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All Journal The Indonesian Biomedical Journal Molecular and Cellular Biomedical Sciences (MCBS)
Anna Meiliana
Department Of Pharmacology And Clinical Pharmacy, Faculty Of Pharmacy, Universitas Padjadjaran, Jl. Raya Bandung-Sumedang Km 21, Jatinangor 45363
Biochemistry, Genetics & Molecular Biology Dentistry Immunology & microbiology Medicine & Pharmacology Neuroscience Public Health

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Chronodisruption and Obesity Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 7, No 3 (2015)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v7i3.184

Abstract

BACKGROUND: Attempts to understand the causes of obesity and develop new therapeutic strategies have mostly focused on caloric intake and energy expenditure. Recent studies have shown that the circadian clock controls energy homeostasis by regulating circadian expression and/or activity of enzymes, hormones, and transport systems involved in metabolism. Moreover, disruption of circadian rhythms leads to obesity and metabolic disorders.CONTENT:Regularly alternating periods of light and darkness, such as normally occur with the rising and the setting of the sun, are essential for the maintenance of undisturbed circadian rhythms in all organisms including humans. The light-dark environment, as detected by specialized photoreceptors in the retinas, impacts the endogenous circadian clock in the anterior hypothalamus, the suprachiasmatic nuclei. These nuclei, via both neural and humoral signals, communicate with cells throughout the organism to establish regular circadian rhythms. The introduction of artificial sources of light roughly 150 years ago has significantly undermined the naturally occurring light-dark environment and, likewise, has disturbed circadian rhythms since light is now available at unusual times, i.e., at night. Light at night is known to cause circadian disruption and melatonin suppression. Many potentially pathophysiological consequences of these artificial light-mediated changes, include cancer, cardiovascular diseases, insomnia, metabolic syndrome, diabetes, and cognitive disorders may be aggravated by the increased exposure to light at night, which is inevitable in well-developed societies that have undergone extensive electrification.SUMMARY: Therefore, it is plausible that resetting of the circadian clock can be used as a new approach to attenuate obesity. Feeding regimens, such as restricted feeding, calorie restriction and intermittent fasting, provide a time cue and reset the circadian clock and lead to better health. In contrast, high-fat diet leads to disrupted circadian expression of metabolic factors and obesity.KEYWORDS: obesity, circadian clock, metabolism, chronodisruption
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  
Mitochondria in Health and Disease Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 11, No 1 (2019)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v11i1.779

Abstract

BACKGROUND: Mitochondrial dysfunction known to be associated with most of human inherited disorders and diseases, including neurodegenerative disorders, cardiomyopathies, metabolic syndrome, muscle weakness, cancer, also obesity.CONTENT: Mitochondria charges for multiple anabolic and catabolic circuitries, as the main provider for adenosine triphosphate (ATP). Mitochondria also responsible for cellwide stress responses and control non-apoptotic cell death routines, such as autophagy and regulated necrosis. In other words, mitochondria play an extended role in regulating cellular functions, both vital and lethal, from physiological metabolism to stress responses and death to maintain adult tissue homeostasis. Furthermore, mitochondria are crucial for both embryonic and postembryonic development. Therefore, any defect or alteration in mitochondria signaling pathways will lead to a large number of diseases in human, including premature aging, neurodegenerative disorders, muscle weakness, cardiovascular disorders, and cancer.SUMMARY: Mitochondria perform a dynamic, integrated interconnected network, to maintain tissue homeostasis, beyond the cell boundaries and regulating cells and tissues communication. Certainly any mitochondrial dysfunction could direct to neurodegenerative diseases and metabolic disorders.KEYWORDS: mitochondria, UPR, mitochondrial quality control, proteostasis, mitohormesis, mitochondrial diseases
Waist Circumference was Positively Correlated with Chemerin, Retinol-Binding Protein 4 and hsCRP Lucia Herminawati; Anna Meiliana; Andi Wijaya
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.v4i1.160

