Visceral Fat-Reducing Effect and Safety of Continuous Consumption of Beverage Containing Resistant Maltodextrin: A Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Clinical Trial.

Obesity is regarded as a global concern with increasing prevalence, most notably in developed countries. Metabolic syndrome is a predictor of cardiovascular disease and type 2 diabetes mellitus and is defined as the accumulation of multiple risk factors caused by abdominal visceral obesity. Resistant maltodextrin (RMD) is a soluble dietary fiber that has been shown to reduce visceral fat in long-term clinical trials when continuously administered at 10 g, three times daily. Herein, we evaluated the effects of long-term consumption of 5 g RMD three times daily. A total of 140 healthy adults were randomly assigned to two intervention groups for a 12-wk randomized, double-blind, placebo-controlled, parallel-group trial. Participants ingested a test beverage containing 5 g RMD or a placebo beverage without RMD. Interviews, anthropometric measurements, physiological examination, blood tests, and urinalyses were conducted at baseline and every 4 wk during the trial. Computed tomography scans were performed at baseline and at the end of week 8 and 12. Results showed that abdominal visceral fat area (VFA) significantly decreased in the test group from 105.33±26.83 cm2 at baseline to 101.15±24.33 cm2 at week 12. Further, a significant difference was observed in the VFA between the test and control groups (p<0.05), confirming the function of continuous RMD consumption in reducing abdominal visceral fat. Furthermore, neither serious adverse events nor adverse clinical findings were observed in the blood or urine tests following consumption of RMD, suggesting that continuous consumption of RMD containing beverages is safe.

DJ-1-dependent protective activity of DJ-1-binding compound no. 23 against neuronal cell death in MPTP-treated mouse model of Parkinson's disease.

Parkinson's disease (PD) is caused by dopaminergic cell death in the substantia nigra, leading to a reduced level of dopamine in the striatum. Oxidative stress is one of the causes of PD. Since symptomatic PD therapies are used, identification of compounds or proteins that inhibit oxidative stress-induced neuronal cell death is necessary. DJ-1 is a causative gene product of familial PD and plays a role in anti-oxidative stress reaction. We have identified various DJ-1-binding compounds, including compound-23, that restored neuronal cell death and locomotion defects observed in neurotoxin-induced PD models. In this study, wild-type and DJ-1-knockout mice were injected intraperitoneally with 1 mg/kg of compound-23 and then with 30 mg/kg of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at 1 h after injection. Five days after administration, the effects of compound-23 on MPTP-induced locomotion deficits, on dopaminergic cell death and on brain dopamine levels were analyzed by rotor rod tests, by staining cells with an anti-TH antibody and by an HPLC, respectively. The results showed that compound-23 inhibited MPTP-induced reduction of retention time on the rotor rod bar, neuronal cell death in the substantia nigra and striatum and dopamine content in wild-type mice but not in DJ-1-knockout mice, indicating a DJ-1-dependent effect of compound-23.