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Protamine from salmon spermaries is a novel dietary protein. Chitooligosaccharide (COS) is an oligosaccharide derived from chitin or chitosan, a long-chain polymer, by chemical or enzymatic hydrolysis. These two compounds are known to enhance lipid metabolism by interrupting the digestion and absorption of fat in the body. Cardiovascular disease (CVD) refers to any type of specific disease that affects the heart and circulatory system. Dyslipidemia, a condition involving high levels of low-density lipoprotein (LDL) cholesterol and low levels of high-density lipoprotein (HDL) cholesterol, is generally known to be a primary cause of CVD development. The risk of CVD is usually associated with the atherogenic index (AI) and cardiac risk factor (CRF). The CVD risk is also closely associated with serum levels of total cholesterol (T-CHO), LDL cholesterol and HDL cholesterol. In the present study, we evaluated alterations in serum lipid contents following the administration of protamine, COS and mixtures of these two compounds to male Sprague-Dawley (SD) rats, and their ability to reduce CVD risk. Based on the results of a serum lipid assay, protamine, COS and their mixtures were found to significantly reduce AI, CRF and CVD risk by decreasing serum levels of TG, T-CHO and LDL cholesterol and increasing serum HDL cholesterol levels. By contrast, TG and T-CHO concentrations in feces were markedly increased. Accumulation of lipids in the liver tissues of the SD rats fed high-fat diets was also inhibited by the intake of protamine and COS. Our findings suggest that protamine, COS and combinations of the two compounds may be used as a dietary therapy for preventing CVD due to their suppressive effects on hyperlipidemia and hypercholesterolemia.

A combination of green tea extract and l-theanine (LGNC-07) has been reported to have beneficial effects on cognition in animal studies. In this randomized, double-blind, placebo-controlled study, the effect of LGNC-07 on memory and attention in subjects with mild cognitive impairment (MCI) was investigated. Ninety-one MCI subjects whose Mini Mental State Examination-K (MMSE-K) scores were between 21 and 26 and who were in either stage 2 or 3 on the Global Deterioration Scale were enrolled in this study. The treatment group (13 men, 32 women; 57.58 ± 9.45 years) took 1,680 mg of LGNC-07, and the placebo group (12 men, 34 women; 56.28 ± 9.92 years) received an equivalent amount of maltodextrin and lactose for 16 weeks. Neuropsychological tests (Rey-Kim memory test and Stroop color-word test) and electroencephalography were conducted to evaluate the effect of LGNC-07 on memory and attention. Further analyses were stratified by baseline severity to evaluate treatment response on the degree of impairment (MMSE-K 21-23 and 24-26). LGNC-07 led to improvements in memory by marginally increasing delayed recognition in the Rey-Kim memory test (P = .0572). Stratified analyses showed that LGNC-07 improved memory and selective attention by significantly increasing the Rey-Kim memory quotient and word reading in the subjects with MMSE-K scores of 21-23 (LGNC-07, n = 11; placebo, n = 9). Electroencephalograms were recorded in 24 randomly selected subjects hourly for 3 hours in eye-open, eye-closed, and reading states after a single dose of LGNC-07 (LGNC-07, n = 12; placebo, n = 12). Brain theta waves, an indicator of cognitive alertness, were increased significantly in the temporal, frontal, parietal, and occipital areas after 3 hours in the eye-open and reading states. Therefore, this study suggests that LGNC-07 has potential as an intervention for cognitive improvement.

To develop a therapeutic agent for obesity-related metabolic disorders, a mixture of dietary components was prepared, including grape extract, green tea extract and l-carnitine (RGTC), and its effects on obesity, hyperlipidemia and non-alcoholic fatty liver disease examined. The RGTC dramatically inhibited the high-fat diet (HFD)-induced increase in body weight and fat in C57BL/6 mice, whereas food consumption was not affected by RGTC treatment. The RGTC also concentration-dependently suppressed the HFD-induced increase in plasma lipids, such as low-density lipoprotein cholesterol and triglycerides. In addition, increases in liver weight and liver steatosis were returned to normal by RGTC treatment in HFD-fed C57BL/6 mice. The plasma levels of glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase were also significantly down-regulated by RGTC treatment. These results suggest that RGTC suppressed HFD-induced obesity, hyperlipidemia and non-alcoholic fatty liver disease, suggesting that RGTC supplementation might be a promising adjuvant therapy for the treatment of these metabolic disorders.

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.

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.