Abstract

BACKGROUND: Central obesity is associated with various chronic metabolic disorders characterized by abnormal cytokine production, increased acute phase reactants, and activation of inflammatory signaling pathways. This study was aimed to investigate the association of waist circumference, chemerin, and retinol binding protein (RBP)-4 with inflammation in men with central obesity.METHODS: The research was conducted with a crosssectional design involving 68 centrally obese male subjects aged 30 to 60 years old, with waist circumference (WC) >90 cm. All subjects fulfilled the inclusion and exclusion criteria. Anthropometric parameters, fasting glucose, creatinine, SGOT, SGPT and hsCRP were measured. Serum concentrations of chemerin and RBP4 were measured by ELISA.RESULTS: The trend lines showed that chemerin, RBP4, and hsCRP increased with WC. Pearson correlation test showed a positively significant correlation between WC and hsCRP (r=0.242, p<0.05); and also between chemerin and hsCRP (r=0.244, p<0.05) and RBP4 (r=0.321, p<0.01). Subjects were stratified into four groups based on their chemerin and RBP4 levels (high chemerin/high RBP4, high chemerin/low RBP4, low chemerin/high RBP4, or low chemerin/low RBP4). Subjects who were in the high chemerin/low RBP4 group were more likely to have high level of inflammation (47.6%), but subjects with high chemerin/high RBP4 showed low level of inflammation (42.9%) as compared with the other three groups.CONCLUSIONS: We concluded that increased WC was correlated with elevated levels of chemerin, RBP4, and hsCRP. High chemerin was correlated with increased level of RBP4 as well as with high level of inflammation.KEYWORDS: waist circumference, chemerin, RBP4, hsCRP, inflammation
A Closer Look at Cardioprotective Function of HDL: Revise the HDL – Cholesterol Hypothesis? Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 6, No 1 (2014)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v6i1.40

Abstract

BACKGROUND: The strong inverse association of plasma levels of high-density lipoprotein (HDL) cholesterol with coronary heart disease (CHD) found in human epidemiological studies led to the development of the ‘HDL cholesterol hypothesis’, which posits that intervention to raise HDL cholesterol will result in reduced risk of CHD. A number of recent developments have brought the potential protective role of HDL into question. Several clinical trials of agents that substantially raise HDL-C have been demonstrated to not reduce CHD event rates.CONTENT: For decades, HDL and HDL-cholesterol (HDL-C) levels were viewed as synonymous, and modulation of HDL-C levels by drug therapy held great promise for the prevention and treatment of cardiovascular disease. Nevertheless, recent failures of drugs that raise HDL-C to reduce cardiovascular risk and the now greater understanding of the complexity of HDL composition and biology have prompted researchers in the field to redefine HDL. As such, the focus of HDL has now started to shift away from a cholesterol-centric view toward HDL particle number, subclasses, and other alternative metrics of HDL. Many of the recently discovered functions of HDL are, in fact, not strictly conferred by its ability to promote cholesterol flux but by the other molecules it transports, including a diverse set of proteins, small RNAs, hormones, carotenoids, vitamins, and bioactive lipids. Based on HDL’s ability to interact with almost all cells and deliver fat-soluble cargo, HDL has the remarkable capacity to affect a wide variety of endocrine-like systems.SUMMARY: There is a significant need to redefine HDL and its benefit. HDL transports a diverse set of functional proteins, including many binding proteins. HDL transports and deliver vitamins, carotenoids, and other small molecules. Moreover, HDL transports hormones, steroids and bile acids, and can modulate multiple endocrine pathways. HDLs also transport and deliver microRNAs to recipient cells and control gene expression. Likewise, HDLs carry bioactive lipids and can activate signaling cascades and receptors that control endothelial apoptosis, migration, survival and activation. Many of HDL’s alternative noncholesterol cargo likely confer many of HDL’s alternative functions.KEYWORDS: HDL, ApoA1, RCT, ABCA1, ABCG1, miRNA, HDL lipidome, HDL proteome
Macrophage Polarization in Metabolism and Metabolic Disease Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 5, No 2 (2013)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v5i2.56

