Effects of high-pressure processing on the physicochemical properties and glycemic index of fruit puree in a hyperglycemia mouse model.

BACKGROUND: In this study, the duration of high-pressure processing (HPP) required to achieve a 5 log reduction of Escherichia coli O157:H7 in fruit purees was evaluated. Banana, cantaloupe, and dragon fruit purees were subjected to HPP at 600 MPa for 300, 270, and 270 s, respectively, and their physicochemical properties and enzyme activities were then analysed. Diabetic mice were fed fresh and HPP-treated purees to observe their effects on the glycemic index (GI) and postprandial blood glucose response. RESULTS: Compared with their fresh counterparts, the HPP-treated banana and dragon fruit purees exhibited significantly higher viscosities, lower glucose concentrations, and higher glucose dialysis retardation indices and showed disrupted sucrose invertase and polygalacturonase activities. The GI and postprandial blood glucose response were not significantly different between the fresh and HPP-treated cantaloupe purees. By contrast, the peak time of glucose response (Tmax ) was delayed from 30 min to 60 min, and the area under the receiver operating characteristic curve was reduced by 40% in the mice fed HPP-treated banana and dragon fruit purees. The GIs of the HPP-treated banana and dragon fruit purees (were 50.3 and 44.8, respectively) were significantly lower than those of their fresh counterparts (85.1 and 75.2, respectively). CONCLUSION: HPP can change the physicochemical properties of fruit purees, resulting in stabilized blood glucose levels and lower GIs after consumption. Therefore, purees processed in this manner would benefit consumers and patients with diabetes/pre-diabetes who need to maintain stable blood glucose levels (Fig. S1). © 2022 Society of Chemical Industry.

Effect of Astaxanthin on the Inhibition of Lipid Accumulation in 3T3-L1 Adipocytes via Modulation of Lipogenesis and Fatty Acid Transport Pathways.

Obesity is defined as a condition of excessive fat tissue accumulation. It was the major factor most closely associated with lifestyle-related diseases. In the present study, we investigated the effect of astaxanthin on the inhibition of lipid accumulation in 3T3-L1 adipocytes. 3T3-L1 adipocytes were treated with 0-25 µg/mL of astaxanthin for 0-48 h. The result indicated that astaxanthin significantly decreased the oil Red O stained material (OROSM), intracellular triglyceride accumulation, and glycerol 3-phosphate dehydrogenase (GPDH) activity in 3T3-L1 adipocytes (p < 0.05). At the molecular level, astaxanthin significantly down-regulated the mRNA expression of peroxisome proliferator-activated receptor-γ (PPARγ) in 3T3-L1 adipocytes (p < 0.05). Moreover, target genes of PPARγ on the inhibition of lipogenesis, such as Acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), fatty acid binding protein (aP2), cluster of differentiation 36 (CD36), and lipoprotein lipase (LPL) in 3T3-L1 adipocytes were significantly down-regulated at a time-dependent manner (p < 0.05). These results suggested that astaxanthin efficiently suppressed lipid accumulation in 3T3-L1 adipocytes and its action is associated with the down-regulation of lipogenesis-related genes and the triglyceride accumulation in 3T3-L1 adipocytes. Therefore, astaxanthin can be developed as a potential nutraceutical ingredient for the prevention of obesity in a niche market.

Antiobesity and Uric Acid-Lowering Effect of Lactobacillus plantarum GKM3 in High-Fat-Diet-Induced Obese Rats.

Objective: Obesity has become one of the world's biggest issues. This condition has a great impact on several metabolic and chronic diseases. For example, obesity is often accompanied by hyperuricemia or gout. However, few drugs are available for the treatment of obesity. The present study is to evaluate the antiobesity effect of Lactobacillus plantarum GKM3 in high-fat-diet-induced obese rats and whether taking L plantarum GKM3 can effectively reduce uric acid accumulation caused by obesity and ameliorate other harmful factors. Method: Sixty male Wistar rats were divided into five groups as follows: ( 1 ) ND group, fed normal diet; ( 2 ) HFC group, fed AIN93G-based high-fat diet containing 65% solids, 7% soybean oil, and 25% lard; ( 3 ) HFL group, fed AIN93G-based high-fat diet supplemented with 102.7 mg/kg/d L plantarum GKM3; ( 4 ) HFM group, fed AIN93G-based high-fat diet supplemented with 205.4 mg/kg/d L plantarum GKM3; and ( 5 ) HFH group, fed AIN93G-based high-fat diet supplemented with 513.5 mg/kg/d L plantarum GKM3. After 6 weeks, the body, organ, and fat weights; food intake; blood serum levels; and adipocyte size were measured. Results: Results showed that rats fed on the high-fat diet showed more body weight, increased feed efficiency, higher fat deposition, higher total liver weight, elevated serum lipid levels, and increased adipocyte size compared with those on the normal diet. All these effects were reversed by supplementation of L plantarum GKM3. Conclusions: In conclusion, we suggest that the L plantarum GKM3 supplement may have beneficial antiobesity and uric acid-lowering effects.

