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Andi Wijaya
Post Graduate Program in Clinical Biochemistry, Hasanuddin University Jl. Perintis Kemerdekaan Km.10. Makassar
Biochemistry, Genetics & Molecular Biology Public Health

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Gut Microbiota, Obesity and Metabolic Dysfunction Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 3, No 3 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i3.147

Abstract

BACKGROUND: The prevalence of obesity and related disorders such as metabolic syndrome and diabetes has vastly increased throughout the world. Recent insights have generated an entirely new perspective suggesting that our microbiota might be involved in the development of these disorders. This represents an area of scientific need, opportunity and challenge. The insights gleaned should help to address several pressing global health problems.CONTENT: Our bowels have two major roles: the digestion and absorption of nutrients and the maintenance of a barrier against the external environment. They fulfill these functions in the context of, and with the help from, tens of trillions of resident microbes, known as the gut microbiota. Studies have demonstrated that obesity and metabolic syndrome may be associated with profound microbiotal changes, and the induction of a metabolic syndrome phenotype through fecal transplants corroborates the important role of the microbiota in this disease. Dietary composition and caloric intake appear to swiftly regulate intestinal microbial composition and function.SUMMARY: The interaction of the intestinal microbial world with its host, and its mutual regulation, will become one of the important topics of biomedical research and will provide us with further insights at the interface of microbiota, metabolism, metabolic syndrome, and obesity. A better understanding of the interaction between certain diets and the human gut microbiome should help to develop new guidelines for feeding humans at various time points in their life, help to improve global human health, and establish ways to prevent or treat various food-related diseases.KEYWORDS: gut microbiota, obesity, metabolic syndrome, type 2 diabetes
Metaflammation, NLRP3 Inflammasome Obesity and Metabolic Disease Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 3, No 3 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i3.148

Abstract

BACKGROUND: Increasing prevalence of obesity gives rise to many problems associated with multiple morbidities, such as diabetes, hypertension, heart disease, sleep apnea and cancer. The mechanism of obesity is very complex, thus its link to various disease is poorly understood. This review highlights important concepts in our understanding of the pathogenesis of obesity and related complications.CONTENT: Many studies have tried to explore the exciting and puzzling links between metabolic homeostasis and inflammatory responses. A form of subclinical, low-grade systemic inflammation is known to be associated with both obesity and chronic disease. This, later called as "metaflammation", refers to metabolically triggered inflammation. The nutrient-sensing pathway and the immune response coordination are facilitated by these molecular sites in order to maintain homeostasis under diverse metabolic and immune conditions. Recent studies have found that the NLRP3 inflammasome during metabolic stress forms a tie linking TXNIP, oxidative stress, and IL-1β production. This provides new opportunities for research and therapy for the disease often described as the next global pandemic: type 2 diabetes mellitus (T2DM).SUMMARY: The crucial role of metaflammation in many complications of obesity shown by the unexpected overlap between inflammatory and metabolic sensors and their downstream tissue responses. Then great interest arose to explore the pathways that integrate nutrient and pathogen sensing, give more understanding in the mechanisms of insulin resistance type 2 diabetes, and other chronic metabolic pathologies. A family of intracellular sensors called NLR family is a critical component of the innate immune system. They can form multiprotein complexes, called inflammasome which is capable of responding to a wide range of stimuli including both microbial and self molecules by activating the cysteine protease caspase-1, leading to processing and secretion of the proinflammatory cytokines IL-1β and IL-18, which play crucial roles in host defense. Inflammasome dysregulation has been linked to some autoinflammatory and metabolic diseases. These provide opportunities to continue to improve our understanding of the nature of metaflammation in the hope of modifying it to prevent and treat diseasese.KEYWORDS: Inflammation, metaflammation, inflammasome, metabolic disease, obesity
Progress and Future Challenges of Human Induced Pluripotents Stem Cell in Regenerative Medicine Anna Meiliana; Andi Wijaya
The Indonesian Biomedical Journal Vol 3, No 2 (2011)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v3i2.138

Abstract

BACKGROUND: Less than a decade ago the prospect for reprogramming the human somatic cell looked bleak at best. It seemed that the only methods at our disposal for the generation of human isogenic pluripotent cells would have to involve somatic cell nuclear transfer (SCNT). Shinya Yamanaka in August 2006 in his publication (Cell) promised to change everything by showing that it was apparently very simple to revert the phenotype of a differentiated cell to a pluripotent one by overexpressing four transcription factors in murine fibroblasts.CONTENT: Mouse and human somatic cells can be genetically reprogrammed into induced pluripotent stem cells (iPSCs) by the expression of a defined set of factors (Oct4, Sox2, c-Myc, and Klf4, as well as Nanog and LIN28). iPSCs could be generated from mouse and human fibroblasts as well as from mouse liver, stomach, pancreatic, neural stem cells, and keratinocytes. Similarity of iPSCs and embryonic stem cells (ESCs) has been demonstrated in their morphology, global expression profiles, epigenetic status, as well as in vitro and in vivo differentiation potential for both mouse and human cells. Many techniques for human iPSCs (hiPSCs) derivation have been developed in recent years, utilizing different starting cell types, vector delivery systems, and culture conditions. A refined or perfected combination of these techniques might prove to be the key to generating clinically applicable hiPSCs.SUMMARY: iPSCs are a revolutionary tool for generating in vitro models of human diseases and may help us to understand the molecular basis of epigenetic reprogramming. Progress of the last four years has been truly amazing, almost verging on science fiction, but if we can learn to produce such cells cheaply and easily, and control their differentiation, our efforts to understand and fight disease will become more accessible, controllable and tailored. Ability to safely and efficiently derive hiPSCs may be of decisive importance to the future of regenerative medicine.KEYWORDS: iPSCs, ESC, reprogramming factor, reprogramming efficiency, somatic cell
Co-Authors Anna Meiliana