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Abstract <p>Obesity is associated with a significant reduction in nicotinamideadenine dinucleotide (NAD<sup>+</sup>) levels andthe activity of the NAD<sup>+</sup>-dependent enzymes suchas sirtuins (SIRTs). Since experimental NAD<sup>+</sup> boostingwas reported to mitigate metabolic and inflammatory dysfunctionassociated with obesity, researchers are now exploring new therapiesdirected to raise NAD<sup>+</sup> levels. This studyaimed at investigating the effects of the CD38-NADase inhibitor,apigenin, in a rat model of high fat diet (HFD)-induced obesity.Forty-eight adult male Wistar rats were divided into a high fatdiet-fed group and a normal diet-fed group for eight weeks. In thelast two weeks, each group was subdivided into four groups accordingto the dose of apigenin given: (1) oral apigenin 10 mg/kg/day, (2)oral apigenin 20&#xa0;mg/kg/day, (3) oral apigenin 40 mg/kg/day, and(4) a vehicle-treated group. Body weight was recorded weekly; after8 weeks, lipid profile and homeostatic model assessment of insulinresistance (HOMA-IR) were measured in serum, while tumor necrosisfactor-α (TNF-α), interleukin 6 (IL-6), NAD<sup>+</sup> levels,relative <i>Sirt1</i> expression,SIRT1 activity, and histopathological changes were evaluated inboth liver and visceral adipose tissues. Apigenin treatment inducedan alleviation of hyperlipidemia, hyperglycemia, and insulin resistance;reduced pro-inflammatory mediators such as TNFα and IL-6; enhancedNAD<sup>+</sup> levels; and increased both the expressionand the activity of SIRT1. This study highlights apigenin-mediated ameliorationof the HFD-induced metabolic and inflammatory dysfunction, whichcould be mediated via enhancing the NAD<sup>+</sup>/Sirt1axis.</p>

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The CD38 Inhibitor, Apigenin, Ameliorates Obesity-Related Metabolic and Inflammatory Dysfunction via Boosting the NAD+/SIRT1 Axis in Rats on High Fat Diet

  • 期刊论文

  • 发表日期：

    2026年4月19日

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  • Basma Tarek Rezk,
  • Mohamed Z. Habib,
  • Noura M. El-Kholy,
  • Magda I. Mohamad,
  • Seham Adel,
  • Marwa N. M. Hassan,
  • Doaa R. Sadek,
  • Wael M. Elayat

摘要

Abstract

Obesity is associated with a significant reduction in nicotinamideadenine dinucleotide (NAD+) levels andthe activity of the NAD+-dependent enzymes suchas sirtuins (SIRTs). Since experimental NAD+ boostingwas reported to mitigate metabolic and inflammatory dysfunctionassociated with obesity, researchers are now exploring new therapiesdirected to raise NAD+ levels. This studyaimed at investigating the effects of the CD38-NADase inhibitor,apigenin, in a rat model of high fat diet (HFD)-induced obesity.Forty-eight adult male Wistar rats were divided into a high fatdiet-fed group and a normal diet-fed group for eight weeks. In thelast two weeks, each group was subdivided into four groups accordingto the dose of apigenin given: (1) oral apigenin 10 mg/kg/day, (2)oral apigenin 20 mg/kg/day, (3) oral apigenin 40 mg/kg/day, and(4) a vehicle-treated group. Body weight was recorded weekly; after8 weeks, lipid profile and homeostatic model assessment of insulinresistance (HOMA-IR) were measured in serum, while tumor necrosisfactor-α (TNF-α), interleukin 6 (IL-6), NAD+ levels,relative Sirt1 expression,SIRT1 activity, and histopathological changes were evaluated inboth liver and visceral adipose tissues. Apigenin treatment inducedan alleviation of hyperlipidemia, hyperglycemia, and insulin resistance;reduced pro-inflammatory mediators such as TNFα and IL-6; enhancedNAD+ levels; and increased both the expressionand the activity of SIRT1. This study highlights apigenin-mediated ameliorationof the HFD-induced metabolic and inflammatory dysfunction, whichcould be mediated via enhancing the NAD+/Sirt1axis.