in sequestration of individual components of mixed micelles. The extent of sequestration of micellar components by these resins and fibers is reasonably correlated with the effects of these same materials on lymphatic absorption of lipids and to their suggested hypocholesteremic properties.