Polymorphism of the CD36 Gene and Cardiovascular Risk Factors in Patients with Coronary Artery Disease Manifested at a Young Age

This study investigates potential associations between CD36 gene variants and the presence of risk factors in Caucasians with coronary artery disease (CAD) manifested at a young age. The study group consisted of 90 patients; the men were ≤ 50 years old and the women were ≤ 55 years old. Amplicons of exons 4 and 5 including fragments of introns were analyzed by DHPLC. Two polymorphisms were found: IVS3-6 T/C (rs3173798) and IVS4-10 G/A (rs3211892). The C allele of the IVS3-6 T/C polymorphism was associated with higher prevalence of obesity and diabetes, higher hsCRP, lower Lp(a) serum concentrations, and younger age at myocardial infarction. The A allele of the IVS4-10 G/A polymorphism was associated with older age of myocardial infarction and higher white blood cell count. The functional role of CD36 polymorphisms in CAD development needs further research

Effects of different protein content and glycemic index of ad libitum diets on diabetes risk factors in overweight adults: the DIOGenes multicentre, randomised, dietary intervention trial.

Aims/hypothesis: Diets with different amounts of protein and glycemic index (GI) may be of importance in the control of body weight and metabolic consequences, especially those related to insulin sensitivity. Methods: In DIOGenes, overweight/obese adults in 8 European countries who lost ≥ 8% of initial body-weight (BW) after following a low calorie diet (LCD) were later randomly assigned into five ad libitum interventional groups during 6 months: Low Protein [LP]/Low GI [LGI]; LP/High GI [HGI]; High Protein [HP]/LGI; HP/HGI and a healthy control diet. BW, fasting plasma glucose and insulin as well as an oral glucose tolerance test (OGTT), HOMA-IR, adiponectin and fructosamine levels were determined at the three time points. Results: The LCD period was initiated by 932 adults, 773 were randomised to the 5 diets and 548 completed the intervention. The HP and LGI diets were related to weight-loss management (p<0.05). The LP/HGI diet induced a higher HOMA-IR increase during the 6 months period. The HP and LGI diets were related to decreasing HOMA-IR changes in those patients with the highest weight-loss (≥10% of initial body-weight). The LGI diet also lead to a decrease in fructosamine levels during the intervention (p<0.05). Plasma insulin response was lower in the HP/LGI after 60 and 90min of the beginning of the OGTT at the end of the 6-months intervention (p<0.05). Conclusion/Interpretation: An increase in dietary protein and a reduction in GI content over a 6-month ad libitum dietary intervention are related to a lower drop-out rate and Accepted Article 4 produced favorable effects on glycaemic control and insulin sensitivity in overweight/obese subjects after an initial body-weight loss. The study was registered with ClinicalTrials.gov, number NCT00390637

Distribution Patterns of the Mexican Species of Carrion Beetles (Coleoptera: Silphidae)

Fig. 3. Individualized tracks of silphid species in Mexico. A) Oxelytrum discicolle (black circles) and Thanatophilus lapponicus (black squares), B) Thanatophilus truncatus. Arrow with continuous line = direction of the track; arrows with discontinuous line = records from North America.Published as part of &lt;i&gt;Márquez, Juan, Escoto-Rocha, Jaime &amp; Goyenechea, Irene, 2015, Distribution Patterns of the Mexican Species of Carrion Beetles (Coleoptera: Silphidae), pp. 813-823 in The Coleopterists Bulletin 69 (4)&lt;/i&gt; on page 816, DOI: 10.1649/0010-065x-69.4.813, &lt;a href="http://zenodo.org/record/10106634"&gt;http://zenodo.org/record/10106634&lt;/a&gt

Obesity-related polymorphisms and their associations with the ability to regulate fat oxidation in obese europeans:The NUGENOB Study

International audienceBoth obesity and insulin resistance have been related to low fat oxidation rates, which may be genetically determined. The association between variation in fat oxidation rates among obese subjects and genotype was studied for 42 common single-nucleotide polymorphisms (SNPs) in 26 candidate genes for fat oxidation, insulin resistance, and obesity, including FTO. Energy expenditure (EE) and fat oxidation were measured with indirect calorimetry during fasting and 3 h after a high fat load containing 95 energy% of fat (60% saturated fat, energy content 50% of estimated resting EE) in 722 obese subjects (541 women, 181 men) from 8 European centers. After adjustment for center and gender, -178 A>C CD36 (rs2232169) (P = 0.02), -22510 C>G SLC6A14 (women, rs2011162) (P = 0.03), and T690S C>G PCSK1 (rs6235) (P = 0.02) were related to a reduced fat oxidation, whereas 17 C>G SREBF1 (17 C>G) (P = 0.01) was related to increased fat oxidation in the fasting state. The ability to increase fat oxidation after a high fat load was increased in subjects with -174 G>C IL6 (rs1800795) (P = 0.01). Effect sizes range from 1.1 to 3.1% differences in fat oxidation (expressed as % of EE). FTO rs9939609 was not related to fat oxidation. At the same time, the results are not adjusted for multiple testing, thus none of the associations can be considered statistically significant. The results should therefore only be considered as leads to new hypotheses about effects of specific genetic polymorphisms on fasting and postprandial fat oxidation

Glucose levels and genetic variants across transcriptional pathways: interaction effects with BMI.

Objective: Much of the genetic variation in glucose levels remains to be discovered. Especially, research on gene–environment interactions is scarce. Overweight is one of the main risk factors for hyperglycemia. As transcriptional regulation is important for both weight maintenance and glucose control, we analyzed 353 single nucleotide polymorphisms (SNPs), occurring in transcriptional pathways of glucose and lipid metabolism in interaction with body mass index (BMI) on glucose levels. Research design and methods: SNPs were measured in 3244 participants of the Doetichem cohort. Non-fasting glucose levels and BMI were measured twice in 6 years. SNP × BMI interactions were analyzed by mixed models and adjusted for age, sex, time since last meal, and follow-up time. False discovery rate (FDR) 28¿kg¿m–2. A small intervention study (n=120) showed similar, though non-significant, results. Conclusions: Using a pathway-based approach, we found that BMI significantly modified the association between two SNPs in the PPARGC1A gene and glucose levels. The association between glucose and PPARGC1A was only present in lean subjects. This suggests that the effect of the PPARGC1A gene, which is involved both in fatty acid oxidation and glucose metabolism, is modified by BM