Modulation of lipid metabolism by mixtures of protamine and chitooligosaccharide through pancreatic lipase inhibitory activity in a rat model.

Overweight and obesity are usually related with high fat and calorie intake, and seriously causative of lifestyle-related diseases such as cardiovascular disorders, arteriosclerosis, and colon cancer. In this study, we propose a novel dietary therapy against overweight and obesity using mixtures of protamine and chitooligosaccharide (COS), which are known to interrupt the lipid metabolism in the body. Protamine is a dietary protein originated from salmon reproductive organ, and COS is an oligosaccharide made from chitin or chitosan by chemical or enzymatic hydrolysis. In the enzyme activity analysis in vitro, protamine and COS strongly suppressed the activity of pancreatic lipase, which is the primary enzyme for the digestion and absorption of lipids in the intestine. In in vivo animal test, the mixtures of protamine and COS significantly reduced the serum levels of triglyceride (TG), total cholesterol (T-CHO), and low density lipoprotein-cholesterol (LDLC) and inhibited the accumulation of lipids in liver tissue of Sprague Dawley (SD) rats fed high fat diets. On the other hand, they increased fecal TG and T-CHO contents. From these alterations in lipid metabolism, we verified that protamine and COS mixtures could effectively interrupt the digestion and absorption of dietary lipids in the body by inhibiting pancreatic lipase activity. In addition, protamine and COS mixtures increased the serum level of high density lipoprotein-cholesterol (HDLC), responsible for removing cholesterol from cells and protecting atherosclerosis, and therefore decreased the potential risks of cardiovascular diseases by lowering values of the atherogenic index (AI) and cardiac risk factor (CRF). Taken together, we suggest protamine and COS mixtures as a prominent dietary therapy for the prevention of overweight, obesity, and further cardiovascular diseases related with hyperlipidemia.

l-Theanine, an amino acid in green tea, attenuates beta-amyloid-induced cognitive dysfunction and neurotoxicity: reduction in oxidative damage and inactivation of ERK/p38 kinase and NF-kappaB pathways.

Amyloid beta (Abeta)-induced neurotoxicity is a major pathological mechanism of Alzheimer disease (AD). In this study, we investigated the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Abeta(1-42)-induced neuronal cell death and memory impairment. Oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Abeta(1-42) (2 microg/mouse, icv), significantly attenuated Abeta(1-42)-induced memory impairment. Furthermore, l-theanine reduced Abeta(1-42) levels and the accompanying Abeta(1-42)-induced neuronal cell death in the cortex and hippocampus of the brain. Moreover, l-theanine inhibited Abeta(1-42)-induced extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase as well as the activity of nuclear factor kappaB (NF-kappaB). l-Theanine also significantly reduced oxidative protein and lipid damage and the elevation of glutathione levels in the brain. These data suggest that the positive effects of l-theanine on memory may be mediated by suppression of ERK/p38 and NF-kappaB as well as the reduction of macromolecular oxidative damage. Thus, l-theanine may be useful in the prevention and treatment of AD.

Effects of a preparation of combined glutathione-enriched yeast and rice embryo/soybean extracts on ethanol hangover.

The effects of a preparation of combined glutathione-enriched yeast (GEY) and rice embryo/soybean (RES) extracts (20:1), GEY/RES, on experimentally induced ethanol hangover were investigated in male Sprague-Dawley rats. To evaluate the preventive effects on hangover, rats were orally administered GEY/RES (50/2.5, 100/5, or 200/10 mg/kg) for 2 weeks. At 30 minutes after the final treatment, they were challenged with 3 mL/kg ethanol (15 mL of 20% in water/kg). The blood concentrations of alcohol and acetaldehyde were analyzed up to 7 hours postchallenge. Hepatic mRNA expression levels of alcohol-metabolizing enzymes, alcohol dehydrogenase (ADH), cytochrome P450 type 2E1 (CYP2E1), and aldehyde dehydrogenase (ALDH), were determined by real-time polymerase chain reaction. Additional rats were challenged with ethanol and, 60 minutes later, administered GEY/RES to evaluate alcohol clearance. Pretreatment with GEY/RES for 2 weeks reduced the blood concentrations of alcohol and acetaldehyde in a dose-dependent manner, lowering by 29.5% and 54.6% at the highest dose (200/10 mg/kg), respectively. The expressions of mRNAs for ADH and ALDH, the major alcohol-metabolizing enzymes, were markedly increased in the livers of rats administered GEY/RES for 2 weeks, whereas CYP2E1 mRNA was suppressed. Postchallenge treatment with GEY/RES enhanced the alcohol clearance rate by lowering blood concentrations of alcohol and acetaldehyde by 24% and 26.6%, respectively, for the highest dose group. GEY/RES remarkably eliminated 2,2-diphenyl-1-picrylhydrazyl hydrate radical and FeCl(3)-mediated lipid peroxidation in vitro and attenuated hepatic lipid accumulation following ethanol administration in vivo. Therefore, it is suggested that GEY/RES reduces the blood concentrations of alcohol and acetaldehyde not only by modulating alcohol-metabolizing enzymes, but also by exerting its antioxidant activity, and that GEY/RES could be a promising candidate for improvements of alcoholic hangover.