Deep Sea Water Improves Abnormalities in Lipid Metabolism through Lipolysis and Fatty Acid Oxidation in High-Fat Diet-Induced Obese Rats.

Deep sea water (DSW) is a natural marine resource that has been utilized for food, agriculture, cosmetics, and medicine. The aim of this study was to investigate whether DSW has beneficial lipid metabolic effects in an animal model. Our previous in vitro study indicated that DSW significantly decreased the intracellular triglyceride and glycerol-3-phosphate dehydrogenase activity in 3T3-L1 adipocytes. DSW also inhibited the gene levels of adipocyte differentiation, lipogenesis, and adipocytokines, and up-regulated gene levels of lipolysis and fatty acid oxidation. In the present study, the results showed that body weight, liver, adipose tissue, hepatic triglycerides and cholesterol, and serum parameters in the high-fat diet (HFD) + DSW groups were significantly lower compared to the HFD group. Moreover, the fecal output of total lipids, triglycerides, and cholesterol in the HFD + DSW groups was significantly higher than that of the HFD group. Regarding gene expression, DSW significantly increased the gene levels of lipolysis and fatty acid oxidation, and decreased the gene levels of adipocytokine in the adipose tissue of rats with HFD-induced obesity. These results indicate a potential molecular mechanism by which DSW can suppress obesity in rats with HFD-induced obesity through lipolysis and fatty acid oxidation.

Chicken surimi fortified by omega-3 fatty acid addition: manufacturing and quality properties.

BACKGROUND: The meat of spent hens is hard to use owing to its small amount and poor quality. A washing process to remove sarcoplasmic proteins and other impurities can prolong the shelf life of surimi-like products. Owing to the benefits of omega-3 polyunsaturated fatty acids (ω-3 PUFAs), functional foods fortified with ω-3 PUFAs are increasingly being marketed. Hence, in this study, ω-3 FA-fortified chicken surimi was manufactured, and how to ameliorate its lipid peroxidation during frozen storage was investigated. RESULTS: A 0.10% (w/v) solution of sodium chloride (NaCl) instead of distilled water in the third washing step decreased (P < 0.05) myofibrillar protein loss and moisture content of spent hen breast protein recoveries. Oil droplets in fish, flaxseed or soybean oil-added chicken surimi were well distributed. Moreover, flaxseed oil addition increased (P < 0.05) total ω-3 FAs and ω-3/ω-6 FA ratio, while only fish oil provided long-chain PUFAs. Oil addition decreased (P < 0.05) hardness and gumminess of chicken surimi, while flaxseed oil resulted in more (P < 0.05) yellow surimi than fish and soybean oil. Fish oil-added samples showed higher (P < 0.05) lipid oxidation than flaxseed or soybean oil-added samples under -15 to -10 °C storage, but α-tocopherol addition ameliorated it. CONCLUSION: A novel semi-manufactured chicken surimi product with nutritional benefits could be developed by fortification with fish or flaxseed oil.

Lemon Peel Water Extract: A Novel Material for Retinal Health, Protecting Retinal Pigment Epithelial Cells against Dynamin-Related Protein 1-Mediated Mitochondrial Fission by Blocking ROS-Stimulated Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Pathway.

