Progress in intestinal adaptation after enterectomy / 中华胃肠外科杂志

Intestinal adaptation is a spontaneous compensation of the remanent bowel after extensive enterectomy, which improves the absorption capacity of the remanent bowel to energy, fluid and other nutrients. Intestinal adaptation mainly occurs within 2 years after enterectomy, including morphological changes, hyperfunction and hyperphagia. Intestinal adaptation is the key factor for patients with short bowel syndrome to weaning off parenteral nutrition dependence and mainly influenced by length of remanent bowel, type of surgery and colon continuity. In addition, multiple factors including enteral feeding, glucagon-like peptide 2 (GLP-2), growth hormone, gut microbiota and its metabolites regulate intestinal adaptation via multi-biological pathways, such as proliferation and differentiation of stem cell, apoptosis, angiogenesis, nutrients transport related protein expression, gut endocrine etc. Phase III clinical trials have verified the safety and efficacy of teduglutide (long-acting GLP-2) and somatropin (recombinant human growth hormone) in improving intestinal adaptation, and both have been approved for clinical use. We aim to review the current knowledge about characteristics, mechanism, evaluation methods, key factors, clinical strategies of intestinal adaptation.

roles of cytochrome P450 and P-glycoprotein in the pharmacokinetics of florfenicol in chickens

The effects of three selective oral inhibitors, fluvoxamine [FLU], ketoconazole [KET], and verapamil [VER], on the pharmacokinetics [PK] of florfenicol [FFC] were investigated in chickens. The chickens were administered orally with saline solution [SAL], FLU [60 mg/kg], KET [25 mg/kg], or VER [9 mg/kg] for 7 consecutive days. Florfenicol was given to the chickens at a single dose of 30 mg/kg orally. Blood samples were collected from each chicken at 0 to 12 h post-administration of FFC. The plasma concentration of FFC was analyzed by high-performance liquid chromatography [HPLC]. The AUC of FFC increased and the Cl[s] of FFC decreased with oral co-administration of KET in chickens, and the C[max] of FFC increased with VER. While the AUC, the Cl[s] and the C[max] of FFC were all invariable with FLU. These data suggested that CYP 3A played a key role in the PK of FFC in chickens, however, P-glycoprotein [P-gp] and CYP 1A did not. The results imply that the adverse drug-drug interaction may occur in the use of FFC if the co-administrated drugs are the substrates, inducers or inhibitors of CYP 3A or/and P-gp