Search

We previously demonstrated improvements of colonic lesions due to dextran sulfate sodium (DSS) in rats after 7 d of supplementation with resistant starch (RS) type 3, a substrate yielding high levels of butyrate ([C.sub.4]), a colonic cell fuel source. In the present study, we hypothesized that if inflammation is related to decreased [C.sub.4] utilization by the colonic mucosa, RS supplementation should restore [C.sub.4] use simultaneously with an increase in the amount of [C.sub.4] present in the digestive tract. Hence, we compared, in vivo, the cecocolonic uptake of [C.sub.4] and its oxidation into C[O.sub.2] and ketone bodies in control and DSS-treated rats fed a fiber-free basal diet (BD) or a RS-supplemented diet. Sprague-Dawley rats (n = 60) were used. DSS treatment was performed to induce acute colitis and then to maintain chronic colitis. After cecal infusion of [[1-.sup.13]C]-C4 (20 [micro]mol in 1 h), concentrations and [sup.13]C-enrichment of [C.sub.4], ketone bodies, and C[O.sub.2] were quantified in the abdominal aorta and portal vein. Portal blood flow was recorded. During acute colitis, [sup.13][C.sub.4] uptake and [sup.13][CO.sub.2] production were lower in DSS rats than in controls. During chronic colitis, DSS rats did not differ from controls. After 7 d of chronic colitis, RS-DSS rats exhibited the same [C.sub.4] uptake as BD-DSS rats in spite of higher [C.sub.4] cecocolonic disposal. After 14 d, [C.sub.4] uptake was higher in RS-DSS than in BD-DSS rats. Thus, the increased utilization of C4 by the mucosa is subsequent to evidence of healing and appears to be a consequence rather than a cause of this RS healing effect. KEY WORDS: * butyrate * metabolism * colitis * rat * resistant starch

The increased prevalence of obesity after neutering in cats is problematic in veterinary practice. Although many factors seem to be involved, the role of prolactin (PRL) and insulin-like growth factor-I (IGF-I), both implicated in adipose tissue development and glucose intolerance, should be considered. Seven male cats were castrated when 11 months old. Body weight was then recorded for 56 weeks and PRL, IGF-I and leptin assayed for 44 weeks. Body weight increased steadily but only significantly after 36 weeks. It stabilised after 44 weeks, and the cats then gained about 20% of their initial body weight. IGF-I increased rapidly and was significantly higher by week 3. PRL and leptin increased with initial peaks during the eighth and eleventh weeks, respectively. This study confirms that castration rapidly modifies the hormonal balance, partly explaining the body weight increase, and that hormonal changes precede this body weight increase. Hyperleptinaemia is apparently a consequence of excess weight.