Special correlation between diet and MASLD: positive or negative?

Cell & Bioscience, Journal Year: 2025, Volume and Issue: 15(1)

Published: April 12, 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic and systemic metabolic characterized by the presence of hepatic steatosis at least one cardiometabolic risk factor (CMRF). The pathogenesis MASLD involves multiple mechanisms, including lipid metabolism disorders, insulin resistance, inflammatory responses, hepato-intestinal axis dysfunction. Among these factors, diet serves as both an inducement potential remedy in disease's development. Notably, high-lipid exacerbates fat accumulation, oxidative stress, thereby promoting progression MASLD. Consequently, dietary induction models have become vital tools for studying pathological mechanisms MASLD, providing foundation identifying therapeutic targets. Additionally, we summarize effects optimization on elucidate role specific components regulating axis, metabolism, inhibiting responses. In conclusion, studies utilizing animal offer significant insights into therapy, particularly concerning regulation metabolism-related hepatoenteric axis-related signaling pathways well beneficial mechanism probiotics regulation. By understanding which different patterns affect can assess clinical applicability current strategies provide new directions research treatment aimed modification.

Language: Английский

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Empagliflozin Alleviates Hepatic Steatosis and Oxidative Stress via the NRF1 Pathway in High-Fat Diet-Induced Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(9), P. 4054 - 4054

Published: April 25, 2025

Empagliflozin (EMPA)—a sodium-glucose cotransporter type 2 inhibitor—reduces endoplasmic reticulum (ER) stress, oxidative and inflammation during metabolic dysfunction-associated steatotic liver disease (MASLD) progression. However, the direct effects of EMPA on hepatic lipid metabolism stress are unclear. Through current study, we seek to explore related mechanisms in MASLD. To this end, MASLD was induced C57BL/6J mice using a high-fat diet (HFD); nuclear respiratory factor 1 (NRF1) downregulated via viral transduction (AAV8-shNrf1). Glucose homeostasis histology were assessed, measured. HFD-fed mice-derived tissue samples exhibited more droplets, higher triglyceride levels, elevated ER than chow (CD)-fed mice. attenuated HFD-induced stress. Additionally, HFD significantly decreased NRF1 Sirtuin (SIRT)7 expression compared with CD, which rescued by treatment. these results did not affect insulin resistance or synthesis-related changes upon treatment Nrf1-knockdown Furthermore, alleviated steatosis stress; however, lost Collectively, study suggest that ameliorates reducing attenuating NRF1.

Language: Английский

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Cysteine‐rich 61 inhibition attenuates hepatic insulin resistance and improves lipid metabolism in high‐fat diet fed mice and HepG2 cells

The FASEB Journal, Journal Year: 2024, Volume and Issue: 38(15)

Published: July 31, 2024

Abstract Metabolic dysfunction‐associated steatotic liver disease (MASLD) is strongly associated with insulin resistance development. Hepatic lipid accumulation and inflammation are considered the main drivers of hepatic in MASLD. Cysteine‐rich 61 (Cyr61 also called CCN1), a novel secretory matricellular protein, implicated inflammation, its role MASLD not clearly understood. Therefore, we investigated Cyr61 metabolism as major factors pathogenesis. In high‐fat diet (HFD)‐fed C57BL/6J mice, was downregulated or upregulated via viral transduction. Measurements glucose homeostasis, histological assessment tissues, gene expression signaling pathways lipogenesis, fatty acid oxidation, were performed using samples from these mice. levels HepG2 cells reduced RNAi‐mediated knockdown. Inflammation evaluated real‐time polymerase chain reaction western blotting. HFD/AAV‐shCyr61 mice exhibited enhanced tolerance protein kinase B pathway, decreased increased oxidation. Notably, showed elevated sirtuin 6 phosphorylated‐AMP‐activated kinase. vitro experiments demonstrated that inhibition pro‐inflammatory cytokines such interleukin‐1 beta, IL‐6, tumor necrosis factor‐alpha nuclear factor kappa B/c‐Jun N‐terminal alleviated resistance. affected metabolism, Inhibition recovered resistance, altered vivo vitro. potential therapeutic target

Language: Английский

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Association of histidine-rich glycoprotein C633T single nucleotide polymorphism and recurrent miscarriage in Iranian women

Molecular Biology Reports, Journal Year: 2024, Volume and Issue: 51(1)

Published: July 13, 2024

Language: Английский

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