Garuda - Garba Rujukan Digital

Endothelial Progenitor Cells in Diabetic Vasculopathy Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 2 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i2.89

BACKGROUND: The discovery of endothelial progenitor cell (EPC) a decade ago by Asahara, et al has refuted the previous belief that vasculogenesis only occurs during embryogenesis. The reduced circulating concentration of EPCs is a surrogate marker of endothelial function and has been implicated in the pathogenesis of many vascular diseases.CONTENT: Diabetes is linked to impaired vascular function, including alterations in both endothelial cells and EPCs. A number of studies have shown that individuals with diabetes have decreased level of circulating EPCs and that the severity of disease is inversely proportional to EPC levels. In vitro, hyperglycemia increases the rate of EPC senescence and the angiogenic function of EPCs from patients with either type 1 or type 2 diabetes is impaired such that they are poorly proliferative and fail to incorporate into forming vessel-like structures. Given the comprehensive role of EPC alterations in diabetes complications, modulation of the levels and/or function of EPCs may be considered a potential therapeutic strategy.SUMMARY: The available data demonstrating that decrease or dysfunction of EPCs may have a prominent role in the pathogenesis of all diabetes complications. Further approaches, such as EPC administration, may represent novel treatments for diabetic vasculopathy in the future. To date, many barriers remain to such a therapeutic approach. Firstly, there is no specific marker for EPC at present. Secondly, techniques of EPC isolation are not standardized, preventing direct comparison between various studies. The long-term effects of transplanted EPCs are currently unknown.

The Relationship of Proinflammatory and Antiinflammatory Adipokines in the Development of Metabolic Syndrome in Centrally Obese Men Anna Meiliana; Andi Wijaya; Suryani As'ad
The Indonesian Biomedical Journal Vol 2, No 3 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i3.125

BACKGROUND: The increased prevalence of obesity worldwide is correlated with increasing prevalence of metabolic syndrome. Studies of adipose tissue have been improved from an inert energy storage to a metabolic active endocrine organ. Adipokines secreted by this tissue play a role in maintaining metabolic homeostasis. The large mass of visceral fat tissue causing the imbalance of these adipokines leading to metabolic abnormality known as the metabolic syndrome (MetS). This study was performed to understand relationship of proinflammatory adipokines (resistin, TNF-α, RBP4 and visfatin) and anti-inflammatory adipokines (adiponectin and vaspin) in the development of MetS.METHODS: This was a cross-sectional study using 122 central obesity men with waist circumference >90 cm, age from 30–60 years old. Proinflammatory adipokines (resistin, TNF-α, RBP4 and visfatin) and anti-inflammatory adipokines (adiponectin and vaspin) was measured by ELISA method.RESULTS: The crosstab study showed that subjects who have >2 high proinflammatory adipokines (17.3%) has higher MetS prevalence (OR = 1.16; p = 0.72) compare to subjects with <2 high proinflammatory adipokines (14.8%), subjects with low anti-inflammatory adipokines profile (18.9%) has higher prevalence of MetS (OR=1.38; p=0.22) compare to subjects with high anti-inflammatory adipokines (13.7%) and the prevalence of MetS became 1.49 times higher (p=0.24) when we combine the high RBP4 and low adiponectin profile (21.1%) compare to subjects with low RBP4 and high adiponectin (14%).CONCLUSIONS: This study showed that each adipokine was not strong enough to induce MetS, so the interaction between proinflammatory and antiinflammatory adipokines were needed to induce a systemic metabolic abnormality. Thus, the adipokines equilibrium was important to prevent MetS especially in centrally obese subjects.KEYWORDS: obesity, metabolic syndrome, adipokines, resistin, TNF-α, RBP4, visfatin, adiponectin, vaspin

Brown Adipose Tissue: A New Target for Antiobesity Therapy Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 2, No 2 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i2.115

BACKGROUND: Human fat consist of white and brown adipose tissue (WAT and BAT). Though most fat is energy-storing WAT, the thermogenic capacity of even small amounts of BAT makes it an attractive therapeutic target for inducing weight loss through energy expenditure.CONTENT: Over the past year, several independent research teams used a combination of positron-emission tomography and computed tomography (PET/CT) imaging, immunohistochemistry and gene and protein expression assays to prove conclusively that adult humans have functional BAT. BAT is important for thermogenesis and energy balance in small mammals and its induction in mice promotes energy expenditure, reduces adiposity and protects mice from diet-induced obesity. The thermogenic capacity of BAT is impressive. In humans, it has been estimated that as little as 50g of BAT could utilize up to 20% of basal caloric needs if maximally stimulated.SUMMARY: The obesity pandemic requires new and novel treatments. The past few years have witnessed multiple studies conclusively showing that adult humans have functional BAT, a tissue that has a tremendous capacity for obesity-reducing thermogenesis. Novel therapies targeting BAT thermogenesis may be available in the near future as therapeutic options for obesity and diabetes. Thermogenic ingredients may be considered as functional agents that could help in preventing a positive energy balance and obesity.KEYWORDS: brown adipose tissue, thermogenesis, energy expenditure, antiobesity therapy