Previous studies showed that NaIO3 can induce oxidative stress-mediated retinal pigment epithelium (RPE) damage to simulate age-related macular degeneration (AMD). Lemon peel is rich in antioxidants and components that can penetrate the blood-retinal barrier, but their role in retinal oxidative damage remains unexplored. Here, we explore the protection of lemon peel ultrasonic-assisted water extract (LUWE), containing large amounts of flavonoids and polyphenols, against NaIO3-induced retinal degeneration. We initially demonstrated that LUWE, orally administered, prevented retinal distortion and thinning on the inner and outer nuclei layers, downregulating cleaved caspase-3 protein expression in RPE cells in NaIO3-induced mice. The effect of LUWE was achieved through the suppression of apoptosis and the associated proteins, such as cleaved PARP and cleaved caspase-3, as suggested by NaIO3-induced ARPE-19 cell models. This is because LUWE reduced reactive oxygen species-mediated mitochondrial fission via regulating p-Drp-1 and Fis1 expression. We further confirmed that LUWE suppresses the expression of p-MEK-1/2 and p-ERK-1/2 in NaIO3-induced ARPE-19 cells, thereby providing the protection described above, which was confirmed using PD98059 and U0126. These results indicated that LUWE prevents mitochondrial oxidative stress-mediated RPE damage via the MEK/ERK pathway. Elucidation of the molecular mechanism may provide a new protective strategy against retinal degeneration.

An Innovative Mei-Gin Formula Exerts Anti-Adipogenic and Anti-Obesity Effects in 3T3-L1 Adipocyte and High-Fat Diet-Induced Obese Rats.

BACKGROUND: To investigate the potential anti-obesity properties of an innovative functional formula (called the Mei-Gin formula: MGF) consisting of bainiku-ekisu, Prunus mume (70% ethanol extract), black garlic (water extract), and Mesona procumbens Hemsl. (40% ethanol extract) for reducing lipid accumulation in 3T3-L1 adipocytes in vitro and obese rats in vivo. MATERIAL AND METHODS: The prevention and regression of high-fat diet (HFD)-induced obesity by the intervention of Japan Mei-Gin, MGF-3 and -7, and positive health supplement powder were investigated in male Wistar rats. The anti-obesity effects of MGF-3 and -7 in rats with HFD-induced obesity were examined by analyzing the role of visceral and subcutaneous adipose tissue in the development of obesity. RESULTS: The results indicated that MGF-1-7 significantly suppressed lipid accumulation and cell differentiation through the down-regulation of GPDH activity, as a key regulator in the synthesis of triglycerides. Additionally, MGF-3 and MGF-7 exhibited a greater inhibitory effect on adipogenesis in 3T3-L1 adipocytes. The high-fat diet increased body weight, liver weight, and total body fat (visceral and subcutaneous fat) in obese rats, while these alterations were effectively improved by the administration of MGF-3 and -7, especially MGF-7. CONCLUSION: This study highlights the role of the Mei-Gin formula, particularly MGF-7, in anti-obesity action, which has the potential to be used as a therapeutic agent for the prevention or treatment of obesity.

Mei-Gin Formula Ameliorates Obesity through Lipolysis, Fatty Oxidation, and Thermogenesis in High-Fat Diet-Induced Obese Rats.

Obesity is a metabolic dysfunction characterized by excessive body fat deposition as a consequence of an energy imbalance. Novel therapeutic strategies have emerged that are safe and have comparatively low side effects for obesity treatment. Functional foods and nutraceuticals have recently received a great deal of attention because of their components with the properties of antimetabolic syndrome. Based on our previous in vitro and in vivo investigations on anti-adipogenesis activity and improved body fat accumulation in serials, the combination of three ingredients (including bainiku-ekisu, black garlic, and Mesona procumbens Hemsl), comprising the Mei-Gin formula (MGF), was eventually selected as a novel inhibitor that exhibited preventive effects against obesity. Herein, we verify the anti-obesity effects of MGF in obese rats induced by a high-fat diet and discuss the potential molecular mechanisms underlying obesity development. Oral administration of MGF significantly suppressed the final body weight, weight change, energy and water intake, subcutaneous and visceral fat mass, liver weight, hepatic total lipids and triglycerides (TG), and serum levels of TG, triglycerides (TC), low-density lipoprotein cholesterol (LDL-C), alanine transaminase (AST), uric acid, and ketone bodies and augmented fecal total lipids, TG, and cholesterol excretion in the high-dose MGF-supplemented groups. Furthermore, the corresponding lipid metabolic pathways revealed that MGF supplementation effectively increased lipolysis and fatty acid oxidation gene expression and attenuated fatty acid synthesis gene expression in the white adipose tissue (WAT) and liver and it also increased mitochondrial activation and thermogenic gene expression in the brown adipose tissue (BAT) of rats with obesity induced by a high-fat diet (HFD). These results demonstrate that the intake of MGF can be beneficial for the suppression of HFD-induced obesity in rats through the lipolysis, fatty oxidation, and thermogenesis pathway. In conclusion, these results demonstrate the anti-obesity efficacy of MGF in vivo and suggest that MGF may act as a potential therapeutic agent against obesity.

