RESUMEN
Lifestyle modification and health behavior practice among the individuals with cardiometabolic diseases (CMD) are important for secondary prevention and disease control. This study was designed to investigate and compare health behavior practices among Chinese and Filipino Americans with CMD. Three hundred seventy-four Asian Americans (211 Chinese and 163 Filipino) who reside in the greater Philadelphia region and had either CMD or no identified disease were included in the study. Information on smoking, alcohol intake, physical activity, and salt and sweets consumption was collected, as well as demographic and acculturative characteristics. Of the 374 participants, 241 (64.4%) had CMD and 133 (35.6%) had no identified disease. The majority of Chinese and Filipino Americans with CMD failed to meet the dietary and physical activity guidelines, and only a small percentage of them restricted their amount of salt added to food and amount of sweets consumption. Compared to participants with no disease, Chinese participants with CMD were more likely to "never" add salt to food (AOR 4.42 compared to "frequently"). Filipino Americans with CMD were less likely to be those who "never" consume sweets than those who frequently consume sweets (AORâ¯=â¯0.12). Among the participants with CMD, Chinese participants with CMD were less likely to restrict drinking (AOR 0.11) than Filipinos with CMD. The findings suggest that tailored interventions for Chinese and Filipino Americans with CMD should be developed to enhance their compliance to behavioral guidelines to prevent further disease progression and complications.
RESUMEN
Cytoplasmic overexpression of Akt in the heart results in a myopathy characterized by organ and myocyte hypertrophy. Conversely, nuclear-targeted Akt does not lead to cardiac hypertrophy, but the cellular basis of this distinct heart phenotype remains to be determined. Similarly, whether nuclear-targeted Akt affects ventricular performance and mechanics, calcium metabolism, and electrical properties of myocytes is unknown. Moreover, whether the expression and state of phosphorylation of regulatory proteins implicated in calcium cycling and myocyte contractility are altered in nuclear-targeted Akt has not been established. We report that nuclear overexpression of Akt does not modify cardiac size and shape but results in an increased number of cardiomyocytes, which are smaller in volume. Additionally, the heart possesses enhanced systolic and diastolic function, which is paralleled by increased myocyte performance. Myocyte shortening and velocity of shortening and relengthening are increased in transgenic mice and are coupled with a more efficient reuptake of calcium by the sarcoplasmic reticulum (SR). This process increases calcium loading of the SR during relengthening. The enhanced SR function appears to be mediated by an increase in SR Ca2+-ATPase2a activity sustained by a higher degree of phosphorylation of phospholamban. This posttranslational modification was associated with an increase in phospho-protein kinase A and a decrease in protein phosphatase-1. Together, these observations provide a plausible biochemical mechanism for the potentiation of myocyte and ventricular function in Akt transgenic mice. Therefore, nuclear-targeted Akt in myocytes may have important implications for the diseased heart.