The Indonesian Biomedical Journal (Prodia Education and Research Institute)
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Gut Hormones and Energy Balance, The Future for Obesity Therapy?
No full textBACKGROUND: 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
Metabolic Syndrome (MetS) and Nonalcoholic Steatohepatitis (NASH): Study of biochemical markers Free Fatty Acid (FFA), Total Antioxidant Status (TAOS), Adiponectin, Transforming Growth Factor (TGF-beta1), in occurence of NASH
Get PDFBACKGROUND: The prevalence of metabolic syndrome (MetS) in USA and Makassar are 22% and 23.7%. The prevalence of Non Alcoholic Steatosis Hepatosis (NASH) in MetS has not been reported. Study in Non-alcoholic Fatty Liver Disease (NAFLD) is 25–90 % in obesity patients. In NASH, there is accumulation of lipid in hepatocyte (raised free fatty acid level), raised stress oxidative (decreased total antioxidant status), raised of inflammation process (decreased adiponectin) and hepatic fibrotic process (raised TGF β1). The aim of this study is to investigate the correlation of free fatty acid, total antioxidant status, adiponectin and TGF-β1 with the occurrence of NASH.METHODS: This was a case control study in man aged ≥30 years old. Metabolic syndrome (MetS) was defined by IDF categories. NASH was defined as fatty liver plus raised type IV collagen level ≥140 ng/ml and Alanine Transferase (ALT) level 1.5x upper normal limit.RESULT: The samples consisted of 8 MetS subjects, 11 MetS subjects with fatty liver and 2 MetS subjects with suspect NASH. Low level of adiponectin and high level free fatty acid led to progression from Fatty Liver (FL) to NASH. Level of total antioxidant and Level of TGF-β1 were relatively steady in NASH.CONCLUSION: The level of Free Fatty acid in subjects with MetS-FL was higher than in subjects with MetS, but was lower than in subjects with MetS-NASH. No difference in total antioxidants status level was observed among all groups. Level of adiponectin decreased in subjects with MetS-FL and MetS-NASH compared with subjects with MetS only. The level of TGF-β1 increased in subjects with MetS-FL more than in subjects with MetS only, and was steady low in subjects with MetS-NASH.KEYWORDS: metabolic syndrome, NASH, free fatty acid, total antioxidant status, adiponectin, transforming growth factor β
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
No full textBACKGROUND: 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, adiponecti
Peroxisome Proliferator–Activated Receptors and The Metabolic Syndrome
Get PDFBACKGROUND: Obesity is a growing threat to global health by virtue of its association with insulin resistance, inflammation, hypertension, and dyslipidemia, collectively known as the metabolic syndrome (MetS). The nuclear receptors PPARα and PPARγ are therapeutic targets for hypertriglyceridemia and insulin resistance, respectively, and drugs that modulate these receptors are currently in clinical use. More recent work on the PPARδ has uncovered a dual benefit for both hypertriglyceridemia and insulin resistance, highlighting the broad potential of PPARs in the treatment of metabolic disease.CONTENT: We have learned much about PPARs, the metabolic fat sensors, and the molecular pathways they regulate. Through their distinct tissue distribution and specific target gene activation, the three PPARs together control diverse aspects of fatty acid metabolism, energy balance, insulin sensitivity glucose homeostasis, inflammation, hypertension and atherosclerosis. These studies have advanced our understanding of the etiology for the MetS. Mechanisms revealed by these studies highlight the importance of emerging concepts, such as the endocrine function of adipose tissue, tissue-tissue cross-talk and lipotoxicity, in the pathogenesis of type 2 diabetes mellitus and CVD.SUMMARY: The elucidation of key regulators of energy balance and insulin signaling have revolutionized our understanding of fat and sugar metabolism and their intimate link. The three ‘lipidsensing’ (PPARα, PPARγ and PPARδ) exemplify this connection, regulating diverse aspects of lipid and glucose homeostasis, and serving as bonafide therapeutic targets.KEYWORDS: Peroxisome Proliferator, Activated Receptor, Metabolic Syndrom
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
No full textBACKGROUND: 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-
The Role of High Concentration of Resistin in Endothelial Dysfunction Through Induction of Proinflammatory Cytokines Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-6 (IL-6) and Chemokin Monocyte Chemotactic Protein-1 (MCP-1)
No full textBACKGROUND: Many previous studies have reported that central obesity is related to inflammation and endothelial dysfunction. It has also been reported that resistin can induce proinflammatory cytokines TNF-α and IL-6, which can result in endothelial dysfunction, although the role of resistin in human remains unclear. The aim of this study was to assess the role of resistin in influencing the proinflammatory cytokines TNF-α, IL-6, and chemokin MCP-1 in nondiabetic, central obese individuals. Results of this study are hoped to be useful to make a strategy for early prevention of endothelial dysfunction especially in obese individuals.METHOD: This was a cross-sectional study on 73 non diabetic obese male subjects (waist circumferences >90 cm). Resistin, hs-TNF-α, IL-6, MCP-1, VCAM-1 were assessed by ELISA. Statistical analysis was performed using SPSS for Windows v.11.5 with significance p<0.05. The correlations among biomarkers were assessed using Spearman’s Rho test.RESULTS: The study results showed a significant correlation between resistin and TNF-α (r=0.274, p<0.005), and a significant correlation between TNF-α and IL-6 (r=0.430, p<0.001). It was found that high concentration of resistin caused the concentration of TNF-α , IL-6 and MCP-1 to increase, and affected the increase of VCAM-1 (p=0.0030), A significant correlation between waist circumference and inflammation (hsCRP, r=0.296, p<0.005; IL-6, r=0.374, p<0.001 and HOMA IR, r=0.331, p<0.001) was also found.CONCLUSION: This study showed that the role of resistin in endothelial dysfunction occurred at a high concentration of resistin through induction of proinflammatory cytokines TNF-α, IL-6, and chemokin MCP-1. We suggest that inflammation in obesity starts with a positive feedback loop mechanism between resistin and TNF-α.KEYWORDS: obesity, inflammation, adipocytokines, resistin, tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, vascular cell adhesion molecule–
