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INDONESIA
The Indonesian Biomedical Journal
Published by The Prodia Education and Research Institute
ISSN : -     EISSN : -     DOI : -
Core Subject : Health, Science,
Biochemistry, Genetics & Molecular Biology Public Health
Arjuna Subject : -
Articles 8 Documents
 1 
Search results for , issue "Vol 1, No 3 (2009)" : 8 Documents clear
Association Between Free Fatty Acid (FFA) and Insulin Resistance: The Role of Inflammation (Adiponectin and high sensivity C-reactive Protein/hs-CRP) and Stress Oxidative (Superoxide Dismutase/SOD) in Obese Non-Diabetic Individual Indriyanti Rafi Sukmawati; Marsetio Donoseputro; Widjaja Lukito
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.102

Abstract

BACKGROUND: Obesity is highly related to insulin resistance, therefore, the increased number of obesity is followed by the increased prevalence of type 2 Diabetes Melitus. Obesity is associated with increased of reactive oxygen species (ROS) in muscle, liver and endothelial cells. The increase of ROS would lead to insulin resistance (IR) and increased proinflamatory protein. FFA plays an important role in IR by inhibiting muscle glucose transport and oxidation via effects on serin/threonine phosphorylation of IRS-1. The aim of this study was discover the existence of SOD, hs-CRP and and adiponectin levels towards the occurrence of insulin resistance which was caused by elevated level of FFA and to discover the interaction between SOD, hs-CRP and adiponectin in non diabetic obese adult male.METHOD: This was observational study with cross sectional design. There were 65 obese male non diabetic subjects and 45 non obese male non diabetic subjects who met the criteria. In this study, measurements were done on body mass index (BMI), fasting glucose, insulin, adiponectin, hs-CRP and SOD. Obese was defined as BMI >25 kg/m2, normal weight was defined as BMI 18.5-23 kh/m2 and Insulin Resistance was defined as HOMA-IR >1.RESULT: This study showed that Hypoadiponectinemia condition, decreased SOD level and high level of hs-CRP is associated with insulin resistance in obese non diabetic subject. Adiponectin and SOD were correlated negatively with insulin resistance in obese non diabetic (Adiponectin, r=-0.455, p<0.001; SOD, r=-0.262, p=0.003), hs-CRP was positively correlated with insulin resistance in obese non diabetic (r=0.592, p<0.001). FFA levels was increased in obese insulin resistance compared with non obese non insulin resistance. The Odds Ratio of Adiponectin, hs-CRP and SOD in this study was analyzed by logistic binary. The OR for SOD 3.6 (p=0.001), hs-CRP 9.1 (p<0.001) and Adiponectin 7.2 (p<0.001).CONCLUSION: This study suggested that FFA levels  increased in obese insulin resistance as compared with non obese non insulin resistance. Hypoadiponectinemia, decreased SOD and elevated hs-CRP were associated with insulin resistance in obese non diabetic subjects.KEYWORDS: obesity, insulin resistance, FFA, SOD, hs-CRP, adiponectin
Adipose Tissue Biology: An Update Review Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.98

