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HOW PRO-INFLAMMATORY WESTERN DIETS AND ANTI-INFLAMMATORY DIETARY INTERVENTIONS INFLUENCE NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) PROGRESSION: A NARRATIVE REVIEW OF NUTRITIONAL MECHANISMS OF ACTION Wedharga, I Gede Putu Adhi
JURNAL WIDYA MEDIKA Vol. 11 No. 2 (2025): October
Publisher : FAKULTAS KEDOKTERAN UNIVERSITAS KATOLIK WIDYA MANDALA SURABAYA

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33508/jwm.v11i2.7560

Abstract

Unhealthy diets, such as Western-type diets, are major contributors to metainflammation underlying the progression of nonalcoholic fatty liver disease (NAFLD). This narrative review analyzed 10 studies (2014–2024) from Google Scholar and PubMed to explore dietary roles in NAFLD progression. Western-type, hypercaloric, high-fructose, and HFHS diets worsen NAFLD by increasing inflammatory biomarkers and reducing oxidative stress. Conversely, dietary interventions, including the DASH diet, freshwater fish–based diets, and the Mediterranean diet, attenuate metainflammation and slow NAFLD progression. The significance of this topic lies in the global health burden of NAFLD and the increasing recognition of metainflammation as a key driver of its progression. While several pharmacological candidates have shown promise, dietary strategies remain essential in clinical practice due to their accessibility, safety, and preventive potential. This review underscores the clinical relevance of targeting metainflammation through specific dietary interventions and offers insights for both therapeutic guidance and public health policy.
Optimized RT-qPCR Detection of Hepatic Lipopolysaccharide-Binding Protein in Diet-Induced Obese Mice Tjahjono, Yudy; Wedharga, I Gede Putu Adhi; Novita, Bernadette Dian; Tahalele, Paul; Wijaya, Hendy; Soediono, Endang Isbandiati; Hendrata, Adi Pramono; Dewi, Sianty; Wijaya, Sumi; Ervina, Martha; Kuncorojakti, Suryo
Jurnal Medik Veteriner Vol. 8 No. 2 (2025): October
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jmv.vol8.iss2.2025.308-317

Abstract

High-throughput RT-qPCR results on hepatic lipopolysaccharide-binding protein (LBP) expression in obese subjects are essential, as they reveal the endotoxin’s role in the development of obesity and non-communicable disease (NCD). This study aimed to optimize RT-qPCR detection of LBP in diet-induced obese mice. This study primarily focused on addressing high variability through reference gene normalization. A total of six male C57BL/6 mice aged 6 weeks were randomly allocated into two dietary treatments (n = 3), consisting of mice fed with the standard chow diet (SCD group) and mice fed with the high-fat and high sucrose diet (HFHS group) ad libitum for 8 weeks. Relative quantification strategies involving the standard 2-ΔΔCt method (calibrator as mean) and the modified 2-ΔΔCt method (calibrator as individual sample-matched biological replicates) were compared in terms of their variability. Obesity was successfully induced in the HFHS treatment group, as indicated by significantly higher body weight, calorie intake, and LBP relative expressions compared to the SCD group. In addition, a sample-specific calibrator approach using the modified 2-ΔΔCt method resulted in lower variability in relative gene expression levels. A modified 2-ΔΔCt method, which utilizes a sample-specific calibrator to counteract sample-specific variability, was successfully employed to address high variability in RT-qPCR results.
Modified High-Fat High-Sucrose Diet Promotes Obesity and Alters Colonic Cytokines Novita, Bernadette Dian; Wedharga, I Gede Putu Adhi; Tjahjono, Yudy; Wijaya, Hendy; Theodora, Imelda; Ervina, Martha; Wilianto, Yufita Ratnasari; Dewi, Sianty; Parengkuan, Irene Lingkan; Herjunianto, Herjunianto; Ghasani, Sabrina Maria; Limantoro, Michael Christian; Jaya, Ferdinand Wiliam
The Indonesian Biomedical Journal Vol 17, No 5 (2025)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v17i5.3807