Geranyl flavonoid derivatives from the fresh leaves of Artocarpus communis and their anti-inflammatory activity.

Breadfruit (Artocarpus communis) is a widely distributed crop in tropical and subtropical regions of the world. It is used in Southeast Asia and India to treat several inflammatory disorders. The aim of this study was to investigate the presence of anti-inflammatory flavonoids in A. communis leaves. Three new geranyl flavonoids, arcommunol C (1), arcommunol D (3), and 5'-geranyl-3,4,2',4'-tetrahydroxychalcone (5), together with four known compounds, prostratol (2), arcommunol E (4), 3'-geranyl-3,4,2',4'-tetrahydroxydihydrochalcone (6), and 3'-geranyl-3,4,2',4'-tetrahydroxychalcone (7), were isolated from the leaves of A. communis. Compound 4 was isolated for the first time from natural sources. The anti-inflammatory activity of the isolated compounds (1-7) was evaluated by determining their inhibitory activity on the production of proinflammatory mediators in lipopolysaccharide (LPS)-activated RAW 264.7 murine macrophage cells. Compounds 2, 3, and 4 suppressed the LPS-induced production of nitric oxide (NO) in RAW 264.7 cells with IC50 values of 8.13 ± 0.17, 18.45 ± 2.15, and 22.74 ± 1.74 µM, respectively. Furthermore, 2 decreased lipopolysaccharide (LPS)-mediated induction of protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in RAW 264.7 cells. It was also found that 2 suppressed LPS-induced phosphorylation of JNK and p38 mitogen-activated protein kinase (MAPK) signaling.

The next generation beneficial actions of novel probiotics as potential therapeutic targets and prediction tool for metabolic diseases.

The prevalence of metabolic disease has rising and affected over 1,000 million populations globally. Since the metabolic disease and its related complication are board, it has become the major health hazard of modern world. However, Long term medication of metabolic disease may cause serious side effects and risk for adverse health problems. Recently, emerging studies focus on exploring the mechanistic details of metabolic state in disease development and progression. Gut bacteria ecosystem was considered to play a pivotal role in regulating energy homeostasis and great associated with the development of metabolic disease. Accumulated evidences indicated that Akkermansia muciniphila, Faecalibacterium prausnitzii, and Roseburia hominis improve the balance of the microecology in the intestine of the host and have positive effects on enhancing nutrients absorption. Hence, the novel probiotics as therapeutic target to modify gut microbiota generally focus on improving microbiota dysbiosis, and offers new prospects for treating metabolic disease. In the present review, we discuss the significant roles and regulatory properties of specific bacterium in the context of intestinal microbial balance, explores the kinds of harmful/beneficial bacteria that were likely to act as indicator for metabolic disease. Further proposed a stepwise procedure in the basis of sequencing technology with that of innovative option to reestablish the microbial equilibrium and prevent metabolic disease.

Anti-fatigue effects of enzyme-hydrolyzed okara in C2C12 myotubes and Sprague-Dawley rats.

Okara is a by-product of tofu or soymilk production processes. The disposal of huge quantities of okara is a significant issue. Based on previous reports, protein hydrolysis can release excess free amino acids and small peptides from okara and exhibit anti-fatigue function. We aimed to investigate the anti-fatigue effect of okara protein hydrolysate (OPH) in vitro and in vivo. In the first phase, we treated C2C12 myotubes with different processed OPHs to detect mitochondrial functions. The results revealed that OPH hydrolyzed with alcalase containing 2% E/S for 2 h increased the mitochondrial mRNA level (cytochrome b and cytochrome c oxidase I) and enzyme activity (citrate synthase and cytochrome c oxidase) most efficiently. In the second phase, we conducted animal studies to assess the anti-fatigue function of OPH. After acclimatization, 8 week-old male Sprague-Dawley (SD) rats were randomly classified into four groups: (1) control group, (2) 1X-OPH, (3) 2X-OPH, and (4) 5X-OPH (8 rats per group, treated for 28 days). The results indicated that the intake of OPH for 28 days increased the exhaustive swimming time of rats and lowered the increment of the lactate ratio, as well as the activity of lactate dehydrogenase and creatine kinase. These results indicated that OPH improves exercise performance and anti-fatigue function in male SD rats. Therefore, OPH could be a potential health supplement for anti-fatigue function.