Abstract

BACKGROUND: Obesity is a major health problem in most countries in the world today. It increases the risk of diabetes, heart disease, fatty liver and some form of cancer. Adipose tissue biology is currently one of the “hot” areas of biomedical science, as fundamental for the development of novel therapeutics for obesity and its related disorders.CONTENT: Adipose tissue consist predominantly of adipocytes, adipose-derived stromal cells (ASCs), vascular endothelial cells, pericytes, fibroblast, macrophages, and extracellular matrix. Adipose tissue metabolism is extremely dynamic, and the supply of and removal of substrates in the blood is acutely regulated according to the nutritional state. Adipose tissue possesses the ability to a very large extent to modulate its own metabolic activities including differentiation of new adipocytes and production of blood vessels as necessary to accommodate increasing fat stores. At the same time, adipocytes signal to other tissue to regulate their energy metabolism in accordance with the body's nutritional state. Ultimately adipocyte fat stores have to match the body's overall surplus or deficit of energy. Obesity causes adipose tissue dysfunction and results in obesity-related disorders.SUMMARY: It is now clear that adipose tissue is a complex and highly active metabolic and endocrine organ. Undestanding the molecular mechanisms underlying obesity and its associated disease cluster is also of great significance as the need for new and more effective therapeutic strategies is more urgent than ever. KEYWORDS: Obesity, Adipocyte, Adipose, Tissue, Adipogenesis, Angiogenesis, Lipid Droplet, Lipolysis, Plasticity, Dysfunction  
Fibroblast Growth Factor 21 (FGF21), Free Fatty Acid (FFA), High Sensitivity C-reactive Protein (hsCRP) and Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) Among Indonesian Obese Non-Diabetic Males Yani Lina; Gatot Susilo Lawrence; Andi Wijaya; Suryani As&#039;ad
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.103

Abstract

BACKGROUND: Fibroblast growth factor-21 (FGF21) is known as an important endocrine and paracrine regulator of metabolic homeostasis. Recent studies have shown that FGF21 attenuates lipolysis in human adipocytes, which is suggested as a FGF21's mechanism as anti-hyperlipidemia, anti-hyperglycemia and anti-obesity. The aim of this study was to measure the correlation between FGF21, FFA, hsCRP and HOMA-IR among Indonesian obese non diabetic males.METHOD: The study was observational with cross sectional design. The analysis was done in 137 subjects aged 30-60 years with non diabetic abdominal obesity. We measured the biochemical markers FGF21, FFA, hsCRP, fasting insulin and fasting glucose. We also measured weight, height, waist circumrefence (WC), creatinine, serum glutamin oxaloacetic transaminase (SGOT), and serum glutamic pyruvic transaminase (SGPT), systolic blood pressure (SBP) and diastolic blood pressure (DBP). Correlation between markers was measured using Pearson and Spearman's analysis.  RESULT: There were significant positive correlations between FGF21-HOMA-IR (r=0.314, p=0.000); FGF21-WC (r=0.173, p=0.043); FFA=hsCRP (r=0.270, p=0.001); and WC-HOMA-IR (r=0.279, p=0.001). There was significant negative correlation between FGF21-FFA (r=-0.038, p=0.657) and FGF21-hsCRP (r=-0.061, p=0.482). CONCLUSION: In this study we found that although there was no significant correlation, FGF21 might act as an anti-lipolytic and anti-inflammation agent among Indonesian obese non-diabetic males. Our findings agree with results of previous studies that the positive correlation between FGF21-WC and FGF21-HOMA-IR moght occur as a compensatory mechanism or resistance to FGF21 in obesity.KEYWORDS: Obesity, FGF21, FFA, hsCRP, HOMA-IR
Gut Hormones and Energy Balance, The Future for Obesity Therapy? Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.99

Abstract

BACKGROUND: The prevalence of obesity is increasing in both developed and developing countries along with associated diseases such as type 2 diabetes and coronary heart disease. The recent discovery of a number of gut hormones that play a role in appetite regulation and are released or suppressed in response to a meal may offer new targets for the treatments of obesity.CONTENT: In addition to the obvious role of the gut in the digestion and absorption of nutrient, the intestine and associated visceral organs, including the pancreas, liver, and visceral adipose depots, have important sensing and signaling roles in the regulation of energy homeostatis. Signals reflecting energy stores, recent nutritional state, and other parameters are integrated in the central nervous system, particularly in the hypotalamus, to coordinate energy intake and expenditure.SUMMARY: Our understanding of the role of the gut in energy balance and insights into gut-derived signals will stimulate previously unexplored therapeutics for obesity and other disorders of energy balance.KEYWORDS: obesity, energy, balance, gut hormones, satiation, satiety  
Visfatin and Adiponectin Have an Opposite Correlation with Inflammation and Metabolic Syndrome in Non-Diabetic Obese Indonesian Men Anna Meiliana; Gatot Susilo Lawrence; Ilhamjaya Patellongi; Andi Wijaya; Suryani As&#039;ad
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.104