Abstract

BACKGROUND: Western dietary patterns are often associated with increasing non-communicable diseases, including inflammatory bowel disease (IBD). In experimental models, a high-fat high-sucrose (HFHS) diet is used to mimic metabolic and inflammatory effects of such diets, however the data regarding colonic inflammation in Indonesia remain limited. Therefore, this study was conducted evaluated the impact of HFHS feeding on colonic interleukin (IL)-6, IL-10 expression, and the IL-6/IL-10 ratio.METHODS: Six weeks old male C57BL/6 mice were randomly assigned to a normal fat diet (NFD) or HFHS diet group and fed ad libitum for 8 weeks. Colonic tissues were collected, and IL-6 and IL-10 expression was analyzed by immunohistochemistry.RESULTS: HFHS-fed mice showed significant increases in body weight (increased by 22.44%, p=0.0047) and caloric intake (increased by 125.17%, p=0.0000), confirming obesity induction. Colitis was also evident, with higher histological colitis scores (p=0.0072). However, colonic IL-6 (increased by 9.12%, p=0.1236), IL-10 (increased by 1.49%, p=0.8013), and the IL-6/IL-10 ratio (increased by 7.38%, p=0.4000) showed no significant differences compared to NFD.CONCLUSION: In C57BL/6 mice, an 8-week modified HFHS diet induced obesity, increased caloric intake, and mucosal injury, but did not significantly alter colonic IL-6, IL-10, or their ratio. This suggests preserved mucosal immune homeostasis consistent with an early compensatory phase rather than overt cytokine-driven inflammation. Longer or more intensive exposure may disrupt this balance, highlighting the need for further studies to define the temporal threshold and clarify immune microbiome interactions in colitis progression.KEYWORDS: high-fat high-sucrose diet, colon inflammation, IL-6, IL-10, obesity mice
STAT3, but not Ki-67, expression is independently associated with tumor progression in colorectal carcinoma: A comparative immunohistochemical biomarker analysis Wedharga, I Gede Putu Adhi; Willianto, Vincentius Michael; Theodora, Imelda; Parengkuan, Irene; Novita, Bernadette Dian
JURNAL INDONESIA DARI ILMU LABORATORIUM MEDIS DAN TEKNOLOGI Vol 7 No 2 (2025): From Natural Compounds to Disease Mechanisms: An Integrated Research Outlook
Publisher : Universitas Nahdlatul Ulama Surabaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33086/ijmlst.v7i2.7711

Abstract

The insidious progression of colorectal carcinoma (CRC) at early stages often hampers timely screening and diagnosis, resulting in delayed intervention and poor clinical outcomes. Ki-67 and Signal Transducer and Activator of Transcription 3 (STAT3) have been widely studied for their roles in tumor proliferation and survival. However, comparative studies assessing their clinicopathological relevance in CRC progression remain limited, and their relative contributions to tumor aggressiveness are unclear. This study aimed to evaluate the clinicopathological significance and association of Ki-67 and STAT3 expression with tumor aggressiveness, focusing on their roles in tumor infiltration and size as indicators of CRC progression. Thirty-eight formalin-fixed, paraffin-embedded (FFPE) CRC tissue specimens were collected from patients undergoing surgical resection for this cross-sectional study. Ki-67 and STAT3 expression were assessed using immunohistochemical (IHC) staining. Clinicopathological data were retrieved from medical records. Protein expression was quantified using inverted mean gray values via digital image analysis. Ki-67 and STAT3 expression levels significantly correlated with tumor infiltration (Ki-67: r = 0.322, p = 0.049; STAT3: r = 0.429, p = 0.007) and size (Ki-67: r = 0.425, p = 0.008; STAT3: r = 0.452, p = 0.004). No significant correlation was found between Ki-67 and STAT3 (r = 0.225, p = 0.175). Only STAT3 was independently associated with infiltration (OR per 1-standard deviation: 4.11, p = 0.043) and size (OR per 1-SD: 3.41, p = 0.047). While both markers are associated with CRC progression, only STAT3 shows an independent association with tumor aggressiveness, underscoring its role beyond cell proliferation and suggesting broader involvement in tumor invasion and progression pathways.