METHODS: The study was on 2322 non-institutionalized Malaysian elderly. The hierarchy logistic regression analysis was applied to estimate the risk of independent variables for urinary incontinence among respondents.
RESULTS: The findings indicated that approximately 3.80% of subjects had urinary incontinence. In addition, constipation was found a significant factor that increased the risk of urinary incontinence in samples (p=0.006; OR=3.77). The increase in dietary monounsaturated fat (p=0.038; OR=0.59) and plasma triglyceride levels (p=0.029; OR=0.56) significantly reduced the risk of incontinence in subjects. Many of suspected variables including socio-demographic factors, diseases, nutritional minerals, blood components and body weight were non-relevant factors to urinary incontinence in respondents.
CONCLUSIONS: Constipation increased the risk of urinary incontinence in subjects, and increase in dietary monounsaturated fat and plasma triglyceride levels decreased the risk.
Methods: The hypolipidaemic effect of (R)-(-)-carvone was investigated in a tyloxapol-induced hyperlipidaemia mice model. Furthermore, its effect on insulin secretion and proliferation of 1.1E7 human pancreatic β-cells was studied. In addition, using molecular docking, the binding affinity of (R)-(-)-carvone against 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase was estimated.
Results: (R)-(-)-carvone (100 mg/kg) decreased plasma triglyceride, total cholesterol, low-density lipoprotein cholesterol (LDL-C) levels and atherogenic index by 90.6%, 49.3%, 56.6% and 70.3%, respectively, but it had no effect on high-density lipoprotein cholesterol (HDL-C). Furthermore, it increased hepatic triglyceride level and catalase activity by 79.6% and 59.6%, respectively. In-vitro, 500 μM (R)-(-)-carvone increased insulin secretion by 454.4% and proliferation of 1.1E7 cells with no cytotoxic effects up to a concentration of 100 μM. Molecular docking simulation demonstrated a good binding affinity with -5.03 Kcal/mol of (R)-(-)-carvone to HMG-CoA reductase.
Conclusion: The hypolipidaemic effect of (R)-(-)-carvone is comparable to that of fenofibrate. (R)-(-)-carvone has the advantage over fenofibrate of not producing hypoglycaemia in animals. Furthermore, (R)-(-)-carvone increased proliferation and insulin secretion of human pancreatic β-cells.
OBJECTIVE: The primary study objective was to evaluate the postprandial fate of tocotrienols and alpha-tocopherol in human plasma and lipoproteins.
DESIGN: Seven healthy volunteers (4 males, 3 females) were administered a single dose of vitamin E [1011 mg palm tocotrienol-rich fraction (TRF) or 1074 mg alpha-tocopherol] after a 7-d conditioning period with a tocotrienol-free diet. Blood was sampled at baseline (fasted) and 2, 4, 5, 6, 8, and 24 h after supplementation. Concentrations of tocopherol and tocotrienol isomers in plasma, triacylglycerol-rich particles (TRPs), LDLs, and HDLs were measured at each interval.
RESULTS: After intervention with TRF, plasma tocotrienols peaked at 4 h (4.79 +/- 1.2 microg/mL), whereas alpha-tocopherol peaked at 6 h (13.46 +/- 1.68 microg/mL). Although tocotrienols were similarly detected in TRPs, LDLs, and HDLs, tocotrienol concentrations were significantly lower than alpha-tocopherol concentrations. In comparison, plasma alpha-tocopherol peaked at 8 h (24.3 +/- 5.22 microg/mL) during the alpha-tocopherol treatment and emerged as the major vitamin E isomer detected in plasma and lipoproteins during both the TRF and the alpha-tocopherol treatments.
CONCLUSIONS: Tocotrienols are detected in postprandial plasma, albeit in significantly lower concentrations than is alpha-tocopherol. This finding confirms previous observations that, in the fasted state, tocotrienols are not detected in plasma. Tocotrienol transport in lipoproteins appears to follow complex biochemically mediated pathways within the lipoprotein cascade.