No abstract

Uncoupling protein 1 (UCP1), a 32-kDa protein located in the inner mitochondrial membrane, is abundant in brown adipose tissue, as a proton transporter in mitochondria inner membrane which uncouples oxidative metabolism from ATP synthesis and dissipates energy through the heat. UCP1 has been reported to play important roles for energy homeostasis in rodents and neonate of larger mammals including human. Recently, numerous candidate genes were searched to determine the genetic factors implicated in the pathogenesis of obesity, related metabolic disorders and diabetes. UCP-1, which plays a major role in thermogenesis, was suggested to be one of the candidates. This review summarizes data supporting the existence of brown adipocytes and the role of UCP1 in energy dissipation in adult humans, and the genetic variety association with the fat metabolism, obesity and diabetes.

The antiobesity and antihyperlipidaemic effects of pu-erh tea in rats with high fat diet (HFD)-induced obesity were investigated. Male Sprague-Dawley rats were randomly divided into five groups and fed varying diets for an 8-week period: control diet, HFD, and HFD supplemented with low, moderate or high doses of pu-erh tea extract (0.5 g, 2 g and 4 g/kg BW/day, respectively). Pu-erh tea significantly reduced the total body weight and the weight of various adipose pads. Pu-erh tea administration also significantly lowered plasma total cholesterol, triglyceride concentrations and low-density lipoprotein-cholesterol levels in rats with HFD-induced obesity, but did not affect high-density lipoprotein-cholesterol levels. Moreover, pu-erh tea significantly increased lipoprotein lipase, hepatic lipase and hormone-sensitive lipase activities in epididymal fat tissue in rats with HFD-induced obesity. Analysis of real-time reverse transcription-polymerase chain reaction results indicated that pu-erh tea significantly enhanced mRNA levels of hormone-sensitive lipase in rats with HFD-induced obesity. These results suggest that pu-erh tea attenuated visceral fat accumulation and improved hyperlipidemia in a rat model of HFD-induced obesity.

This study aimed to investigate the probiotic potential of lactic acid bacteria (LAB) strains isolated from De'ang pickled tea, a traditional food consumed by the De'ang nationality of Yunnan, China. Twenty-six LAB strains isolated from De'ang pickled tea were subjected to identification based on 16S rRNA gene sequence analysis. Twenty-four belonged to Lactobacillus plantarum, one belonged to Enterococcus casseliflavus, and one belonged to Lactobacillus acidophilus. Eighteen out of 26 LAB strains which showed a higher capability to tolerate simulated gastrointestinal juices were chosen to further evaluate their probiotic properties. Varied adhesive abilities and auto-aggregative capacities of selected LAB strains were dependent on species and even strains. All tested LAB strains were resistant to kanamycin, streptomycin, gentamycin, and vancomycin and sensitive to tetracycline and chloramphenicol. Ten out of the 18 strains are resistant to ampicillin, and the remaining strains are sensitive to ampicillin; 4 out of the 18 strains showed resistance to erythromycin. Compared to reference strain Lactobacillus rhamnosus strain GG, these LAB strains had a greater or comparative antimicrobial activity against Salmonella typhimurium or Escherichia coli. In contrast, eight out of the 18 strains suppressed growth of Shigella flexneri. Two L. plantarum strains, ST and STDA10, not only exhibited good probiotic properties but also showed a good ability of scavenging DPPH and ABTS. This study suggests that L. plantarum ST and STDA10 could be used as potential probiotics applied in functional foods.

The present study investigated the neuroprotective effects of aucubin on hydrogen peroxide (H₂O₂)-induced apoptosis in PC12 cells. Exposure of PC12 cells to 0.25 mm H₂O₂ induced a leakage of lactate dehydrogenase and decreased cell viability, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. In a dose over 0.1 mm, aucubin increased PC12 cellular viability and markedly attenuated H₂O₂-induced apoptotic cell death. Quantitation of apoptosis by flow cytometry indicated that aucubin inhibited H₂O₂-induced apoptosis in PC12 cells. Nuclear damage was alleviated by aucubin, as shown by Hoechst staining. In addition, the levels of malondialdehyde were reduced and the activity of superoxide dismutase, catalase and glutathione peroxidase was augmented in these cells. These results indicated that aucubin inhibited H₂O₂-induced apoptosis in PC12 cells through regulation of the endogenous oxidant-antioxidant balance. Our results suggest that aucubin is a potential protective agent for the treatment of oxidative-stress-induced neurodegenerative disease.