The dipeptidyl peptidase-4 inhibitor vildagliptin has the capacity to repair ß-cell dysfunction and insulin resistance.

The aim of the present study was to determine whether the dipeptidyl peptidase (DPP)-4 inhibitor could repair pancreatic ß-cell dysfunction and insulin resistance. Ten subjects with type 2 diabetes who had never received DPP-4 inhibitor treatment were enrolled in the study. Just before and 3 months after twice-daily administration of vildagliptin (50 mg tablets), insulin secretion and insulin sensitivity were estimated using 2-compartment model analysis of C-peptide kinetics and insulin-modified minimal model parameters, respectively. The first-phase insulin secretion (CS1) was determined as the sum of the C-peptide secretion rate (CSR) from 0 to 5 min (normal range 6.8-18.5 ng/ml/min). The whole-body insulin sensitivity index (SI) was calculated using a minimal model software program (normal range 2.6-7.6×10(-4)/min/µU/ml). After vildagliptin treatment, reductions in mean (± SE) HbA1c were noted (43.28±1.53 vs. 40.98±1.77 mmol/mol; p=0.019). Vildagliptin treatment increased the area under the curve for the C peptide reactivity (CPR) (AUCCPR; 26.66±5.15 vs. 33.02±6.12 ng/ml · 20 min; p=0.003) and CS1 (0.80±0.20 vs. 1.35±0.38 ng/ml/min; p=0.037) in response to an intravenous glucose load. -Vildagliptin treatment significantly increased SI (0.46±0.27 vs. 1.21±0.48×10(-4)/min/µU/ml; p=0.037). The long-term administration of vildagliptin improved CS1 and Si suggesting that this drug has the capacity to repair impairments in pancreatic ß-cell function and insulin resistance in type 2 diabetes.

The outcome of Japanese anorexia nervosa patients treated with an inpatient therapy in an internal medicine unit.

OBJECTIVE: To investigate the outcome of Japanese anorexia nervosa (AN) patients who were treated with the standard Japanese inpatient therapy. METHOD: Of the 88 female AN patients treated with our inpatient therapy between January 1997 and December 2002, 67 (76.1%) who agreed to cooperate in this study were assessed by the Global Clinical Score (GCS) at admission and follow-up, 6.3±1.8 years after discharge. Their clinical characteristics at admission and discharge were also examined. RESULTS: Four (6.0%) patients had died before follow-up. BMI was significantly increased during inpatient therapy. At follow-up, excellent, much improved, symptomatic, and poor outcomes on GCS were 57.1%, 14.3%, 14.3% and 14.3%, respectively. Younger age at admission and larger BMI at discharge were significantly associated with a better outcome. DISCUSSION: This study shows the potential for the use of this method for the treatment of AN patients in countries without specialized eating disorder units.

Specific immune response to the 40-kDa outer-membrane protein of Porphyromonas gingivalis in mice.

Whether B-cell activation to Porphyromonas gingivalis in periodontal diseases is the consequence of a specific immune response or is due to non-specific polyclonal activation is still not clear. Here the immune response of mice to a purified 40-kDa recombinant protein antigen, a major outer-membrane protein specific to P. gingivalis, was investigated. Patients' sera strongly reacted to this recombinant antigen. Purified splenic T and B cells from mice immunized with 40-kDa antigen or from normal mice were reconstituted in vitro and cultured in the presence or absence of the P. gingivalis 40-kDa protein antigen and antigen-presenting cells (APCs). In vitro antibody production to this particular antigen was analysed with respect to the requirement of helper T cells and APCs by enzyme-linked immunosorbent assay. The results clearly showed that an effective secondary response required the presence of B cells, T cells and APCs. In the absence of CD4+ helper T cells, an antibody response to the 40-kDa protein was not observed. In addition, the requirement of H-2 restricted, Ia-positive APCs was evident for an adequate response to the 40-kDa protein of P. gingivalis. Thus the antibody response to the 40-kDa protein of P. gingivalis was generated in an immunologically antigen-specific manner and was not simply the result of polyclonal B-cell activation. This in vitro system could be used in the detection of antigen-specific memory B or T cells in patients with periodontal diseases.