These results suggest that LMP promotes healing of colonic anastomosis more effectively than HMP, which may be explained by the mechanical stresses generated by the movement of normally formed stool though the colon.

Inactivity leads to skeletal muscle atrophy, whereas intermittent loading (IL) during hind limb unloading (HU) attenuates muscle atrophy. However, the combined effects of IL and protein supplementation on disuse muscle atrophy are unclear. Therefore, we investigated the effects of IL and a high-protein oral nutritional supplement (HP) during HU on skeletal muscle mass and protein synthesis/breakdown. Male F344 rats were assigned to the control (CON), 14-day HU (HU), IL during HU (HU + IL), and IL during HU followed by HP administration (2.6 g protein/kg/day; HU + IL + HP) groups. Soleus and gastrocnemius muscles were sampled 30 min after the last IL and HP supplementation. HU decreased relative soleus and gastrocnemius muscle masses. Relative muscle masses and p70 ribosomal protein S6 kinase/ribosomal protein S6 phosphorylation in soleus and gastrocnemius muscles were higher in the HU + IL group than the HU group and further higher in the HU + IL + HP group than the HU + IL group in gastrocnemius muscle. Therefore, protein administration plus IL effectively prevented skeletal muscle atrophy induced by disuse, potentially via enhanced activation of targets downstream of mammalian target of rapamycin complex 1 (mTORC1) signaling pathway.

Vascular endothelial function deteriorates with age and disease, and the production of vasodilator factors like nitric oxide (NO) decreases. The free amino acid l -citrulline increases vasodilation and blood flow through increased NO production. We examined the effects of oral l -citrulline administration on vascular delivery of substances to skeletal muscles. In Experiment 1, following oral l -citrulline administration and subsequent intravenous Evans blue dye (EBD) administration to rats, EBD levels delivered to skeletal muscles were measured after 60 min. In Experiment 2, plasma concentrations of amino acids and NOx, an indicator of vasodilation, were measured over time after oral l -citrulline administration. In Experiment 3, we measured EBD levels in skeletal muscles of streptozotocin-induced type 1 diabetic rats following l -citrulline administration. In these experiments, EBD levels in the soleus muscle were higher in the l -citrulline group than in the control group (19.9 ± 0.7 vs. 22.5 ± 1.9 μg/g tissue, p < 0.05). Plasma l -arginine, l -citrulline, and NOx levels were increased within 30 min after l -citrulline administration. EBD levels in the soleus and gastrocnemius muscles were higher in diabetic rats with l -citrulline administration (18.7 ± 2.2 vs. 25.0 ± 4.3 μg/g tissue, p < 0.05 and 8.0 ± 0.5 vs. 9.2 ± 0.8 μg/g tissue, p = 0.05, respectively). These data suggest that oral l -citrulline administration may increase the level of substances delivered to skeletal muscles by increasing the NO production in both normal and vascular endothelial dysfunction models.

This study has the following aims: (1) to confirm a methodology for a fecal indocyanine green (ICG) imaging test for measuring gastro‐intestinal transit time (GITT); and (2) to compare GITT in mice given a liquid diet in which viscosity increases under acidic conditions to that in mice given stable liquid diets with comparable viscosity or regular chow. To address Aim 1, mice received ICG orally along with intraperitoneal injection of atropine in Study 1, and mice were given ICG orally with concurrent carmine red for Study 2. Fluorescence imaging of feces collected for 8 h thereafter was used to detect the first feces with fluorescence and thereby determine GITT. To address Aim 2, mice were fed ad libitum for 1 week with either liquid diet or regular chow for Study 3, or with liquid diet containing low‐methoxyl (LM) pectin or high‐methoxyl (HM) pectin, or regular chow for Study 4. GITT was then determined by fecal ICG imaging. Atropine delayed GITT in a dose‐dependent manner. The GITT of ICG completely corresponded to that of carmine red (correlation coefficient, 1.00). The first ICG excretion in the loose/some diarrheal feces of mice given a liquid diet was seen at 170 min. Feces of mice given liquid diet were loose with LM pectin and loose/some diarrhea with HM pectin. GITT of mice given liquid diet with HM pectin was significantly delayed (280 min) compared to that of mice given liquid diet with LM pectin (111 min) or regular chow (130 min). Fecal imaging of ICG enables measurements of GITT. LM pectin supplementation in a liquid diet may normalize GITT in mice to that of a normal meal and may be associated with changes in fecal properties.

Both intravenous saline administration and oral hydration with ORS decreased the severity of CIN. Hydration with ORS was comparable to intravenous saline infusion in preventing CIN-associated abnormalities.