Abstract

BACKGROUND: Obesity is now recognized as the main cause of the worldwide epidemic of type 2 diabetes. Obesity-associated chronic inflammation is a contributing key factor for type 2 diabetes and cardiovascular disease. Numbers of studies have clearly demonstrated that the immune system and metabolism are highly integrated.CONTENT: Macrophages are an essential component of innate immunity and play a central role in inflammation and host defense. Moreover, these cells have homeostatic functions beyond defense, including tissue remodeling in ontogenesis and orchestration of metabolic functions. Diversity and plasticity are hallmarks of cells of the monocyte-macrophage lineage. In response to interferons (IFNs), toll-like receptor (TLR), or interleukin (IL)-4/IL-13 signals, macrophages undergo M1 (classical) or M2 (alternative) activation. Progress has now been made in defining the signaling pathways, transcriptional networks, and epigenetic mechanisms underlying M1, M2 or M2-like polarized activation.SUMMARY: In response to various signals, macrophages may undergo classical M1 activation (stimulated by TLR ligands and IFN-γ) or alternative M2 activation (stimulated by IL-4/IL-13); these states mirror the T helper (Th)1–Th2 polarization of T cells. Pathology is frequently associated with dynamic changes in macrophage activation, with classically activated M1 cells implicate in initiating and sustaining inflammation, meanwhile M2 or M2-like activated cells associated with resolution or smoldering chronic inflammation. Identification of the mechanisms and molecules that are associated with macrophage plasticity and polarized activation provides a basis for macrophage centered diagnostic and therapeutic strategies.KEYWORDS: obesity, adipose tissue, inflammation, macrophage polarization
MicroRNAs in Obesity, Metabolic Syndrome and Diabetes Mellitus 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.v3i1.130

Abstract

BACKGROUND: MicroRNAs (miRNAs) are small regulatory RNAs that play important roles in development of diseases. Several studies have provided evidences showing that miRNAs affect pathways that are fundamental for metabolic control in adipocyte and skeletal muscle differentiations. Some miRNAs have been implicated in lipid, amino acid, and glucose homeostasis. This leads to the possibility that miRNAs may contribute to common metabolic diseases and point to novel therapeutic opportunities based on targeting of miRNAs.CONTENT: miRNAs have been recognized as a class of epigenetic regulators of metabolism and energy homeostasis, primarily because the simultaneous regulation of a large number of target genes can be accomplished by a single miRNA. Emerging evidences suggest that miRNAs play a key role in the pathological development of obesity by affecting adipocyte differentiation. miRNAs have been implicated as novel protagonists in the pathogenesis of Diabetes Mellitus (DM), regulation of insulin production, secretion and action. They also appear to play a role in the development of diabetic complications such as nephropathy and cardiac hypertrophy.SUMMARY: Involvement of miRNAs in glucose and lipid metabolism has provided strong evidences to confirm their roles as key players in regulation of complex metabolic pathways. Additionally, it indicates potential outlook for novel therapeutic strategies in the management of obesity, metabolic syndrome and DM. Further research in this field is needed to ascertain the full potential of miRNAs as novel metabolic biomarkers and potent therapeutic agents against obesity and its metabolic disorders.KEYWORDS: obesity, metabolic syndrome, diabetes, miRNAs, adipogenesis, insulin, pancreatic cells
Telomeres and Telomerase in The Aging Heart Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 9, No 3 (2017)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v9i3.389

Abstract

BACKGROUND: Aging per se is a risk factor for reduced cardiac function and heart diseases, even when adjusted for aging-associated cardiovascular risk factors. Accordingly, aging-related biochemical and cell-biological changes lead to pathophysiological conditions, especially reduced heart function and heart disease.CONTENT: Telomere dysfunction induces a profound p53-dependent repression of the master regulators of mitochondrial biogenesis and function, peroxisome proliferator-activated receptor gamma coactivator (PGC)-1a and PGC-1b in the heart, which leads to bioenergetic compromise due to impaired oxidative phosphorylation and ATP generation. This telomere-p53-PGC mitochondrial/metabolic axis integrates many factors linked to heart aging including increased DNA damage, p53 activation, mitochondrial, and metabolic dysfunction and provides a molecular basis of how dysfunctional telomeres can compromise cardiomyocytes and stem cell compartments in the heart to precipitate cardiac aging.SUMMARY: The aging myocardium with telomere shortening and accumulation of senescent cells restricts the tissue regenerative ability, which contributes to systolic or diastolic heart failure. Moreover, patients with ion-channel defects might have genetic imbalance caused by oxidative stress-related accelerated telomere shortening, which may subsequently cause sudden cardiac death. Telomere length can serve as a marker for the biological status of previous cell divisions and DNA damage with inflammation and oxidative stress. It can be integrated into current risk prediction and stratification models for cardiovascular diseases and can be used in precise personalized treatments.KEYWORDS: aging, telomere, telomerase, aging heart, mitochondria, cardiac stem cell
Adipose Tissue, Inflammation (Meta-inflammation) and Obesity Management Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 7, No 3 (2015)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v7i3.185

