Objectives Noncommunicable disease (NCD) including obesity, cancer, and diabetes has become particular concern worldwide due to its morbidity and mortality which keep increasing annually. Adiponectin and insulin-like growth factor-1 (IGF-1) are known to be substances that are involved in the development of NCD. Several diet regimens have been developed to treat NCD, one of which is the ketogenic diet (KD). This study aimed to analyze the long-term KD effect on serum adiponectin and IGF-1 levels in mice. Methods This study was a real experimental with post-test only controls group design. The subjects were 14 male mice (2–3 months, 20–30 g) were randomly divided into two groups, K1 (n=7, standard diet) and K2 (n=7, KD with a composition of 60% fat, 30% protein, and 10% fiber). All subjects were given diet intervention for 8 weeks ad libitum. Serum adiponectin and IGF levels were measured in post-intervention using Enzyme-Linked Immunosorbent Assay. Distribution of normality was analyzed by the Shapiro–Wilk Test, mean difference using Independent T-Test, and linear correlation using Pearson’s Correlation Test. Data analysis was performed using Statistic Package for Social Science Version 16. Results Serum adiponectin levels in K1 (0.080 ± 0.012) pg/mL and K2 (0.099 ± 0.005) pg/mL, with p=0.003. Serum IGF-1 levels in K1 (133.535 ± 25.702) ng/mL and K2 (109.987 ± 27.118) ng/mL, with p=0.121. Coefficient correlation between serum adiponectin and serum IGF-1 levels [r]=−0.401, with p=0.155. Conclusions Long-term KD increases serum adiponectin levels and has no effect on serum IGF-1 levels. There was no significant correlation between serum adiponectin and serum IGF-1 levels.
Introduction: CagA, an oncogenic virulence factor of Helicobacter pylori, may present with 39-bp deletions in the preepiya region of East-Asian strains resulting in a virulent genotype. This study aims to compare the morphological changes, protein expressions, and interleukin-8 (IL-8) production in AGS cells infected with H. pylori East-Asian strains containing 39-bp deletion. Methods: Cultured AGS cells, infected with H. pylori strains obtained from gastric biopsy, were incubated for 24 h (MOI 50, 37°C, 5% CO2). The subsequent changes in cell appearances (Hummingbird phenotype and cell death), protein expressions (CagA, Py99, UreB, and β-actin), and IL-8 production were analyzed through microscopic observation, western blot analysis, and sandwich enzyme-linked immunosorbent assay, respectively. Results: Two H. pylori strains (KPG15 and TN2) and negative H. pylori infection negative control (NC) were observed. Cell death was observable in all three groups. Hummingbird phenotype, inducible by CagA, was present in 39-deletion strains. KPG15 and TN2 exhibited positive bands in UreB, CagA, and Py99-confirming H. pylori presence, CagA expression and phosphorylation, respectively. The higher IL-8 concentrations in KPG15 (820.6 pg/ml) compared to TN2 (742.5 pg/ml) and NC (37.1 pg/ml) may be attributable to CagA-independent IL-8 production. These results support the fact that 39-bp deletion induces more severe inflammation. Conclusions: KPG15 and TN2 displayed similar in silico profiles, cell appearances, and protein expressions. Although both cases induced IL-8 production, KPG15 had a higher result.
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