Short-Term Oral Quercetin Supplementation Improves Post-exercise Insulin Sensitivity, Antioxidant Capacity and Enhances Subsequent Cycling Time to Exhaustion in Healthy Adults: A Pilot Study.

Aim: Quercetin has been reported to have antioxidant and anti-inflammatory properties on health promotion in human studies. The main purpose of this study was to investigate the effect of short-term oral quercetin supplementation on post-exercise whole-body energy metabolism. This study also aimed to determine the effects of supplementation on oxygen stress, inflammation, muscle damage, and high-intensity cycling exercise performance. Method: Twelve healthy participants, physically active students, were recruited to perform a randomized, single-blind crossover study. All subjects completed 7-days of quercetin (quercetin:1,000 mg per day for 7-days) and placebo supplementation in a randomized order. Supplement/placebo was combined with exercise consisting of 70% V̇O2max cycling for 60-min, followed by 3-h of recovery, then a subsequent single bout of cycling exercise with 75% V̇O2max to exhaustion. Time to exhaustion, indicators of muscle damage, as well as blood and gaseous parameters relating to energy metabolism, oxidative stress, inflammatory response, respectively, were determined. Results: The results showed that 7-day quercetin supplementation significantly attenuated the post-exercise glucose-induced insulin response, increased total antioxidant capacity (TAC) and superoxidase dismutase (SOD) activities, and mitigated malondialdehyde (MDA) levels during the recovery period (p < 0.05). While subsequent 75% V̇O2max cycling performance was significantly improved after quercetin treatment and accompanied by lower responses of interleukin 6 and creatine kinase at 24-h. However, it's noted that there were no significant responses in glucose, respiratory exchange rate, tumor necrosis factor-α (TNF-α), myoglobin, and high sensitivity C-reactive protein between quercetin and placebo trials. Conclusion: Our findings concluded that 7-day oral quercetin supplementation enhances high-intensity cycling time to exhaustion, which may be due in part to the increase in whole-body insulin-stimulated glucose uptake and attenuation of exercise-induced oxygen stress and pro-inflammation. Therefore, quercetin may be considered an effective ergogenic aid for enhancing high-intensity cycling performance among young adults.

Supplementation of Lactobacillus plantarum (TCI227) Prevented Potassium-Oxonate-Induced Hyperuricemia in Rats.

Hyperuricemia (HC) is one of the important risk factors for gout, arteriosclerosis, and cardiovascular disease. Animal studies have shown that Lactobacillus plantarum can improve microbiota and immune regulation, as well as inhibit uric acid production. However, it is not clear whether L. plantarum can improve HC and intestinal microbiota. We used potassium oxonate (PO) to induce HC in male SD rats and then treated them with L. plantarum TCI227 in a dose-dependent manner (HC + LD, HC + MD, HC + HD) for 4 weeks. We examined organ weight, conducted biochemical examinations of blood and urine, and analyzed the intestinal microbiota in feces through a 16s rDNA sequence analysis. In this study, TCI227 improved body weight, decreased creatinine and serum uric acid, and increased urine uric acid compared to the HC group. Furthermore, TCI227 increased short-chain fatty acids (SCFAs). In the fecal microbiota (family), TCI227 increased the level of Lactobacillaceae and then decreased the levels of Deferribacteres and Prevotellaceae compared to the HC group. Finally, in the fecal microbiota (genus), TCI227 decreased the level of Prevotella and then increased the levels of Lactobacillus and Ruminococcus compared to the HC group. This study suggested that TCI227 can improve HC and can change the composition of intestinal microbiota in PO-induced male HC SD rats.

Cardiovascular protection of deep-seawater drinking water in high-fat/cholesterol fed hamsters.

