Methods: Freeze-dried pineapple vinegar was evaluated for its in vitro apoptosis and metastasis inhibitory potential using MTT, cell cycle, Annexin V and scratch assays. The in vivo test using BALB/c mice challenged with 4 T1 cells was further investigated by pre-treating the mice with 0.08 or 2 ml/kg body weight of freshly-prepared pineapple vinegar for 28 days. The tumor weight, apoptotic state of cells in tumor, metastasis and immune response of the untreated and pineapple vinegar treatment group were evaluated and compared.
Results: From the in vitro study, an IC50 value of 0.25 mg/mL after 48 h of treatment was established. Annexin V/PI and scratch closure assays showed that pineapple vinegar induced 70% of cell population to undergo apoptosis and inhibited 30% of wound closure of 4 T1 cells. High concentration of pineapple vinegar (2 ml/kg body weight) led to the reduction of tumor weight and volume by 45%as compared to the untreated 4 T1-challenged mice. This effect might have been contributed by the increase of T cell and NK cells population associated with the overexpression of IL-2 andIFN-γ cytokines and splenocyte cytotoxicity. Furthermore, fewer instances of metastasis events were recorded in the pineapple vinegar treatment group and this could be explained by the downregulation of inflammation related genes (iNOS, NF-kB and COX2), metastasis related genes (iCAM, VEGF and MMP9) and angeogenesis related genes (CD26, TIMP1, HGF, MMP3, IGFBP-1 and IGFBP-2).
Conclusion: The ability of pineapple vinegar to delay cancer progression portrayed its potential as chemopreventive dietry intervention for cancer therapy.
Method: The mRNA expression of PI3K/AKT axis from 100 non-obese and obese participants with insulin sensitivity and insulin resistance states were compared in this study toward the understanding of obesity heterogeneity molecular mechanism.
Result: In present study, there was no statistically significant difference in gene expression levels of IRS1 and PTEN between groups, whereas PI3K, AKT2 and GLUT4 genes were expressed at a lower level in obese diabetic group compared to other groups and were statistically significant. PDK1 gene was expressed at a higher level in non-obese diabetic group compared to obese diabetic and non-obese non-diabetics groups. No statistically significant difference was identified in gene expression pattern of PI3K/AKT pathway between obese non-diabetics and non-obese non-diabetics.
Conclusion: The components of PI3K/AKT pathway which is related to the fasting state, showed reduced expression in obese diabetic group due to the chronic over-nutrition which may induced insensitivity and reduced gene expression. The pathogenesis of insulin resistance in the absence of obesity in non-obese diabetic group could be due to disturbance in another pathway related to the non-fasting state like gluconeogenesis. Therefore, the molecular mechanism of insulin signalling in non-obese diabetic individuals is different from obese diabetics which more investigations are required to study insulin signalling pathways in greater depth, in order to assess nutritional factors, contribute to insulin resistance in obese diabetic and non-obese diabetic individuals.
Methods: CSSI was induced in male Sprague Dawley rats by intraperitoneal injection of LPS three times per week for 28 days, and SBH (4.6 and 9.3 g/kg/day) was supplemented for 30 days.
Results: LPS-induced rats showed significant leukocytosis, and elevated serum levels of CRP, TNF-α, IL-1β, IL-6, IL-8, MCP-1, malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), accompanied with diminished antioxidants. Treatment with SBH significantly ameliorated inflammatory markers, MDA and 8-OHdG, and enhanced antioxidants in LPS-induced rats. In addition, SBH decreased NF-κB p65 and p38 MAPK, and increased Nrf2 expression in the liver, kidney, heart and lung of LPS-induced rats. Furthermore, SBH prevented LPS-induced histological and functional alterations in the liver, kidney, heart and lung of rats.
Conclusion: SBH has a substantial protective role against LPS-induced CSSI in rats mediated via amelioration of inflammation, oxidative stress and NF-κB, p38 MAPK and Nrf2 signaling.
Methods: This is a cross-sectional study among 335 adolescents who provided both dietary information assessed using a validated food frequency questionnaire (FFQ) and biochemical parameters including lipid profile, blood glucose, serum insulin and homeostatic model assessment-insulin resistance (HOMA-IR). Anthropometric measurements included weight (kg), height (cm) and waist circumference (cm), while body mass index (BMI) in kg/m2 was estimated, respectively. Reduced rank regression (RRR) identified a DP with percentage of energy from sugar and total fat, DED and fibre density intake as response variables.
Results: The identified 'high sugar, high fibre, high DED and low fat' DP was characterised by high intakes of sugar-sweetened beverages, fruits, sweets and low intakes of meat and cereal. Adolescents in the highest tertile of the identified DP had about 3.0 (OR = 2.7; 95%CI: 1.3, 5.6) and 2.0 (OR = 1.9; 95%CI: 1.0, 3.5) times higher odds of having dyslipideamia or elevated total cholesterol and LDL-cholesterol level, respectively compared to adolescents in the lowest tertile DP after adjusting for sex, school location, maternal education, physical activity, dietary misreporting and BMI z-score. This DP was not significantly associated with overweight and obesity.
Conclusions: Higher adherence to a DP characterised mainly by free sugars and DED was associated with greater odds of having dyslipideamia, elevated total cholesterol and LDL-cholesterol levels in Malaysian adolescents.
METHODS: Thirty human volunteers were fed complete, whole food diets during 4 wk periods, where total fat (approximately 31% daily energy, >70% from the test fats) and fatty acid composition were tightly controlled. A crossover design was used with 3 randomly-assigned diet rotations and repeated-measures analysis. One test fat rotation was based on palm olein (POL) and provided 12.0 percent of energy (%en) as palmitic acid (16:0); a second contained trans-rich partially hydrogenated soybean oil (PHSO) and provided 3.2 %en as trans fatty acids plus 6.5 %en as 16:0, while the third used an interesterified fat (IE) and provided 12.5 %en as stearic acid (18:0). After 4 wk the plasma lipoproteins, fatty acid profile, as well as fasting glucose and insulin were assessed. In addition, after 2 wk into each period an 8 h postprandial challenge was initiated in a subset of 19 subjects who consumed a meal containing 53 g of test fat.
RESULTS: After 4 wk, both PHSO and IE fats significantly elevated both the LDL/HDL ratio and fasting blood glucose, the latter almost 20% in the IE group relative to POL. Fasting 4 wk insulin was 10% lower after PHSO (p > 0.05) and 22% lower after IE (p < 0.001) compared to POL. For the postprandial study the glucose incremental area under the curve (IAUC) following the IE meal was 40% greater than after either other meal (p < 0.001), and was linked to relatively depressed insulin and C-peptide (p < 0.05).
CONCLUSION: Both PHSO and IE fats altered the metabolism of lipoproteins and glucose relative to an unmodified saturated fat when fed to humans under identical circumstances.