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<p>Metabolic associated steatotic liver disease (MASLD) is a globally prevalent metabolic disorder characterized by hepatic steatosis, inflammation, and impaired lipid homeostasis. Vitamin D exhibits anti-inflammatory and insulin-sensitizing properties, whereas intermittent fasting (IF) has recently emerged as a metabolic intervention capable of improving hepatic and systemic energy balance. To compare the therapeutic effects of vitamin D and IF on high-fat and fructose diet-induced MASLD in rats, with emphasis on lipid metabolism, oxidative stress, and inflammatory signaling pathways. Twenty-four male Sprague–Dawley rats were allocated into four groups (<i>n</i> = 6/group): Control, MASLD (HFD), HFD + vitamin D, and HFD + IF. Biochemical analyses included fasting glucose, serum insulin, ALT, AST, lipid profile, MDA, and GSH. Immunohistochemistry quantified hepatic expression of SREBP1, AQP9, TLR4, and NF-κB. Numerical comparisons were reported as mean ± SD and percentage changes relative to HFD. Both interventions significantly improved MASLD outcomes. Vitamin D and IF reduced ALT by <b>42%</b> and <b>47%</b>, respectively, and lowered AST by <b>38%</b> and <b>45%</b> compared with HFD. Triglycerides and LDL-C decreased by <b>31–48%</b>, while HDL-C increased by <b>18–24%</b>. Oxidative stress improved, with MDA reduced by <b>36%</b> (vitamin D) and <b>54%</b> (IF), and GSH elevated by <b>61%</b> and <b>82%</b>, respectively. Both treatments markedly downregulated hepatic SREBP1 and the AQP9 glycerol transport pathway, and suppressed activation of TLR4/NF-κB signaling. Vitamin D and intermittent fasting exert significant hepatoprotective effects in MASLD by improving metabolic parameters, enhancing antioxidant capacity, and attenuating inflammatory signaling. These findings support their potential as complementary, non-pharmacological strategies for MASLD management and warrant further translational investigation.</p>

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Therapeutic effects of vitamin D and intermittent fasting on metabolic associated steatotic liver disease in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月3日

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  • Ola Mohammed Youssef,
  • Amira Osman,
  • Ahmed El-Sayed Nour El-Deen,
  • Dalia H. El-Kashef,
  • Salma M. Eraky,
  • Dina Abdalla Arida

摘要

Metabolic associated steatotic liver disease (MASLD) is a globally prevalent metabolic disorder characterized by hepatic steatosis, inflammation, and impaired lipid homeostasis. Vitamin D exhibits anti-inflammatory and insulin-sensitizing properties, whereas intermittent fasting (IF) has recently emerged as a metabolic intervention capable of improving hepatic and systemic energy balance. To compare the therapeutic effects of vitamin D and IF on high-fat and fructose diet-induced MASLD in rats, with emphasis on lipid metabolism, oxidative stress, and inflammatory signaling pathways. Twenty-four male Sprague–Dawley rats were allocated into four groups (n = 6/group): Control, MASLD (HFD), HFD + vitamin D, and HFD + IF. Biochemical analyses included fasting glucose, serum insulin, ALT, AST, lipid profile, MDA, and GSH. Immunohistochemistry quantified hepatic expression of SREBP1, AQP9, TLR4, and NF-κB. Numerical comparisons were reported as mean ± SD and percentage changes relative to HFD. Both interventions significantly improved MASLD outcomes. Vitamin D and IF reduced ALT by 42% and 47%, respectively, and lowered AST by 38% and 45% compared with HFD. Triglycerides and LDL-C decreased by 31–48%, while HDL-C increased by 18–24%. Oxidative stress improved, with MDA reduced by 36% (vitamin D) and 54% (IF), and GSH elevated by 61% and 82%, respectively. Both treatments markedly downregulated hepatic SREBP1 and the AQP9 glycerol transport pathway, and suppressed activation of TLR4/NF-κB signaling. Vitamin D and intermittent fasting exert significant hepatoprotective effects in MASLD by improving metabolic parameters, enhancing antioxidant capacity, and attenuating inflammatory signaling. These findings support their potential as complementary, non-pharmacological strategies for MASLD management and warrant further translational investigation.