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Sarcopenia as a Risk of Modern Obesity Treatments: A Review of Molecular Mechanisms and Prevention Strategies Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 17, No 6 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i6.3583

While lifestyle interventions and metabolic surgery for obesity have limitations, incretin-based therapies have emerged as highly effective treatments. However, their success is shadowed by a significant risk, which is the loss of lean skeletal muscle, which can induce sarcopenia or sarcopenic obesity. Given the vital role of skeletal muscle in overall health, it is crucial to accurately assess this condition using standard clinical measures. Exercise stands as the most potent countermeasure, acting as medicine to preserve muscle and improve metabolic health. Its benefits are driven by a complex interplay of mechanisms. Different exercise types trigger the release of myokines and exerkines, while a regulated inflammatory response is essential for muscle adaptation and regeneration. This regenerative process, involving muscle stem cells, is further governed by epigenetic factors and critical molecular pathways like Akt and insulin that maintain muscle mass. To optimize these effects, adequate protein intake and targeted nutritional strategies are essential, supporting muscle protein synthesis and recovery. Supplementation, particularly with leucine-rich amino acids or vitamin D, may further enhance anabolic responses, especially in older adults. Clinical monitoring of muscle mass, strength, and nutritional biomarkers should be integrated into obesity care to detect early signs of sarcopenia and guide individualized interventions. Therefore, it is imperative that obesity therapy evolves to prevent muscle loss. This review highlights the risk of therapy-induced sarcopenia from modern obesity treatments, emphasizing the need for integrated prevention strategies, centered on exercise, and reinforced by nutrition, supplementation, and clinical monitoring to ensure healthy, sustainable weight loss.KEYWORDS: sarcopenia, skeletal muscle, inflammation, obesity, incretin

Roles of Mesenchymal Stem Cell-derived Extracellular Vesicles in Cancer: Development and Target Therapy Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 17, No 1 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i1.3408

Extracellular vesicles (EVs) are membrane structures that enclose proteins, lipids, RNAs, metabolites, growth factors, and cytokines. EVs derived from mesenchymal stem cells (MSCs) can either stimulate or inhibit tumor growth in various malignancies through paracrine signaling. Tumor-associated MSCs (TA-MSCs), often described as "wounds that never heal," actively participate in the development, propagation, and metastasis of tumors, impacting the immunological state of the tumor microenvironment. For instance, TA-MSCs can alter immune cell recruitment and cytokine production, leading to a pro-tumorigenic environment. Consequently, both the tumor and its microenvironment undergo functional alterations, the cargo of exosomes is modified, and an abnormal tumor-associated MSC phenotype is acquired. MSC-EVs contain exosome microRNA with both tumor-inhibitory and tumor-supportive effects. For example, MSC-EVs have been shown to deliver tumor-suppressive microRNAs that inhibit cancer cell proliferation and induce apoptosis. This review outlines the criteria for the modification, isolation, and characterization of exosomes, as well as their application in cancer, providing insights for clinical use. By understanding these mechanisms, we can better harness MSC-EVs for therapeutic purposes.Keywords: mesenchymal stem cell, extracellular vesicle, exosome, cancer therapy, drug delivery

Resveratrol: The Multifaceted Roles and Mechanisms of Polyphenol to Improve Longevity, Immunomodulation, and Age-related Diseases Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 17, No 2 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i2.3486

High in polyphenols diet has been known to protect human against chronic metabolic diseases including cancer, diabetes, neurological and cardiovascular disorders. Resveratrol (RSV) is a natural polyphenol that presents in fruits, vegetables, and nuts. The polyphenols content of RSV possesses anti-inflammatory, antioxidant, immunomodulatory, and anticancer properties by influencing the nuclear factor-kappaB (NF-κB), p53, adenosine monophosphate-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathways, enzymatic antioxidants expressions, and the levels of microRNAs. Therefore, this review article will focus on the potential of RSV in improving aging and metabolic diseases, which mostly induced by low-chronic inflammation and oxidative stress. RSV is also known as calorie restriction (CR)-mimetics to activate sirtuins family which improve mitochondrial function, repair DNA and genomic stability and reduce inflammation thus become a promising substance to extend health span and longevity. RSV can be useful as a supplement to prevent aging-related diseases, with a dose range between 250–1,000 mg depending on the intended health benefit and individual factors. More clinical data is needed to determine the impact of RSV metabolites and the relationship between dose, concentration, and effect, particularly in the context of chronic illness.KEYWORDS: mesenchymal stem cell, extracellular vesicle, exosome, cancer therapy, drug delivery

