Serum levels of undercarboxylated osteocalcin are related to cardiovascular risk factors in patients with type 2 diabetes mellitus and healthy subjects

Introduction: Vitamin D receptor (VDR) is encoded by the VDR gene. Several studies have supported that this gene is associated with diabetes. Heterodimer VDR/RXR functions as an enhancer of the BGLAP gene and increases the basal transcription rate of osteocalcin (OC) during osteoblast differentiation. OC is a regulator of glucose metabolism in mice. Moreover, OC level is decreased in patients with type 2 diabetes (T2D). Although inversely correlated with serum glucose insulin and glycated haemoglobin, it is unclear whether OC reduction is caused by diabetes or plays a role in the pathogenesis and/or progression of the disease. In this study we analysed the association between TaqI and ApaI VDR gene polymorphisms and OC serum concentration in T2D subjects. Material and methods: Patients underwent clinical and nutritional assessment. Genomic DNA was extracted from leucocytes using a standard salting-out procedure. The polymorphisms were genotyped by PCR-RFLP method. ELISA was used to measure OC and insulin concentrations. Results: Association between TT genotype of TaqI polymorphism and low levels of OC was observed only in the population with overweight and obesity. No association between TaqI and ApaI polymorphisms and T2D was observed (p > 0.05). Furthermore, in T2D subjects, no correlation between ApaI and TaqI genotypes and age, sex, Body Mass Index (BMI), glucose, or OC was observed. Conclusions: The TT genotype of TaqI VDR gene polymorphism was correlated with low levels of OC in overweight and obese subjects. However, TaqI and ApaI VDR gene polymorphisms were not associated with T2D. (Endokrynol Pol 2015; 66 (4): 329–333) Introduction: Vitamin D receptor (VDR) is encoded by the VDR gene. Several studies have supported that this gene is associated with diabetes. Heterodimer VDR/RXR functions as an enhancer of the BGLAP gene and increases the basal transcription rate of osteocalcin (OC) during osteoblast differentiation. OC is a regulator of glucose metabolism in mice. Moreover, OC level is decreased in patients with type 2 diabetes (T2D). Although inversely correlated with serum glucose insulin and glycated haemoglobin, it is unclear whether OC reduction is caused by diabetes or plays a role in the pathogenesis and/or progression of the disease. In this study we analysed the association between TaqI and ApaI VDR gene polymorphisms and OC serum concentration in T2D subjects. Material and methods: Patients underwent clinical and nutritional assessment. Genomic DNA was extracted from leucocytes using a standard salting-out procedure. The polymorphisms were genotyped by PCR-RFLP method. ELISA was used to measure OC and insulin concentrations. Results: Association between TT genotype of TaqI polymorphism and low levels of OC was observed only in the population with overweight and obesity. No association between TaqI and ApaI polymorphisms and T2D was observed (p > 0.05). Furthermore, in T2D subjects, no correlation between ApaI and TaqI genotypes and age, sex, Body Mass Index (BMI), glucose, or OC was observed. Conclusions: The TT genotype of TaqI VDR gene polymorphism was correlated with low levels of OC in overweight and obese subjects. However, TaqI and ApaI VDR gene polymorphisms were not associated with T2D. (Endokrynol Pol 2015; 66 (4): 329–333)

Studies report that increased body fat can lead to health risks for individuals. However, some methods used for analyzing adiposity did not identify its distribution in the human body because they are typically measured using bioimpedance scales. This study aims to associate the presence of cardiometabolic risk factors in sedentary and active adult populations through anthropometric methods based on skinfold thickness measurements. A cross-sectional study was conducted on 946 adults aged between 18 and 79 years with prior informed consent. Clinical, anthropometric, and biochemical parameters, as well as some cardiometabolic risk factors, were evaluated. Almost half of the population (45.1%; n = 427) is sedentary. A significant association was found between the sum of the skinfolds (bicipital, tricipital, subscapular, and suprailiac) and the cardiometabolic risk factors evaluated, highlighting the cardiovascular risk associated with abdominal obesity, risk of insulin resistance, as well as the development of hyperglycemia, and hypertriglyceridemia. The bicipital fold was thicker (19.67 mm) in the population with a sedentary lifestyle than in the physically active population (18.30 mm). Furthermore, the skinfolds that predict higher metabolic risks were suprailiac and subscapular in sedentary and active populations. Thus, these skinfold measurements could be considered in assessing the adult population for early cardiometabolic risk detection, even in healthy and physically active people.

This study aimed to screen relevant interactions between DRD2/ANKK1 TaqIA polymorphism and dietary intakes with reference to phenotypical features in patients with T2D from western Mexico. In this cross-sectional study, a total of 175 T2D patients were enrolled. Dietary intake was evaluated using 3-day food records and appropriate software. Glycemic and blood lipid profiles were measured by standardized methods. Genotyping of the DRD2/ANKK1 TaqIA polymorphism was performed by the RFLP method. Gene-diet interactions regarding anthropometric and metabolic phenotypes were screened by adjusted multiple linear regression analyses. Genotype frequencies of the DRD2/ANKK1 TaqIA polymorphism were A1A1 (16.0%), A1A2 (52.6%), and A2A2 (31.4%). Statistically significant interactions between the DRD2/ANKK1 TaqIA genotypes and dietary factors in relation to blood triglyceride (TG) levels were found. Carriers of the A1 allele (A1A1 homozygotes plus A1A2 heterozygotes) were protected from TG increases by maltose intake (P int. = 0.023). Instead, A2A2 homozygotes were susceptible to TG rises through consumptions of total fat (P int. = 0.041), monounsaturated fatty acids (P int. = 0.001), and dietary cholesterol (P int. = 0.019). This study suggests that the interactions between DRD2/ANKK1 TaqIA polymorphism and dietary factors (sugar and fats) influence TG levels in diabetic patients.