Abstract

BACKGROUND: Obesity-induced inflammation contributes to the development of type 2 diabetes, metabolic syndrome, and cardiovascular disease.CONTENT:The last decade has seen a sharp increase in our appreciation for the macrophage as a critical regulator of metabolic status in obesity. Activation of adipose tissue (AT) macrophages within fat depots is coupled with the development of obesity-induced proinflammatory state and insulin resistance (IR). The activation of classically activated M1 macrophages at the expense of anti-inflammatory M2 macrophages has been causally linked to the development of AT inflammation and metabolic syndrome, a pathophysiological state aptly termed as ‘metainflammation’. It is recognized that several proinflammatory cytokines, including interleukin (IL)-1β, are implicated in disrupting insulin signaling. Our developing appreciation of links among obesity, inflammation and cardiovascular disease will require multiple complementary approaches to leverage new concepts into translatable outcomes. Careful characterization of human patients, particularly analysis of AT distribution, will be needed to stratify subjects that are most likely obese/metabolically healthy from those that are obese/metabolically unhealthy.SUMMARY: It has been suggested that individuals with the condition known as metabolically healthy obese (MHO) may not have the same increased risk for the development of metabolic abnormalities as their non-metabolically healthy counterparts. A complications-centric model for the medical management of obesity emphasizes the identification and staging of complications, and treatment paradigm directed at patients who would gain the most benefit from weight loss.KEYWORDS: obesity, inflammation, insulin resistance, M1/M2 macrophage.
In Search for Anti-Aging Strategy: Can We Rejuvenate Our Aging Stem Cells? Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 7, No 2 (2015)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v7i2.72

Abstract

BACKGROUND: Recent evidence suggested that we grow old partly because of our stem cells grow old as a result of mechanisms that suppress the development of cancer over a lifetime. We believe that a further, more precise mechanistic understanding of this process will be required before this knowledge can be translated into human anti-aging therapies.CONTENT: A diminished capacity to maintain tissue homeostasis is a central physiological characteristic of aging. As stem cells regulate tissue homeostasis, depletion of stem cell reserves and/or diminished stem cell function have been postulated to contribute to aging. It has further been suggested that accumulated DNA damage could be a principal mechanism underlying age-dependent stem cell decline. It is interesting that many of the rejuvenating interventions act on the stem cell compartments, perhaps reflecting shared genetic and biochemical pathways controlling stem cell function and longevity. Strategy to slow down the aging processes is based on caloric restriction refers to a dietary regimen low in calories but without undernutrition. Sirtuin (SIRT)1 and 3, increases longevity by mimicking the beneficial effects of caloric restriction. SIRT3 regulates stress-responsive mitochondrial homeostasis, and more importantly, SIRT3 upregulation rejuvenates aged stem cells in tissues. Resveratrol (3,5,4’-trihydroxystilbene), a natural polyphenol found in grapes and wine, was the most powerful natural activator of SIRT1. In fact, resveratrol treatment has been demonstrated to rescue adult stem cell decline, slow down bodyweight loss, improve trabecular bone structure and mineral density, and significantly extend lifespan.SUMMARY: Tissue-specific stem cells persist throughout the entire lifespan to repair and maintain tissues, but their self-renewal and differentiation potential become dysregulated with aging. Given that adult stem cells are thought to be central to tissue maintenance and organismal survival, SIRT3 may promote organismal longevity by maintaining the integrity of tissue-speciic stem cells.KEYWORDS: rejuvenation, aging, stem cell, DNA damage, sirtuin activator
Co-Authors Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya Andi Wijaya ANDI WIJAYA Andi Wijaya Arifin, Arief Riadi Babikian, Haig Chandra Agung Purnama Eli Halimah, Eli Erizal Sugiono, Erizal Ferdy Ferdian Gatot S. Lawrence Gatot Susilo Lawrence Iceu Dimas Kulsum Ida Paulina Sormin Ilhamjaya Patellongi Ilhamjaya Patellongi Irma Ruslina Defi Ismail, Efriadi Keri Lestari lhamjaya Patellongi Lucia Herminawati Melisa Intan Barliana Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi Nurrani Mustika Dewi, Nurrani Mustika Prayudi Santoso Qiantori, Adziqa Ammara Rina Triana Rosalia E Napitupulu Rosdianto, Aziiz Mardanarian Setiawan Setiawan Sumalim, Yelsen Suryani As&#039;ad Suryani As&#039;ad Suryani As’ad Yovita Hartantri