Cardiovascular protection of deep-seawater (DSW) drinking water was assessed using high-fat/cholesterol-fed hamsters in this study. All hamsters were fed a high-fat/cholesterol diet (12% fat/0.2% cholesterol), and drinking solutions were normal distiled water (NDW, hardness: 2.48ppm), DSW300 (hardness: 324.5ppm), DSW900 (hardness: 858.5ppm), and DSW1500 (hardness: 1569.0ppm), respectively. After a 6-week feeding period, body weight, heart rates, and blood pressures of hamsters were not influenced by DSW drinking waters. Serum total cholesterol (TC), triacylglycerol (TAG), atherogenic index, and malondialdehyde (MDA) levels were decreased (p<0.05) in the DSW-drinking-water groups, as compared to those in the NDW group. Additionally, increased (p<0.05) serum Trolox equivalent antioxidant capacity (TEAC), and faecal TC, TAG, and bile acid outputs were measured in the DSW-drinking-water groups. Hepatic low-density-lipoprotein receptor (LDL receptor) and cholesterol-7α-hydroxylase (CYP7A1) gene expressions were upregulated (p<0.05) by DSW drinking waters. These results demonstrate that DSW drinking water benefits the attenuation of high-fat/cholesterol-diet-induced cardiovascular disorders in hamsters.

Rutin and Gallic Acid Regulates Mitochondrial Functions via the SIRT1 Pathway in C2C12 Myotubes.

Mitochondria are highly dynamic organelles, balancing synthesis and degradation in response to increases in mitochondrial turnover (i.e., biogenesis, fusion, fission, and mitophagy) and function. The aim of this study was to investigate the role of polyphenols in the regulation of mitochondrial functions and dynamics in C2C12 myotubes and their molecular mechanisms. Our results indicate that gallic acid and rutin are the most potential polyphenol compounds in response to 15 phenolic acids and 5 flavonoids. Gallic acid and rutin were associated with a significantly greater mitochondrial DNA (cytochrome b and COX-II), mitochondrial enzymatic activities (including citrate synthase and cytochrome c oxidase), and intracellular ATP levels in C2C12 myotubes. Moreover, gallic acid and rutin significantly increased the gene expressions of mitochondrial turnover in C2C12 myotubes. Our findings indicated that gallic acid and rutin may have a beneficial effect on mitochondrial dynamics via regulation of the SIRT1-associated pathway in C2C12 myotubes.

The potential role of phenolic compounds on modulating gut microbiota in obesity.

Obesity is a rising public health issue and challenge which is tightly correlated with socio-economic development paralleled with increased energy intake and sedentary behavior that subsequently cause adipose tissue accumulation. Physiological and metabolic status changes during obesity development have been suggested with low grade inflammation of gastrointestinal tract. The gut microbiota plays an essential role in regulating whole body energy metabolism and also lipid accumulation, and immunity of host. However, the detail mechanism of which the gut microbiota composition influence obesity development in humans still need deeper investigation owing to the complex pathophysiology of such disease. Recently, the consumption of phenols-rich food has been showed to have physiological function that attribute to improve gut microbiota and benefit body weight management. Here, we review the current knowledge regarding phenolic compounds that regulate the development of obesity and the importance of the axis that link dietary-induced gut microbiota change and metabolic health of host. We also discuss dietary intervention reshaping gut bacterial community to modulate obesity.

Effects of Oral Resveratrol Supplementation on Glycogen Replenishment and Mitochondria Biogenesis in Exercised Human Skeletal Muscle.

The present study aimed to investigate the effect of oral resveratrol supplementation on the key molecular gene expressions involved in mitochondria biogenesis and glycogen resynthesis in human skeletal muscle. Nine young male athletes participated in the single-blind and crossover designed study. All subjects completed a 4-day resveratrol and placebo supplement in a randomized order while performing a single bout of cycling exercise. Immediately after the exercise challenge, the subjects consumed a carbohydrate (CHO) meal (2 g CHO/Kg body mass) with either resveratrol or placebo capsules. Biopsied muscle samples, blood samples and expired gas samples were obtained at 0 h and 3 h after exercise. The muscle samples were measured for gene transcription factor expression by real-time PCR for glucose uptake and mitochondria biogenesis. Plasma glucose, insulin, glycerol, non-esterified fatty acid concentrations and respiratory exchange ratio were analyzed during post-exercise recovery periods. The results showed that the muscle glycogen concentrations were higher at 3 h than at 0 h; however, there were no difference between resveratrol trial and placebo trial. There were no significantly different concentrations in plasma parameters between the two trials. Similarly, no measured gene expressions were significant between the two trials. The evidence concluded that the 4-day oral resveratrol supplementation did not improve post-exercise muscle glycogen resynthesis and related glucose uptake and mitochondrial biosynthesis gene expression in men.