Abstract

BACKGROUND: Along with the increase in obesity is a parallel increase in the prevalence of metabolic complications of obesity, often referred to as the metabolic syndrome (MetS). The role of adipose tissue in MetS has continued to evolve with the description of numerous secretory peptides from adipocytes named adipocytokines or adipokines. Recent studies have found visfatin as the regulation of inflammatory and immunomodulating prosesses, meanwhile adiponectin was known to have a potent anti-inflammatory properties. Here we try to assess the correlation between those two adipokines to MetS, via an inflammatory pathway.METHODS: This was a cross-sectional study on 128 non diabetic obese male subject (waist circumferences ≥90 cm). Visfatin and adiponectin were assessed by ELISA. Statistical analysis was performed using SPSS for Windows v.16.00 with signifcantly p<0.05. The correlations among biomarkers were assessed using Spearman's Rho test.RESULTS: This study showed a significant positive correlation between levels of visfatin and inflammatory markers TNF-α (r=0.22, p<0.005), and hsCRP (r=0.12, p=0.19), significant negative correlation between levels of adiponectin and TNF-α (r=-0.22-8, p<0.005-1), adiponectin and hsCRP (r=-0.14, p=0.11) and visfatin (r=-0.029, p<0.01). Plasma visfatin levels were increased along with the number MetS components, white plasma adiponectin showed inversely relation.CONCLUSION: Our present study has shown that visfatin has a proinflammatory properties and adiponectin has an anti-inflammatory properties, and how they have an opposite effects on MetS. Visfatin was found to have a positive correlaton while adiponectin was found to have a negative correlation with the number of MetS components.KEYWORDS: Obesity, Inflammation, Metabolic Syndrome, Adipocytokines, Visfatin, Adiponectin, TNF-α, hsCRP
Laboratory Diagnosis of von Willebrand's Disease Mansyur Arif
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.100

Abstract

von Willebrand's disease (vWD) is an autosomally inherited bleeding disorder caused by a deficiency or abnormality of von Willebrand factor (vWF). vWF is a multimeric adhesive protein that plays an important role in primary hemostasis by promoting platelet adhesion to the subendothelium at the sites of vascular injury. It is also the carrier of factor VIII (FVIII), thus indirectly contributing to the coagulation process. Bleeding symptoms are usually mucocutaneous and postsurgical with varying severity. The diagnosis of vWD requires a personal and family history of bleeding and confirmation by laboratory analysis involving vWF antigen level, vWF ristocetin cofactor, FVIII activity, ristocetin-induced platelet aggregation, and vWF multimer analysis.KEYWORDS: von Willebrand's disease, von Willebrand factor
Porphyromonas gingivalis Induced Fragmentation of Type IV Collagen Through Macrophage-Activated MMP-9: (In Vitro Study of Collagenolytic Mechanism in Pathogenesis of Atherosclerotic Plaque Rupture) Siti Nurul Mubarokah; I Dewa Agung Susilawati; Sumarno Sumarno; I Ketut Gedhe Muliartha; Djanggan Sargowo
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.105