Microparticles Novel Mechanisms of Intracellular Communication: Implication in Health and Disease Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 3, No 1 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i1.131

BACKGROUND: The prevailing view that eukaryotic cells are restrained from intercellular exchange of genetic information has been challenged by recent reports on nanotubes, exosomes, apoptotic bodies, and nucleic acid—binding peptides that provide novel pathways for cell—cell communication, with implications in health and disease.CONTENT: Microparticles (MPs) are a heterogeneous population of small plasma membrane structures that serve as important signaling structures between cells. MPs are composed of a phospholipid bilayer that exposes transmembrane proteins and receptors and encloses cytosolic components such as enzymes, transcription factors, and mRNA derived from their parent cells. Growing evidence suggests that MPs regulate inflammation, stimulate coagulation, affect vascular functions and apoptosis, and can also play a role in cell proliferation or differentiation. MPs circulate in the bloodstream, can be detected in the peripheral blood, and may originate from different vascular cell types (eg, platelets, monocytes, endothelial cells, red blood cells, and granulocytes).SUMMARY: Cells of various types release small membrane vesicles called MP on their activation, as well as during the process of apoptosis. The properties and roles of MP generated in different contexts are diverse and are determined by their parent cell and the pathway of their generation, which affects their content. MP are involved in multiple cellular functions, including immunomodulation, inflammation, coagulation, and intercellular communication. MPs are able to deliver molecular signals in the form of lipids, proteins, nucleic acids, or functional trans-membrane proteins from the parent cell to distantly located targets. From a clinical point of view, MP may serve as biomarkers for disease status and may be found useful for developing novel therapeutic strategies.KEYWORDS: microparticles, microvesicle, membrane remodeling, Intercellular communication

The Relationship of Fetuin-A, Adiponectin, Retinol Binding Protein-4 (RBP-4) and High Sensitivity C-Reactive Protein (hsCRP) with Insulin Resistance (HOMA-IR) in Obese Non Diabetic Men Imelda Novianti; Andi Wijaya; Marsetio Donosepoetro
The Indonesian Biomedical Journal Vol 4, No 1 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i1.157

BACKGROUND: Central obesity is the accumulation of visceral (intra-abdominal) fat and is strongly known to be associated with insulin resistance and type 2 diabetes mellitus (T2DM). Obesity can cause adipocyte hypertrophy that results in dysregulation of adipokine expression. The abnormal function of adipocytes may play an important role in the development of a chronic low-grade proinflammatory state associated with obesity. Adiponectin, retinol binding protein (RBP)-4 and fetuin-A play a role in the pathophysiology of insulin resistance. Expression of fetuin-A is increased due to fat accumulation in the liver. Elevated concentration of fetuin-A in the circulation can impair insulin signaling in muscle and liver as well as suppress adiponectin secretion, although its molecular mechanism is still unclear. The aim of this study was to identify the relationship of fetuin-A, adiponectin, RBP-4 and hsCRP with insulin resistance in obese non diabetic men.METHODS: This was an observational study with a cross-sectional design. The study subjects were 64 men with non diabetic abdominal obesity, characterized by waist circumference of 98.47 ± 5.88 cm and fasting blood glucose of 85.75±8.36 mg/dL.RESULTS: This study showed that fetuin-A was positively correlated with HOMA-IR in obese non diabetic men with insulin resistance (r = 0.128; p = 0.570), although not significant. Fetuin-A was found to be correlated with adiponectin, RBP-4 and hsCRP (r=0.150; p=0.233; r=0.050; p=0.711; r=-0.04; p=0.445), although not significant.CONCLUSIONS: The concentration of fetuin-A showed a tendency to be positively correlated with HOMA-IR and with RBP-4 in obese non diabetic men, although statistically not significant. The concentration of fetuin-A showed a tendency to be negatively correlated with adiponectin and hsCRP although statistically not significant. There was no interrelationship between fetuin-A, adiponectin, RBP-4, hsCRP and HOMA-IR. Elevated concentrations of fetuin-A were noted in obese subjects, which in turn might impair insulin signaling. This finding might suggest that fetuin-A may represent a new target for the prevention of insulin resistance. Further studies might be needed on obese population with fatty liver.KEYWORDS: fetuin-A, adiponectin, RBP-4, hsCRP, insulin resistance