Phenolic compounds: evidence for inhibitory effects against obesity and their underlying molecular signaling mechanisms.

Phenolic compounds are widely present in the plant kingdom. Many epidemiological studies have indicated that consumption of some plant-derived foodstuffs with high phenolic content is associated with the prevention of some diseases and that these compounds may have similar properties to antioxidants, antimutagenic agents, antithrombotic agents, anti-inflammatory agents, anti-HIV-1, and anticancer agents. However, obesity is an important topic in the world of public health and preventive medicine. Relationships between body mass index, waist circumference, or waist-to-hip ratio and the risk of development of some diseases (such as heart disease, dyslipidemia, hypertension, non-alcoholic fatty liver disease, diabetes, kidney failure, cancer, stroke, osteoarthritis, and sleep apnea) have been observed. Evidence that phenolic compounds have beneficial effects in fighting obesity is increasingly being reported in the scientific literature. These in vitro and in vivo effects of phenolic compounds on the induction of pre-adipocytic and adipocytic apoptosis and inhibition of adipocytic lipid accumulation are considered in detail here. This review presents evidence of their inhibitory effects on obesity and their underlying molecular signaling mechanisms.

Inhibitory effect of vanillic acid on methylglyoxal-mediated glycation in apoptotic Neuro-2A cells.

Methylglyoxal is a reactive dicarbonyl compound generated as an intermediate of glycolysis during the physical glycation in the diabetic condition. It is considered to be a potent precursor of advanced glycation end products (AGEs) formation. Methylglyoxal itself and methylglyoxal-derived AGEs have been commonly implicated in the development of diabetic neuropathy. Our previous study indicated that vanillic acid showed an inhibitory effect against methylglyoxal-mediated Neuro-2A cell apoptosis, suggesting that vanillic acid might possess cytoprotective properties in the prevention of diabetic neuropathy complication. In this study, the effects of vanillic acid on the methylglyoxal-mediated glycation system involved in the progression of Neuro-2A cell apoptosis were further investigated. Our findings indicated that methylglyoxal-induced Neuro-2A cell apoptosis was mediated through the possible glycation mechanism of oxidative stress, activation of the MAPK signaling pathway (p38 and JNK) and oxidation-sensitive protein expression (PKC and p47(phox)) and methylglyoxal-derived N-epsilon-(carboxymethyl)lysine (CML) formation. Vanillic acid, however, suppressed methylglyoxal-induced Neuro-2A cell apoptosis via inhibition of glycation mechanisms including ROS, p38 and JNK, PKC and p47(phox), and methylglyoxal-derived CML formation. In the present study, we established the first evidence that vanillic acid might contribute to the prevention of the development of diabetic neuropathy by blocking the methylglyoxal-mediated intracellular glycation system.

Lucidenic acid B induces apoptosis in human leukemia cells via a mitochondria-mediated pathway.

Ganoderma lucidum is known as a medicinal mushroom used in traditional Chinese medicine. In the present study, the effect of lucidenic acids (A, B, C, and N) isolated from a new G. lucidum (YK-02) on induction of cell apoptosis and the apoptotic pathway in HL-60 cells were investigated. The results demonstrated that lucidenic acids decreased cell population growth of HL-60 cells, assessed with the MTT assay. The cell cycle assay indicated that treatment of HL-60 cells with lucidenic acid A, C, and N caused cell cycle arrest in the G 1 phase. Lucidenic acid B (LAB) did not affect the cell cycle profile; however, it increased the number of early and late apoptotic cells but not necrotic cells. Treatment of HL-60 cells with LAB caused loss of mitochondria membrane potential. Moreover, the ratio of expression levels of pro- and antiapoptotic Bcl-2 family members was changed by LAB treatment. LAB-induced apoptosis involved release of mitochondria cytochrome c and subsequently induced the activation of caspase-9 and caspase-3, which were followed by cleavage of poly(ADP-ribose) polymerase (PARP). Pretreatment with a general caspase-9 inhibitor (Z-LEHD-FMK) and caspase-3 inhibitor (Z-DEVD-FMK) prevented LAB from inhibiting cell viability in HL-60 cells. Our finding may be critical to the chemopreventive potential of lucidenic acid B.