Effects Of Exercise Training And Chlorogenic Acid Supplementation On Hepatic Lipid Metabolism In Prediabetes Mice

Background@#Since prediabetes is a risk factor for metabolic syndromes, it is important to promote a healthy lifestyle to prevent prediabetes. This study aimed to determine the effects of green coffee (GC), chlorogenic acid (CGA) intake, and exercise training (EX) on hepatic lipid metabolism in prediabetes male C57BL/6 mice. @*Methods@#Forty-nine mice were randomly divided into two groups feeding with a normal diet (n=7) or a high-fat diet (HFD, n=42) for 12 weeks. Then, HFD mice were further divided into six groups (n=7/group): control (pre-D), GC, CGA, EX, GC+EX, and CGA+EX. After additional 10 weeks under the same diet, plasma, and liver samples were obtained. @*Results@#HFD-induced prediabetes conditions with increases in body weight, glucose, insulin, insulin resistance, and lipid profiles were alleviated in all treatment groups. Acsl3, a candidate gene identified through an in silico approach, was lowered in the pre-D group, while treatments partly restored it. HFD induced adverse alterations of de novo lipogenesis- and β oxidation-associated molecules in the liver. However, GC and CGA supplementation and EX reversed or ameliorated these changes. In most cases, GC or CGA supplementation combined with EX has no synergistic effect and the GC group had similar results to the CGA group. @*Conclusion@#These findings suggest that regular exercise is an effective non-therapeutic approach for prediabetes, and CGA supplementation could be an alternative to partially mimic the beneficial effects of exercise on prediabetes.

Genetic approaches toward understanding the individual variation in cardiac structure, function and responses to exercise training

Cardiovascular disease (CVD) accounts for approximately 30% of all deaths worldwide and its prevalence is constantly increasing despite advancements in medical treatments. Cardiac remodeling and dysfunction are independent risk factors for CVD. Recent studies have demonstrated that cardiac structure and function are genetically influenced, suggesting that understanding the genetic basis for cardiac structure and function could provide new insights into developing novel therapeutic targets for CVD. Regular exercise has long been considered a robust nontherapeutic method of treating or preventing CVD. However, recent studies also indicate that there is inter-individual variation in response to exercise. Nevertheless, the genetic basis for cardiac structure and function as well as their responses to exercise training have yet to be fully elucidated. Therefore, this review summarizes accumulated evidence supporting the genetic contribution to these traits, including findings from population-based studies and unbiased large genomic-scale studies in humans.

Genetic approaches toward understanding the individual variation in cardiac structure, function and responses to exercise training

Cardiovascular disease (CVD) accounts for approximately 30% of all deaths worldwide and its prevalence is constantly increasing despite advancements in medical treatments. Cardiac remodeling and dysfunction are independent risk factors for CVD. Recent studies have demonstrated that cardiac structure and function are genetically influenced, suggesting that understanding the genetic basis for cardiac structure and function could provide new insights into developing novel therapeutic targets for CVD. Regular exercise has long been considered a robust nontherapeutic method of treating or preventing CVD. However, recent studies also indicate that there is inter-individual variation in response to exercise. Nevertheless, the genetic basis for cardiac structure and function as well as their responses to exercise training have yet to be fully elucidated. Therefore, this review summarizes accumulated evidence supporting the genetic contribution to these traits, including findings from population-based studies and unbiased large genomic-scale studies in humans.

Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed across SED groups. For responses to exercise training, there was a significant interaction between mouse strain and training intensity on EDR. Exercise training had no effect on EDR in aortas from 129S1 and B6 mice. In NON, EDR was improved in aortas from MOD and HIT compared with respective SED, accompanied by diminished responses to PE in those groups. Interestingly, EDR was impaired in aorta from SJL HIT compared with SED. The transcriptional activation of endothelial genes was also influenced by the interaction between mouse strain and training intensity. The number of genes altered by HIT was greater than MOD, and there was little overlap between genes altered by HIT and MOD. HIT was associated with gene pathways for inflammatory responses. NON MOD genes showed enrichment for vessel growth pathways. These findings indicate that exercise training has non-uniform effects on endothelial function and transcriptional activation of endothelial genes depending on the interaction between genetic background and training intensity.

Diagnostic Utility of Carbohydrate-deficient Transferrin as a Marker of Alcohol Dependence / 대한진단검사의학회지

BACKGROUND: Biochemical markers can provide objective evidence of heavy alcohol drinking. In this study, we investigated the diagnostic usefulness of carbohydrate-deficient transferrin (CDT), a relatively new marker of alcohol consumption. METHODS: We consecutively enrolled 81 participants aged between 28 and 69 years, consisting of 44 alcohol-dependent patients and 37 age-matched controls. Relative values (%) of CDT were determined in their sera with turbidimetric immunoassay (Bio-Rad %CDT assay, Axis-Shield ASA, Oslo, Norway), and were compared with two conventional markers of alcohol consumption, gammaglutamyl transferase (GGT) and mean corpuscular volume (MCV). RESULTS: The distribution patterns of %CDT among alcohol-dependent patients and controls were significantly different from each other (P=0.0000). Of the 44 alcohol-dependent patients, positive results of %CDT (> or =2.6%), GGT (>50 IU/L), and MCV (>98 fL) were observed in 43 (97.7%), 35 (79.5%), and 24 (54.5%) patients, respectively. The areas under the receiver operating characteristic (ROC) curves (95% confidence interval) for %CDT, GGT, and MCV were 0.995 (0.946-1.000), 0.894 (0.805-0.951), and 0.768 (0.661-0.855), respectively. Discrimination between alcohol-dependent patients and controls, as measured by the areas under the ROC curves, was significantly better for %CDT than for GGT and MCV (P=0.000 and P=0.006, respectively). CONCLUSIONS: CDT seems to be the most reliable of the three markers tested for chronic alcohol consumption, and it may provide a useful information to for the objective detection of alcohol-dependent patients.