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
No full textBACKGROUND: 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-I
Biochemical Markers for Determining Vulnerable Atherosclerotic Plaque in Stenotic Patient: Biochemical Markers Study of Myeloperoxidase (MPO), Matrix Metallo-Proteinase-9 (MMP-9), Secretory Phospholipase A2 (SPLA2) and CD40 Ligand
No full textBACKGROUND: Thrombus is a main cause of cardiac death. Therefore identifying which coronary artery plaque is vulnerable to rupture is a critical step for cardiac intervention to prevent future cardiac events. Systemic biochemical markers are used for predicting rupture of coronary plaque or identifying stenotic coronary artery plaque(s) vulnerable to rupture.METHODS: Blood samples of 2x24 locations (2x10 controls, 2x12 stable plaques and 2x2 unstable plaques) of 13 patients to undergo stent placement were taken from an artery which showed no stenosis (control), 70% or more stenosis of stable plaques and unstable plaques, respectively. The blood samples were taken by using microcatheter distally and proximally. Concentrations of MPO, MMP-9, SPLA2 and CD40L of each sample were assayed.RESULTS: Concentration of MMP-9 in unstable coronary artery plaque (94.7+14.4 ng/ml) significantly increased compared with that of stable coronary artery plaque (71.0+67.8 ng/ml, p=0.024). SPLA2 concentration significantly decreased in unstable coronary artery plaque (45.9+14.0 pg/ml) compared with that of stable coronary artery plaque (80.9+39.3 pg/ml, p=0.015). Nine of ten studied subjects showed an average of 14.5% (range: 0.0-28.8%) decrease of the SPLA2 concentration in stable plaques compared with that of the non-stenotic coronary artery.CONCLUSION: MMP-9 increased in unstable coronary artery plaque compared with that of stable coronary plaque. Unstable coronary artery plaques absorbed SPLA2 from the vasculars more than the stable plaques and control plaques. MMP-9 and SPLA2 may be used as markers of stability of a plaque in coronary artery in relation to its rupture potential.KEYWORDS: stable and unstable plaque, myeloperoxidase, matrix metalloproteinase-9, secretory phospholipase A2, CD40 Ligan
Development of Immunopathobiogenesis on SIRS-Sepsis
Get PDFOver the past decade, sepsis has been diagnosed according to consensus guidelines established in 1991 as an infection in addition to the symptoms of systemic inflammatory response syndrome (SIRS). In addition to the previous criteria, the 2001 conference added several new diagnostic criteria for sepsis. Of particular interest was the inclusion of the biomarkers procalcitonin (PCT) and C-reactive protein (CRP), despite the overall conclusion that it was premature to use biomarkers for sepsis diagnosis. The primary recommendation of the panel was the implementation of the Predisposition, insult Infection, Response, and Organ dysfunction (PIRO).The immune system has traditionally been devided into innate and adaptive components, each of which has a different role and function in defending the host against infectious agents. Stimulation of different TLRs induces distinct patterns of gene expression, which not only leads to the activation of innate immunity but also increasing evidence supports an additional critical role for TLRs in orchestrating the development of adaptive immune responses.The superantigens are able to induce toxic shock syndrome and can sometimes cause multiple organ failure via adaptive immune system. The superantigenic activity of the bacterial exotoxins can be attributed to their ability to cross-link major histocompatibility complex class II molecules on antigen-presenting cells outside the peptide groove with T-cell receptors to form a trimolecular complex. This trimolecular interaction leads to uncontrolled release of a number of proinflammatory cytokines. Proinflammatory cytokines especially IFN-γ and TNF-α, the key cytokines causing toxic shock syndrome.KEYWORDS: sepsis, innate immunity, adaptiv
Biochemical Markers for Differential Diagnosis of Stroke: A Biochemical Markers Study of S100B Protein, Neuron Spesific Enolase (NSE), Myelin Basic Protein (MBP), and Heart-Type Fatty Acid Binding Protein (H-FABP)
Get PDFBACKGROUND: Differential diagnosis between hemorrhagic and ischemic stroke, which determine how to treat the patients, was performed by CT-Scan. CT-Scan is not always available in all Indonesian health care facility. Other alternative using biochemical markers needed to be studied.METHODS: In total of 44 stroke patients consist of 25 ischemic and 19 hemorrhagic strokes according to CTScan, participated in this study. S100B Protein, NSE, MBP and H-FABP concentration in the blood of each stroke patient was determined.RESULTS: Among the biochemical markers used, only MBP at cut off point 0,712 ng/ml could be used for diagnosing hemorrhagic from ischemic stroke for serum samples obtained until 72 hours after onset of the stroke. If samples could be obtained within 24 hours, S100B Protein and MBP could be used for diagnosing hemorrhagic from ischemic stroke. If both markers increased (S100B Protein >7.55 pg/ml and MBP >0.109 ng/ml) sensitivity and specificity would be 77.8% and 84.6% respectively.CONCLUSIONS: MBP and S100B Protein are promising markers for differential diagnosis of hemorrhagic from ischemic stroke. Using serum samples obtained within 24 hours after onset and multiple markers (MBP and S100B Protein) will improved diagnostic performance of the test.KEYWORDS: Stroke, S100B Protein, Neuron Specific Enolase, Myelin Basic Protein, and Heart-Type Fatty Acid Binding Protei