METHODS: Subjects underwent a randomized double-blind crossover trial, consuming diets supplemented with 20 g/day of either soybean oil-based mayonnaise (SB-mayo) or palm olein-based mayonnaise (PO-mayo) for 4 weeks each with a 2-week wash-out period. The magnitude of changes for metabolic outcomes between dietary treatments was compared with PO-mayo serving as the control. The data was analyzed by ANCOVA using the GLM model. Analysis was adjusted for weight changes.
RESULTS: Treatments resulted in significant reductions in TC (diff = -0.25 mmol/L; P = 0.001), LDL-C (diff = -0.17 mmol/L; P = 0.016) and HDL-C (diff = -0.12 mmol/L; P 0.05). Lipoprotein particle change was significant with large LDL particles increasing after PO-mayo (diff = +63.2 nmol/L; P = 0.007) compared to SB-mayo but small LDL particles remained unaffected. Plasma glucose, apolipoproteins and oxidative stress markers remained unchanged.
CONCLUSIONS: Daily use with 20 g of linoleic acid-rich SB-mayo elicited reductions in TC and LDL-C concentrations without significantly changing LDL-C:HDL-C ratio or small LDL particle distributions compared to the PO-mayo diet.
TRIAL REGISTRATION: This clinical trial was retrospectively registered with the National Medical Research Register, National Institute of Health, Ministry of Health Malaysia, (NMRR-15-40-24035; registered on 29/01/2015; https://www.nmrr.gov.my/fwbPage.jsp?fwbPageId=ResearchISRForm&fwbAction=Update&fwbStep=10&pk.researchID=24035&fwbVMenu=3&fwbResearchAction=Update ). Ethical approval was obtained from the National University of Malaysia's Medical Ethics Committee (UKM 1.5.3.5/244/SPP/NN-054-2011, approved on 25/05/2011).
METHODS: This is a cross sectional study conducted in adults living at urban area of Yogyakarta, Indonesia. Data of adiposity, lifestyle, triglyceride, high density lipoprotein (HDL) cholesterol, leptin and UCP2 gene polymorphism were obtained in 380 men and female adults.
RESULTS: UCP2 gene polymorphism was not significantly associated with adiposity, leptin, triglyceride, HDL cholesterol, dietary intake and physical activity (allp> 0.05). Leptin was lower in overweight subjects with AA + GA genotypes than those with GG genotype counterparts (p= 0.029). In subjects with AA + GA genotypes there was a negative correlation between leptin concentration (r= -0.324;p< 0.0001) and total energy intake and this correlation was not seen in GG genotype (r= -0.111;p= 0.188).
CONCLUSIONS: In summary, we showed how genetic variation in -866G/A UCP2 affected individual response to leptin production. AA + GA genotype had a better leptin sensitivity shown by its response in dietary intake and body mass index (BMI) and this explained the protective effect of A allele to obesity.
PRACTICAL APPLICATION: Kenaf seed oil-in-water nanoemulsion (KSON) has the potential to be used as a natural alternative to the synthetic hypocholesterolemic drug in the future. However, larger sample size and clinical trial are needed to confirm on this potential application. In addition, treatment with KSON was suggested to prevent cardiovascular disease and fatty liver.
METHODS: A sample of 3895 individuals without known diabetes underwent detailed interview and health examination, including anthropometric and biochemical evaluation, between 2004 and 2007. Pearson's correlation, analysis of variance and multiple linear regression analyses were used to examine the influence of ethnicity on HbA(1c) .
RESULTS: As fasting plasma glucose increased, HbA(1c) increased more in Malays and Indians compared with Chinese after adjustment for age, gender, waist circumference, serum cholesterol, serum triglyceride and homeostasis model assessment of insulin resistance (P-interaction < 0.001). This translates to an HbA(1c) difference of 1.1 mmol/mol (0.1%, Indians vs. Chinese), and 0.9 mmol/mol (0.08%, Malays vs. Chinese) at fasting plasma glucose 5.6 mmol/l (the American Diabetes Association criterion for impaired fasting glycaemia); and 2.1 mmol/mol (0.19%, Indians vs. Chinese) and 2.6 mmol/mol (0.24%, Malays vs. Chinese) at fasting plasma glucose 7.0 mmol/l, the diagnostic criterion for diabetes mellitus.
CONCLUSIONS: Using HbA(1c) in place of fasting plasma glucose will reclassify different proportions of the population in different ethnic groups. This may have implications in interpretation of HbA(1c) results across ethnic groups and the use of HbA(1c) for diagnosing diabetes mellitus.