METHODS: Using 3 d of dietary records, FA intakes of 333 recruited patients were calculated using a food database built from laboratory analyses of commonly consumed Malaysian foods. Plasma triacylglycerol (TG) and erythrocyte FAs were determined by gas chromatography.
RESULTS: High dietary saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) consumption trends were observed. Patients on HD also reported low dietary ω-3 and ω-6 polyunsaturated fatty acid (PUFA) consumptions and low levels of TG and erythrocyte FAs. TG and dietary FAs were significantly associated respective to total PUFA, total ω-6 PUFA, 18:2 ω-6, total ω-3 PUFA, 18:3 ω-3, 22:6 ω-3, and trans 18:2 isomers (P < 0.05). Contrarily, only dietary total ω-3 PUFA and 22:6 ω-3 were significantly associated with erythrocyte FAs (P < 0.01). The highest tertile of fish and shellfish consumption reflected a significantly higher proportion of TG 22:6 ω-3. Dietary SFAs were directly associated with TG and erythrocyte MUFA, whereas dietary PUFAs were not.
CONCLUSION: TG and erythrocyte FAs serve as biomarkers of dietary PUFA intake in patients on HD. Elevation of circulating MUFA may be attributed to inadequate intake of PUFAs.
METHODS: This cross-sectional study was conducted among 392 schoolchildren aged 9-11 years, cluster sampled from five randomly selected schools in Kuala Lumpur. Whole-grain and fatty acids intakes were assessed by 3-day, 24-h diet recalls. All whole-grain foods were considered irrespective of the amount of whole grain they contained.
RESULTS: In total, 55.6% (n = 218) were whole-grain consumers. Mean (SD) daily intake of whole grain in the total sample was 5.13 (9.75) g day-1 . In the whole-grain consumer's only sample, mean (SD) intakes reached 9.23 (11.55) g day-1 . Significant inverse associations were found between whole-grain intake and saturated fatty acid (SAFA) intake (r = -0.357; P
METHODS: Using a randomized, crossover and double-blinded design, 15 men and 15 women with metabolic syndrome consumed high-fat meals enriched with SFA, MUFA or n-6 PUFA, or a low-fat/high-sucrose (SUCR) meal. C-peptide, insulin, glucose, gastrointestinal peptides and satiety were measured up to 6 h.
RESULTS: As expected, SUCR meal induced higher C-peptide (45 %), insulin (45 %) and glucose (49 %) responses compared with high-fat meals regardless of types of fatty acids (P < 0.001). Interestingly, incremental area under the curve (AUC0-120min) for glucagon-like peptide-1 was higher after SUCR meal compared with MUFA (27 %) and n-6 PUFA meals (23 %) (P = 0.01). AUC0-120min for glucose-dependent insulinotropic polypeptide was higher after SFA meal compared with MUFA (23 %) and n-6 PUFA meals (20 %) (P = 0.004). Significant meal x time interaction (P = 0.007) was observed for ghrelin, but not cholecystokinin and satiety.
CONCLUSIONS: The amount of fat regardless of the types of fatty acids affects insulin and glycemic responses. Both the amount and types of fatty acids acutely affect the gastrointestinal peptide release in metabolic syndrome subjects, but not satiety.
OBJECTIVE: To assess the chronic effects of the substitution of refined carbohydrate or MUFA for SAFA on insulin secretion and insulin sensitivity in centrally obese subjects.
METHODS: Using a crossover design, randomized controlled trial in abdominally overweight men and women, we compared the effects of substitution of 7% energy as carbohydrate or MUFA for SAFA for a period of 6 weeks each. Fasting and postprandial blood samples in response to corresponding SAFA, carbohydrate, or MUFA-enriched meal-challenges were collected after 6 weeks on each diet treatment for the assessment of outcomes.
RESULTS: As expected, postprandial nonesterified fatty acid suppression and elevation of C-peptide, insulin and glucose secretion were the greatest with high-carbohydrate (CARB) meal. Interestingly, CARB meal attenuated postprandial insulin secretion corrected for glucose response; however, the insulin sensitivity and disposition index were not affected. SAFA and MUFA had similar effects on all markers except for fasting glucose-dependent insulinotropic peptide concentrations, which increased after MUFA but not SAFA when compared with CARB.
CONCLUSION: In conclusion, a 6-week lower-fat/higher-carbohydrate (increased by 7% refined carbohydrate) diet may have greater adverse effect on insulin secretion corrected for glucose compared with isocaloric higher-fat diets. In contrast, exchanging MUFA for SAFA at 7% energy had no appreciable adverse impact on insulin secretion.