Abstrak (156,8 ± 33,1 vs 116,03 ± 5,66) . Begitu pula dengan konsentrasi VEGF pada kelompok anaerobik konsentrasi tertinggi terjadi pada hari pertama (36,37 ± 2,35), sedangkan pada kelompok aerobik konsentrasi VEGF tertinggi terjadi pada hari ke-3 (40,66 ± 1,73). Terdapat korelasi antara konsentrasi HIF-1α dan konsentrasi VEGF jaringan dengan tingkat korelasi sedang (r = 0,59) pada kelompok aerobik dan korelasi yang kuat pada kelompok anaerobik (r = 0,69). Kesimpulan: Aktivitas fisik aerobik dan anaerobik mengakibatkan peningkatan konsentrasi HIF-1α dan VEGF AbstractBackground: Exercise increases the need for oxygen to generate ATP through oxidative phosphorylation. If the high energy demand during exercise is not balanced by sufficient oxygen supply, hypoxia occurs in skeletal muscle tissue leading to upregulation of hypoxia inducible factor-1α (HIF-1α). The activity of HIF-1α increases the expression of various genes in order to reduce the metabolic dependence on oxygen and to increase oxygen supply to the tissue, e.g., VEGF which plays a role in angiogenesis. In myocardium, it is unlcear whether exercise leads to hypoxia and whether HIF-1α and VEGF play a role in the mechanism of hypoxic adaptation. This study aimed to investigate the correlation of HIF-1α and VEGF in heart muscle tissue of rats during aerobic and anaerobic exercise.

Background: Liver is sensitive against hypoxia and hypoxia will stabilize HIF-1α. At the same time, hypoxia will produce reactive oxygen species (ROS) which can be scavenged by Cygb. The purpose of our study is to know, if normobaric hypoxia can induce Cygb expression and its association with HIF-1α stabilization.Methods: This is an experimental study using 28 male Sprague-Dawley rats, 150-200 g weight. Rats are divided into 7 groups: control group and treatment groups that are kept in hypoxic chamber (10% O2: 90% N2) for 6 hours, 1, 2, 3, 7 and 14 days. All rats are euthanized after treatment and liver tissue are isolated, homogenized and analyzed for oxidative stress parameter, expression of Cygb and HIF-1α.Results: Expression of Cygb mRNA and protein was increased on the day-1 after treatment and reach the maximum expression on the day-2 of hypoxia treatment. But, the expression was decreased after the day-3 and slightly increased at the day-14 of hypoxia. The correlation between expression of Cygb and oxidative stress parameter was strongly correlated. Cygb mRNA, as well as protein, showed the same kinetic as the HIF-1, all increased about day-1 and day-2.Conclusion: Systemic chronic hypoxia and/or oxidative stress up-regulated HIF-1α mRNA which is correlated with the Cygb mRNA and protein expression. Cygb mRNA as well as Cygb protein showed the same kinetic as the HIF-1, all increased about day-1 and day-2 suggesting that Cygb could be under the regulation of HIF-1, but could be controlled also by other factor than HIF-1.

Background. Despite significant therapeutic advances, heart failure (HF) remains unacceptably high in morbidity and mortality. Additionally, its high-care and costs make HF a deadly and costly disease. First reported independently by two group of researchers, Apela/Elabela/Toddler (ELA) is the second endogenous apelin-receptor ligand discovered which is encoded from a previously classified non-coding gene, and has emerged as a key signalling-pathway in the cardiovascular system.Aims. To explore and summarise the biological effects and diagnostic potential of ELA as a new biomarker for heart failure.Results. ELA (prepro-ELA 54 AA) is a molecule with three isoforms (ELA 11,16 and 32), recently identified as the second endogenous ligand to APJ-receptor and functions to mediate early cardiac development during zebrafish embryogenesis by inducing cardiogenesis, vasculogenesis and bone formation. In adults, it enhances cardiac contractility, promotes vasodilatory effects, mediates fluid homeostasis, reduces food intake, limits kidney dysfunction and exerts anti-atherosclerotic as well as anti-oxidative properties.Conclusion. These results show that ELA, an endogenous agonist of the APJ-receptor exerts cardiovascular effects comparable and potentially more potent than apelin and is found to be downregulated in experimental models and humans with heart failure.

