Effects of dietary gamma-cyclodextrin on voluntary activity and muscle strength in mice.

Gamma-cyclodextrin (γCD) is a cyclic oligosaccharide consisting of eight α-(1,4)-linked glucopyranose subunits, which is often used in the food and pharmaceutical industries. However, little is known regarding the metabolic activity of "empty" γCD per se. Therefore, in the present study young C57BL/6 male mice received a control diet (CON) or an experimental diet that was supplemented with 12.88% γCD exchanged against corn starch. After 6 weeks of treatment, the voluntary wheel running activity was monitored and the muscle strength of mice was measured by employing Kondziela's inverted screen test and forelimb grip strength assay. The γCD-treated mice covered a significantly larger distance per night (CON 8.6 km, γCD 12.4 km) and were significantly longer active (CON 340 min, γCD 437 min). Moreover, γCD-treated mice significantly performed better at the inverted screen test indicated by an enhanced Kondziela score (CON 3.10, γCD 4.63). These data suggest that dietary γCD leads to an increased endurance. We also found a slightly anti-glycemic effect of γCD during oral glucose tolerance test. However, our mice from the γCD group exhibited no difference in terms of GLUT2 protein level in ileum tissue nor increased muscle glycogen storage. Furthermore, γCD exhibited no DPP-4 inhibitory activity in vitro. By analysing candidate muscle genes and proteins related to endurance and muscle performance we did not observe any differences in terms of Sirt1, Pgc1α, Cpt1b, Mef2c, Myh1 and Myh2 gene expression levels as well as total oxidative phosphorylation (OXPHOS), mtTFA and GLUT4 protein expression levels in skeletal muscle in response to γCD. We could not fully establish the exact underlying molecular mechanisms of the fitness improvement by dietary γCD which warrants further investigations.

[An analysis of gp 70 expressed on Friend virus-infected rat tumor cells and the mouse melanoma antigen cross-reacting with it].

In order to analyse a virus-associated antigen which is expressed on Friend virus-infected rat tumor cells and induces strong resistance to their transplantability. I made monoclonal antibodies against it by using spleen cells of the syngeneic rats in whom the Friend virus-associated tumor cells spontaneously regressed. As a result, I was able to obtain a monoclonal antibody, named TF 1, to react specifically to the infection of Friend virus and found out that TF1 antibody reacted to gp 70, a product of the envelope gene of Friend virus, on Friend virus-infected rat tumor cells. And also I found out that B16BL6 cells, which are mouse melanoma cells and are not infected with Friend virus, were positive to TF1 antibody and made it clear that the melanoma antigen which reacted to TF 1 antibody was not gp 70, but a protein of 80-85 KD. Immunizing therefore with gp 70 cross-reacting with the melanoma antigen, I was able to observe that resistance to the transplantability of B16BL6 cells was induced. The result suggests that the melanoma antigen played a role as a tumor rejection antigen. I thus consider that gp 70 is able to induce resistance to transplantability of B16BL6 cells in mice and affects spontaneous regression of Friend virus-infected tumor cells as a virus-associated antigen in rats.