Abstract

BACKGROUND: Periodontitis is caused mostly by Porphyromonas gingivalis (P.gingivalis) and it is related to acute coronary syndrome. P.gingivalis  readily invades blood circulation and potentially induces collagenolytic activity of inflammatory cells that results in collagen vascular degradation leading to atherosclerotic plague rupture (APR). APR is responsible for the occurence of fatal cardiovascular events such as acute myocardial infraction (AMI).AIMS: To show that P.gingivalis potentially induces fragmentation of the type IV vascular collagen due to macrophage-activated MMP-9.MATERIAL AND METHODS: The ability of P.gingivalis to induce the type IV collagen fragmentation, shown by digesting type IV collagen with the supernatant of monocyte-derived macrophage activated by exposure to P.gingivalis suspension for 18 hours, 37oC, 5%CO2. The type IV collagen fragments were analyzed by SDS-PAGE and confirmed by Western-blotting. Antibody of type IV collagen produced and confirmed by dot-blotting prior to its being used as primary antibody of Western-blotting. The existence of MMP-9 was detected by Dot-blot and Western-blot technique, while the MMP-9 activity was assessed by SDS-PAGE and zymograms.RESULTS: Our data showed that P.gingivalis induced macrophage to produce MMP-9 as one of collagenolytic components, and interaction with P.gingivalis proteases enhanced the proteolytic activity and resulted in degradation of type IV collagen with molecular weight of 88 kDa into two smaller fragments with molecular weight of 80 kDa and 60 kDa. CONCLUSION: P.gingivalis induced macrophage to activate its MMP-9 that led to fragmentation of vascular type IV collagen in the pathogenesis of atherosclerotic plaque rupture. KEYWORDS: P.gingivalis, macrophage, type IV collagen fragmentation, atherosclerotic plaque rupture, AMI
The Different Concentrations of Transforming Growth Factor-Beta1 (TGF-Beta1), Matrix Metalloproteinase-9 (MMP-9) and Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2) in Normoalbuminuria Normotension, Normoalbuminuria Hypertension Johnson Wijaya; Marsetio Donosepoetro; Syakib Bakri
The Indonesian Biomedical Journal Vol 1, No 3 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i3.101

Abstract

BACKGROUND: Vascular remodeling was an adaptive process of the vascular wall that occured in response to long-term changes in hemodynamic conditions that contribute to the changes of the vascular structure and the pathophysiology of vascular disease. On the other hand, Endothelial Progenitor Cells (EPC) derived from bone marrow had the capacity to migrate to the peripheral circulation and to differentiate into mature endothelial cells. Therefore, EPC could contribute in the endothelial repairing after endothelial injury.METHODS: This study was a cross sectional design. Analysis was done among 30 subjects with normoalbuminuria normotension, 55 subjects with normoalbuminuria hypertension and 30 subjects with with microalbuminuria hypertension. TGF-β1, MMP-9 and VEGFR-2 testing were performed by ELISA method. All statistical calculations were performed using the SPSS 11.5 statistical software package. We used the Independent sample T test, Mann-Whitney, One Way Annova and Kruskal Wallis to establish the difference among various biochemical measures.RESULTS: TGF-β1 concentration was increased from normoalbuminuria normotension to normoalbuminuria hypertension and to microalbuminuria hypertension (27.63178±12.97246 vs. 38.61193±17.09546 vs. 38.73939±12.63911 ng/mL). TGF-β1 concentration was higher significantly in normotension as compared to hypertension (27.63178±12.97246 vs. 38.65692±15.58950, p<0.001) and to microalbuminuria hypertension (38.73939±12.63911, p<0.001). MMP-9 concentration was increased in normotension to normoalbuminuria hypertension but was decreased in microalbuminuria hypertension (438.1967±156.4268 vs. 564.5873±291.2876 vs. 418.6900±188.3801 ng/mL). MMP-9 concentration was higher significantly in normoalbuminuria hypertension as compared to microalbuminuria hypertension (p=0.028). VEGFR-2 concentration was decreased from normotension to normoalbuminuria hypertension to microalbuminuria hypertension (9.90552±1.85185 vs. 9.39561±1.75413 vs. 9.00506±1.47173 ng/mL). VEGFR-2 concentration was higher significantly in normotension as compared to microalbuminuria hypertension (p=0.042). CONCLUSIONS: The increasing concentration level of TGF-β1 and decreasing concentration level of MMP-9 in microalbuminuria hypertension showed that the remodeling process was getting increased. The decreasing concentration level of VEGFR-2 in microalbuminuria hypertension showed that the repairing process was getting decreased.KEYWORDS: vascular remodelling, vascular repairing, TGF-β1, MMP-9, VEGFR-2

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