Latar belakang: Aktivitas fisik sangat dianjurkan dalam program pencegahan, pengobatan, dan rehabilitasi, yang bertujuan untuk mempromosikan kesehatan khususnya kesehatan kardiovaskular. Selain meningkatkan fungsi jantung, ternyata aktivitas fisik juga dapat mengakibatkan kematian mendadak. Pada atlet kematian mendadak sering kali terjadi saat pertandingan olahraga dengan penyebab terbanyak adalah infark miokard. Diduga, pola latihan tanpa hari istirahat turut berperan dalam terjadinya kerusakan otot jantung dan kematian mendadak dalam pertandingan. Penelitian ini bertujuan untuk mempelajari adaptasi otot jantung terhadap aktivitas fisik aerobik dan anaerobik yang dilakukan setiap hari tanpa hari istirahat. Metode: Jaringan otot jantung berasal dari tikus yang diberi aktivitas fisik aerobik dan anaerobik menggunakan treadmill selama 1,3,7 dan 10 hari tanpa hari istirahat. Kemudian dilakukan analisis gas darah dan pemeriksaan hematologi sebagai parameter hipoksia dan adaptasi sistemik tubuh terhadap aktivitas fisik, dan gambaran histopatologi otot jantung sebagai parameter terjadinya kerusakan sel otot jantung. Hasil: Hasil penelitian menunjukkan bahwa aktivitas fisik aerobik dan anaerobik mengakibatkan terjadinya hipoksia sistemik dan menimbulkan respon adaptasi. Kerusakan sel otot jantung terjadi pada hari ke-10 pada kedua kelompok perlakuan, dengan tingkat kerusakan yang lebih berat pada kelompok aktivitas fisik anaerobik. Tingkat protein jaringan pada kelompok anaerobik meningkat secara progresif pada hari ke-10. Kesimpulan: Aktivitas fisik mengakibatkan terjadinya hipoksia dan adaptasi sistemik. Aktivitas fisik aerobik dan anaerobik yang dilakukan selama 10 hari tanpa hari istirahat mengakibatkan kerusakan sel otot jantung.

Worldwide statins are considered to be the first-line pharmacological treatment for dyslipidemia and reducing the risk of coronary heart disease. However, recently various studies have shown its adverse effect on glucose control among diabetic patients and the U.S. Food and Drug Administration have revised statin drug labels to include information that increases in fasting serum glucose and glycated hemoglobin levels have been reported. This systematic review objective is to evaluate the risks and benefits of statins in glucose control management of type 2 diabetes patients based on the 44 published journal articles included and obtained through MEDLINE full text, PubMed, Science Direct, Pro Quest, SAGE, Taylor and Francis Online, Google Scholar, High Wire, and Elsevier Clinical Key. Statins were found to affect glucose control through several ways, namely, by affecting insulin production and secretion by β-pancreatic cells, insulin resistance, insulin uptake by the muscles and adipocytes and production of adipokines. Current evidence available shows that most of the statins give unfavorable side effects with regards to glucose control among diabetic patients. A dose-dependent and time-dependent effect was also observed in some statins which may be present among other statins as well.

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Apelin is a novel adipokine identified as an endogenous ligand of the specific orphan receptor APJ. Among the various isoforms of apelin, an increase in the apelin-36 plasma level has been associated with oxidative stress, and this isoform has various biological effects, such as positive inotropic, vasodilatory, and antiatherosclerotic effects. Therefore, apelin-36 may be used as a biomarker of heart failure (HF). Advances in the understanding of the molecular mechanisms underlying HF cannot be achieved without the use of animal models. However, it is unclear whether chronic systemic hypoxia can cause HF in rats. The present study aimed to determine whether chronic systemic hypoxia can cause HF in rats and whether apelin-36 can be used as a biomarker of HF. The study included Sprague–Dawley rats. The rats were randomly divided into seven groups (n = 4). One of the groups was a control group, and the six other groups were exposed to hypoxia (8% O2) for different durations (6 hours, 1 day, 3 days, 5 days, 7 days, and 14 days). The exposure groups showed ventricular hypertrophy accompanied by myocardial structural damage, which indicated ventricular remodeling. In addition, the exposure groups showed elevated apelin-36 plasma levels and signs of oxidative stress. Moreover, gel electrophoresis of heart tissue showed five bands that corresponded to apelin isotypes, including apelin-36. In an experimental rat HF model with chronic systemic hypoxia, apelin-36 was elevated along with oxidative stress. Apelin-36 along with oxidative stress may serve as a biomarker of HF in this model.