A metabolically healthy profile is a transient stage when exercise and diet is not supervised: long-term effects in the EXERDIET-HTA study

Metabolically unhealthy obesity (MUO) is a regular state in people with primary hypertension (HTN), obesity and physically inactive. To become and maintain a metabolically healthy overweight/obese (MHO) state should be a main treatment. The aims of the study were 1) to determine differences in metabolic profiles of overweight/obese, physically inactive individuals with HTN following a 16-week (POST) supervised aerobic exercise training (SupExT) intervention with an attentional control (AC) group and, 2) to determine whether the changes observed were maintained following six months (6M) of unsupervised time. Participants (n=219) were randomly assigned into AC or SupExT groups. All participants underwent a hypocaloric diet. At POST all participants received diet and physical activity advice for the following 6M, with no supervision. All measurements were assessed pre-intervention (PRE), POST, and after 6M. From PRE to POST, MUO participants became MHO with improved (P<0.05) total cholesterol (TC, ∆=-12.1 mg/dL), alanine aminotransferase ∆=-8.3 U/L), glucose (∆=-5.5 mg/dL), C-reactive protein (∆=-1.4 mg/dL), systolic blood pressure (SBP) and CRF compared to unhealthy optimal cut-off values. However, after 6M, TC, glucose, and SBP returned to unhealthy values (P<0.05). In a non-physically active population with obesity and HTN, a 16-week SupExT and diet intervention significantly improves cardiometabolic profile from MUO to MHO. However, after 6M of no supervision, participants returned to MUO. The findings of this study highlight the need for regular, systematic and supervised diet and exercise programs to avoid subsequent declines in cardiometabolic health

Association of Candidate Gene Polymorphisms With Chronic Kidney Disease: Results of a Case-Control Analysis in the Nefrona Cohort

Chronic kidney disease (CKD) is a major risk factor for end-stage renal disease, cardiovascular disease and premature death. Despite classical clinical risk factors for CKD and some genetic risk factors have been identified, the residual risk observed in prediction models is still high. Therefore, new risk factors need to be identified in order to better predict the risk of CKD in the population. Here, we analyzed the genetic association of 79 SNPs of proteins associated with mineral metabolism disturbances with CKD in a cohort that includes 2, 445 CKD cases and 559 controls. Genotyping was performed with matrix assisted laser desorption ionizationtime of flight mass spectrometry. We used logistic regression models considering different genetic inheritance models to assess the association of the SNPs with the prevalence of CKD, adjusting for known risk factors. Eight SNPs (rs1126616, rs35068180, rs2238135, rs1800247, rs385564, rs4236, rs2248359, and rs1564858) were associated with CKD even after adjusting by sex, age and race. A model containing five of these SNPs (rs1126616, rs35068180, rs1800247, rs4236, and rs2248359), diabetes and hypertension showed better performance than models considering only clinical risk factors, significantly increasing the area under the curve of the model without polymorphisms. Furthermore, one of the SNPs (the rs2248359) showed an interaction with hypertension, being the risk genotype affecting only hypertensive patients. We conclude that 5 SNPs related to proteins implicated in mineral metabolism disturbances (Osteopontin, osteocalcin, matrix gla protein, matrix metalloprotease 3 and 24 hydroxylase) are associated to an increased risk of suffering CKD