Lifestyle Modifications and Nutraceutical Interventions in the Prevention and Management of Metabolic Syndrome Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 17, No 3 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i3.3412

Abdominal obesity, dyslipidemia, hypertension, and hyperglycemia are metabolic risk factors that are grouped together to define metabolic syndrome (MetS). It is now widely recognized that MetS is linked to a higher risk of type 2 diabetes (T2DM) and cardiovascular disease (CVD). Overall, the pathophysiology of MetS initiated by the imbalance of nutrition intake and physical activity. It involves a complex interplay of insulin resistance (IR), inflammation, dysregulated adipocyte function, and genetic susceptibility, all of which contribute to the metabolic dysfunction. Lifestyle modifications play a crucial role in managing and preventing MetS. Key strategies include adopting a balanced diet like Mediterranean diet, Dietary Approaches to Stop Hypertension (DASH), or caloric restriction (CR), engaging in regular physical activity, and maintaining a healthy weight. Nutraceuticals, including polyphenols and CR-mimetic agents, improve insulin sensitivity, reduce inflammation, lower blood pressure and cholesterol levels, reducing oxidative stress, and promoting autophagy. In addition to lifestyle changes, drug therapy may be necessary for some individuals to manage specific risk factors, such as diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), calcium channel blockers, and beta blockers for hypertension; biguanides, sulfonylureas, dipeptidyl peptidase-4 (DPP-4) inhibitors, glucagon-like peptide 1(GLP-1) receptor agonists, sodium-glucose co-transporter 2 (SGLT2) inhibitors, and thiazolidinediones for hyperglycemia; and statins for dyslipidemia. Early diagnosis, including waist circumference and blood pressure measurement, serum cholesterol and glucose testing, and intervention, is essential to effectively manage MetS and prevent the progression of associated diseases. In conclusion, understanding the risk factors and associated risks of MetS, along with the implementation of lifestyle modifications such as dietary and nutraceutical interventions including polyphenols and CR-mimetic agents, is vital for reducing the burden of this syndrome. Early diagnosis and proactive management are key to improving long-term health outcomes.KEYWORDS: metabolic syndrome, abdominal obesity, insulin resistance, diet, nutraceuticals

Therapeutic Potential of Gut Microbiota in Hypertension: Mechanisms of Immune Modulation and Inflammation Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 17, No 4 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i4.3565

Emerging evidence links gut dysbiosis to numerous ailments, including hypertension and metabolic diseases. Multi-omics techniques have revealed that hypertensive individuals exhibit distinct alterations in their gut bacterial composition and metabolite profiles. The gut microbiome influences blood pressure through several mechanisms. For instance, microbiota-derived metabolites can have beneficial effects, such as those from short-chain fatty acids (SCFAs), or detrimental ones, like trimethylamine N-oxide (TMAO). These molecules modulate downstream signaling pathways via G protein-coupled receptors or direct immune cell activation. Furthermore, dysbiosis can compromise the gut epithelial barrier, leading to systemic inflammation that activates key regulatory pathways like the renin-angiotensin-aldosterone system (RAAS), the autonomic nervous system, and the immune system. Given these connections, the gut microbiome is a promising therapeutic target for hypertension. This review explores the potential of modulating the gut microbiota to manage blood pressure, focusing on the underlying mechanisms of immune modulation, inflammation, and microbial metabolites. By focusing on the 'how' rather than the 'what' of hypertension, it is identified that immune-mediated inflammation is orchestrated by the gut microbiota, as the core mechanism driving the disease. Gut dysbiosis is triggered by environmental factors like high-salt diets, perpetuates a pro-inflammatory state that undermines the efficacy of conventional antihypertensive drugs and contributes to treatment-resistant hypertension. Consequently, modulating the gut microbiota through targeted interventions, including dietary fiber, probiotics, and fecal transplantation, might represents a critical evolution in treatment. This approach moves beyond managing symptoms to directly correcting the inflammatory dysfunction at the heart of the disease, offering a powerful strategy to complement existing therapies.KEYWORDS: hypertension, inflammation, gut microbiota, metabolite

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