METHODS AND STUDY DESIGN: A cross-sectional study was conducted on 112 healthy men and women from 3 main ethnic group (Malay, Chinese, and Indian) who were aged 18-60 years. The participants were categorized into normal body mass index (BMI), overweight and obese groups according to WHO criteria for BMI in Asian populations (18.5 kg/m2overweight, and obese groups (p<0.05). Contrastingly, the PLT did not vary significantly among the 3 groups. In addition, sP-sel levels correlated significantly with BMI (r=0.36, p=0.001) and WC (r=0.25, p=0.007) and MPV correlated significantly with BMI (r=0.2, p=0.001) and WC (r=0.2, p=0.003).
CONCLUSIONS: Higher MPV and sPsel levels in the obese participants than in the overweight and normal BMI participants indicated potentially higher activation of platelets in people with obesity. Moreover, we observed higher sCD40L levels in obese participants than in the overweight and normal BMI participants, suggesting a proinflammatory state in obese individuals.
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.
METHODS: The study involved 235 Malaysian subjects who were randomly selected (66 normal weight subjects, 97 overweight, 59 obese subjects, and 13 subjects who were underweight). Serum sDPP4 and active GLP-1 levels were examined by enzyme-linked immunosorbent assay (ELISA). Also, body mass index kg/m(2) (BMI), lipid profiles, insulin and glucose levels were evaluated. Insulin resistance (IR) was estimated via the homeostasis model assessment for insulin resistance (HOMA-IR).
RESULTS: Serum sDPP4 levels were significantly higher in obese subjects compared to normal weight subjects (p=0.034), whereas serum levels of active GLP-1 were lower (p=0.021). In obese subjects, sDPP4 levels correlated negatively with active GLP-1 levels (r(2)=-0.326, p=0.015). Furthermore, linear regression showed that sDPP4 levels were positively associated with insulin resistance (B=82.28, p=0.023) in obese subjects.
CONCLUSION: Elevated serum sDPP4 levels and reduced GLP-1 levels were observed in obese subjects. In addition, sDPP4 levels correlated negatively with active GLP-1 levels but was positively associated with insulin resistance. This finding provides evidence that sDPP4 and GLP-1 may play an important role in the pathogenesis of obesity, suggesting that sDPP4 may be valuable as an early marker for the augmented risk of obesity and insulin resistance.