Correlation of Apo B-48 and Apo B-100 with Oxidized LDL in Men with Central Obesity Maria Diah Fibriani; Andi Wijaya; Burhanuddin Bahar
The Indonesian Biomedical Journal Vol 2, No 2 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i2.120

BACKGROUND: Obesity has a central role in the metabolic syndrome, which raises the risk for atherosclerotic cardiovascular disease (ASVCD). Apo B-48 and Apo B-100 are the necessary structural proteins required for the assembly and secretion of chylomicron and VLDL which have role in atherogenesis. The key initiating process in atherogenesis is the subendothelial retention of apolipoprotein B-containing lipoproteins. Oxidation of LDL is a hallmark of atherosclerosis development. The aim of this study was to asses the association between Apo B-48 and Apo B-100 with Oxidized-LDL as marker of atherosclerosis risk in central obesity. We hope that the result of this study can help to make a new strategy for the prevention and treatment of vascular disease.RESULTS: There were 68 patients aged 39.6±7.3 years, Apo B-48 concentration was 7.47±5.36 μg/mL, Apo B-100 was 117.26±25.74 mg/dL, and ox-LDL was 137.05±18.88 U/L. This study showed a significant correlation between Apo B-100 and ox-LDL (r=0.608, p<0.05) and correlation between Apo B-48 and ox-LDL (r=0.171, p<0.05). The levels of Apo B-100 were significantly different between obese with Mets and obese without Mets individuals (p<0.05).CONCLUSIONS: This study suggested that Apo B-100 concentration increase in obese in Mets as compared with obese without Mets. Apo B-48 and Apo B-100 were correlated with Oxidized LDL, but correlation between Apo B-100 and ox-LDL more significant that Apo B-48and ox-LDL.KEYWORDS: obesity, atherogenesis, Apo B-48, Apo B-100, ox-LDL

Molecular Regulators of Metabolism and Cardiometabolic Disease Indriyanti Rafi Sukmawati; Andi Wijaya
The Indonesian Biomedical Journal Vol 4, No 3 (2012)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v4i3.173

BACKGROUND: The mechanisms that are responsible for energy management in cells in an organism require a complex network of transcription of factors and cofactors.CONTENT: All living system must maintain a tight equilibrium between energy intake, storage and expenditure for optimal performance. This tight equilibrium must be both robust and flexible to allow for adaptation to every situation such as exercise or rest and famine or feast. Organisms rely on finely tuned and complex signaling network to confront with all possibilities. Metabolic imbalance can cause dysfunction and pertubation of these networks, which if uncorrected will induce disease such as obesity and diabetes mellitus.SUMMARY: During the last decades the understanding of the transcriptional regulation of diverse metabolic pathways has contributed to the elucidation of mechanisms of metabolic control and to a better knowledge of the pathogenesis of metabolic diseases. KEYWORDS: AMPK, SIRT1, PGC-1α, FGF21, mTORC1

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) Anna Meiliana; Ilhamjaya Patellongi; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 2 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i2.90

BACKGROUND: 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–1

Peroxisome Proliferator–Activated Receptors and The Metabolic Syndrome Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 1, No 1 (2009)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v1i1.79

BACKGROUND: 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 Syndrome

Circadian Clock and The Cardiometabolic Risk Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 2, No 2 (2010)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v2i2.116

BACKGROUND: Epidemiological data reveal parallel trends of decreasing sleep duration and increases in metabolic disorders such as obesity, diabetes and hypertension. There is growing evidence that these trends are mechanistically related.CONTENT: The circadian system orchestrates the temporal organization of many aspects of physiology, including metabolism, in synchrony with the 24 hours rotation of the Earth. The circadian system is a complex feedback network that involves interactions between the central nervous system and peripheral tissues. Circadian regulation is intimately linked to metabolic homeostasis and that dysregulation of circadian rhythms can contribute to disease. Conversely, metabolic signals also feed back into the circadian system, modulating circadian gene expression and behavior.SUMMARY: Both inter- and intraorgan desynchrony may be involved in the pathogenesis of cardiometabolic disease attributable to effects in brain and multiple metabolic tissues including heart, liver, fat, muscle, pancreas and gut. Efforts to dissect the molecular mediators that coordinate circadian, metabolic, and cardiovascular systems may ultimately lead to both improved therapeutics and preventive interventions.KEYWORDS: circadian rhythms, clock genes, nuclear receptor, sleep, obesity, cardiometabolic risk

Title

Found 28 Documents
Search

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Title Search

Found 28 Documents Search

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Abstract

Title

Found 28 Documents
Search