The role of high fat diet on serum uric acid level among healthy male first degree relatives of type 2 diabetes mellitus.

First-degree relatives (FDR) of type 2 diabetes mellitus have increased risk of developing insulin resistance-related disorders including hyperuricemia. We investigated metabolic profile and serum uric acid (SUA) metabolism in response to high-fat diet among healthy male FDR in comparison to those without family history of diabetes. A total of 30 FDR and 30 non-FDR subjects completed a 5-days-hypercaloric diet with fat added to regular daily intake. Despite similar insulin response, FDR displayed different changes in SUA compared to non-FDR subjects (0.26 ± 0.83 mg/dL vs - 0.21 ± 0.78 mg/dL, p = 0.028). In subgroup analyses stratified by body mass index and waist circumference, significant different SUA changes between FDR and non-FDR subjects were only found in obese (0.48 ± 0.87 mg/dL vs - 0.70 ± 0.71 mg/dL, p = 0.001) and centrally obese (0.59 ± 0.83 mg/dL vs - 0.55 ± 0.82 mg/dL, p = 0.011) subgroups. In multivariate analysis, visceral adiposity seemed mediating the different response in SUA metabolism between FDR and non-FDR subjects induced by short-term obesogenic diet.

Increased intestinal-fatty acid binding protein in obesity-associated type 2 diabetes mellitus.

BACKGROUND: Obesity is a traditional risk factor for type 2 diabetes mellitus (T2DM). However, recent studies reported that metabolically unhealthy obesity (MUO) exerts a higher risk of developing T2DM than metabolically healthy obesity (MHO) because of its higher state of insulin resistance. This may happen due to metabolic endotoxemia through gut dysbiosis and increased intestinal permeability. Our study aimed to know the association of intestinal permeability using intestinal fatty acid-binding protein (I-FABP) with obesity-related T2DM patients in Indonesia. METHODS: This was a cross-sectional study that recruited 63 participants with obesity defined using body mass index (BMI) classification for the Asia-Pacific population (BMI ≥25 kg/m2). All participants were then grouped into T2DM and non-T2DM based on American Diabetes Association (ADA) diagnostic criteria. The I-FABP levels were measured using the enzyme-linked immunosorbent assay method. RESULTS: The I-FABP level of T2DM group was higher compared to non-T2DM group, namely 2.82 (1.23) ng/mL vs. 1.78 (0.81) ng/mL (p<0.001; mean difference 1.033 with 95% CI 0.51-1.55). This difference was not attenuated even after adjustment for age. The fitted regression model using linear regression was: i-FABP = 1.787+1.034*(DM) (R2 = 18.20%, standardized ß = 0.442, p<0.001). CONCLUSIONS: This study underscores the association of intestinal permeability with T2DM in people with obesity and supports the evidence of the potential role of intestinal permeability in the pathogenesis of obesity-related T2DM.

Determinant of postprandial triglyceride levels in healthy young adults.

BACKGROUND: Fasting lipid profile does not necessarily illustrate the exact lipid dynamic in 24 h as human spends most of their time in postprandial state. Postprandial triglyceride (TG) has been reported to have advantages compared to fasting TG in terms of practicality and ability to predict cardiovascular events. This study aims to assess the determinant of postprandial TG in healthy young adults. METHODS: This is a quasy-experimental study that involved 200 healthy young adults. This study compared fasting with postprandial TG and analyzed the relationship between postprandial TG with various demographic and metabolic parameters after ingestion of standardized high fat liquid meal. RESULT: There was an upward trend from fasting TG to 2 h postprandial TG and 4 h postprandial TG. There was strong correlation between fasting TG and 2 h postprandial TG with 4 h postprandial TG (r = 0.731; p < 0.0001 dan r = 0.669; p < 0.0001, respectively). Whereas body mass index (BMI) and age showed weak correlation with 4 h postprandial TG (r = 0.141; p < 0.0001 dan r = 0.0747; p < 0.0001), fasting TG was the strongest predictor of 4 h postprandial TG (r = 0.669, B = 1.722 (95% CI 1.552 to 1.892), p < 0.0001). CONCLUSION: Fasting TG was the strongest determinant of 4 h postprandial TG in healthy young adults. We also observed strong correlation between 4 h postprandial TG and fasting TG. Hence, 4 h postprandial TG might potentially replaced fasting TG when measurement of fasting TG is not feasible.