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  1. Moderate-intensity exercise decreases the circulating level of betatrophin and its correlation among markers of obesity in women
    Rejeki PS, Baskara PG, Herawati L, Pranoto A, Setiawan HK, Lesmana R, et al.
    J Basic Clin Physiol Pharmacol, 2022 Nov 01;33(6):769-777.
    PMID: 35286051 DOI: 10.1515/jbcpp-2021-0393
    OBJECTIVES: Positive energy homeostasis due to overnutrition and a sedentary lifestyle triggers obesity. Obesity has a close relationship with elevated levels of betatrophin and may increase the risk of developing metabolic syndrome. Therefore, lifestyle modification through a nonpharmacological approach based on physical exercise is the right strategy in lowering betatrophin levels. This study aimed to analyze the effect of moderate-intensity interval and continuous exercises on decreased betatrophin levels and the association between betatrophin levels and obesity markers in women.

    METHODS: A total of 30 women aged 20-24 years old were randomly divided into three groups. Measurement of betatrophin levels using Enzyme-Linked Immunosorbent Assay (ELISA). Data analysis techniques used were one-way ANOVA and parametric linear correlation.

    RESULTS: The results showed that the average levels of betatrophin pre-exercise were 200.40 ± 11.03 pg/mL at CON, 203.07 ± 42.48 pg/mL at MIE, 196.62 ± 21.29 pg/mL at MCE, and p=0.978. Average levels of betatrophin post-exercise were 226.65 ± 18.96 pg/mL at CON, 109.31 ± 11.23 pg/mL at MIE, 52.38 ± 8.18 pg/mL at MCE, and p=0.000. Pre-exercise betatrophin levels were positively correlated with age, BMI, FM, WHR, FBG, and PBF (p≤0.001).

    CONCLUSIONS: Our study showed that betatrophin levels are decreased by 10 min post-MIE and post-MCE. However, moderate-intensity continuous exercise is more effective in lowering betatrophin levels than moderate-intensity interval exercise. In addition, pre-exercise betatrophin levels also have a positive correlation with obesity markers.

  2. Formononetin-induced apoptosis in hepatocellular carcinoma: insights from mTOR inhibition and caspase-3 activation through in silico and in vitro approaches
    Hidayah N, Sudjarwo SA, Herawati L, Kurnijasanti R, Mustafa MR, Yunani R
    Med Oncol, 2025 Jun 16;42(7):264.
    PMID: 40522515 DOI: 10.1007/s12032-025-02778-2
    Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer and remains a major contributor to global cancer-related deaths. The progression of HCC is strongly influenced by the dysregulation of the mechanistic target of rapamycin (mTOR) signaling pathway and impaired apoptotic mechanisms, particularly due to caspase-3 suppression. These molecular aberrations promote oncogenic proliferation and confer resistance to conventional therapeutic regimens. Existing treatment modalities are frequently constrained by limited efficacy, the emergence of drug resistance, and dose-limiting toxicities, highlighting the critical need for innovative and targeted therapeutic approaches to improve patient outcomes. This study investigates the dual anticancer mechanisms of formononetin, a bioactive isoflavone, focusing on its ability to suppress the mTOR signaling pathway and induce caspase-3 activation in hepatocellular carcinoma (HCC). By targeting these critical molecular pathways, formononetin exhibits therapeutic potential by impeding tumor progression and counteracting apoptosis resistance in HCC. In silico analyses employing molecular docking, PASS Online, and ProTox 3.0 were utilized to predict formononetin's biological activity, pharmacokinetic properties, and toxicity profile. These computational tools provided valuable insights into formononetin's potential therapeutic properties. To validate these predictions, in vitro studies were conducted, including cytotoxicity assays (MTT), apoptosis quantification via Annexin V-FITC/PI staining, and protein expression analysis of mTOR and caspase-3 using flow cytometry. The experimental results substantiated formononetin's capacity to suppress mTOR signaling and induce apoptotic cell death in HCC models. In silico analyses demonstrated that formononetin exhibited high binding affinities to mTOR (- 8.7 kcal/mol) and caspase-3 (- 7.2 kcal/mol), supported by favorable pharmacokinetic properties and low toxicity profiles. Cytotoxicity assays revealed selective activity against HepG2 cells, with an IC50 of 10.397 µg/mL, while showing minimal effects on normal Vero cells. Flow cytometry confirmed a dose-dependent induction of apoptosis, evidenced by a significant increase in caspase-3 expression and a corresponding decrease in mTOR levels at a concentration of 10.397 µg/mL (p 
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