No abstract

Our results suggested that incorporation of almonds into a healthy diet could ameliorate inflammation and oxidative stress in patients with T2DM.

Cardiovascular disease (CVD) is the most important adult health problem in the world. Epidemiological studies and laboratory experiments have shown that fruit and vegetable consumption has protective effects against CVD. The purpose of the study was to investigate the effects of consumption of two kiwifruit per day on the lipid profile, antioxidants and markers of lipid peroxidation in hyperlipidemic adult men and women in Taiwan. Forty-three subjects who had hyperlipidemia, including 13 males and 30 females, participated in this study. They were asked to consume two kiwifruit per day for 8 weeks. Anthropometric measurements were made. Before the intervention and at 4 and 8 weeks of the intervention, fasting blood samples were analyzed for total cholesterol, triacylglycerol, low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein cholesterol (HDL-C). Additionally vitamin E and vitamin C, the malondialdehyde + 4-hydroxy-2(E)-nonenal concentration, and the lag time of LDL oxidation were determined. No significant differences from baseline to 8 weeks of the intervention were detected for triacylglycerol, total cholesterol, or LDL cholesterol. However, after 8 weeks of consumption of kiwifruit, the HDL-C concentration was significantly increased and the LDL cholesterol/HDL-C ratio and total cholesterol/HDL-C ratio were significantly decreased. Vitamin C and vitamin E also increased significantly. In addition, the lag time of LDL oxidation and malondialdehyde + 4-hydroxy-2(E)-nonenal had significantly changed at 4 and 8 weeks during the kiwifruit intervention. Regular consumption of kiwifruit might exert beneficial effects on the antioxidative status and the risk factors for CVD in hyperlipidemic subjects.

The aim of this study was to evaluate the effects of purple sweet potato leaves (PSPL) consumption on oxidative stress markers in a healthy, nontrained, young male population after completing a running exercise protocol. A crossover design was applied, with 15 subjects participating in a two-step dietary intervention period. Each subject was given a high- (PSPL group) or low-polyphenol (control group) diet for 7 days with a 14-day washout period. After each dietary intervention period, all subjects performed 1 h of treadmill running at a speed corresponding to 70% of each subject's individual maximal oxygen uptake (Vo(2max)). Blood samples were taken before exercise and at 0, 1, and 3 h after exercise. Compared with the control group, PSPL consumption significantly increased plasma total polyphenols concentration and total antioxidant power (i.e., the ferric-reducing ability of plasma) in the PSPL group. The markers of oxidative damage, plasma TBARS and protein carbonyl, significantly decreased. Plasma IL-6 concentration also decreased. However, no significant difference was found in HSP72 levels between the two groups. These findings indicate that consuming a high-polyphenol diet for 7 days can modulate antioxidative status and decrease exercise-induced oxidative damage and pro-inflammatory cytokine secretion.

Na؉ /Ca 2؉ exchanger (NCX) is one of the major mechanisms for removing Ca 2؉ from the cytosol especially in cardiac myocytes and neurons, where their physiological activities are triggered by an influx of Ca 2؉ . NCX contains a large intracellular loop (NCXIL) that is responsible for regulating NCX activity. Recent evidence has shown that proteins, including kinases and phosphatases, associate with NCX1IL to form a NCX1 macromolecular complex. To search for the molecules that interact with NCX1IL and regulate NCX1 activity, we used the yeast twohybrid method to screen a human heart cDNA library and found that the C-terminal region of sarcomeric mitochondrial creatine kinase (sMiCK) interacted with NCX1IL. Moreover, both sMiCK and the muscle-type creatine kinase (CKM) coimmunoprecipitated with NCX1 using lysates of cardiacmyocytes and HEK293T cells that transiently expressed NCX1 and various creatine kinases. Both sMiCK and CKM were able to produce a recovery in the decreased NCX1 activity that was lost under energy-compromised conditions. This regulation is mediated through a putative PKC phosphorylation site of sMiCK and CKM. The autophosphorylation and the catalytic activity of sMiCK and CKM are not required for their regulation of NCX1 activity. Our results suggest a novel mechanism for the regulation of NCX1 activity.