The Indonesian Biomedical Journal

33-56

Authors: Anna Meiliana, Andi Wijaya

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.

65-70

Authors: Johnson Wijaya, Marsetio Donosepoetro, Syakib Bakri

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.

76-80

Authors: Yani Lina, Gatot Susilo Lawrence, Andi Wijaya, Suryani As'ad

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.

88-96

Authors: Siti Nurul Mubarokah, I Dewa Agung Susilawati, Sumarno Sumarno, I Ketut Gedhe Muliartha, Djanggan Sargowo

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.