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Purpose <p>This study investigated the direct (cigarette smoke extract, CSE) and indirect (low nutrient) effects of cigarette smoking on intervertebral disc cell energy metabolism, with a focus on glucose consumption and lactate production in lumbar discs.</p> Methods <p>Lumbar IVDs from Sprague–Dawley rats were harvested and dissected into nucleus pulposus (NP), annulus fibrosus (AF), and cartilaginous endplate (CEP) regions. Minced tissue cultures from each region were exposed to physiological control (5.5&#xa0;mM glucose, 5% oxygen), CSE-treated (physiological + 10% CSE), or low-nutrient conditions (1.5&#xa0;mM glucose, 1% oxygen). Glucose consumption rates (GCR) and lactate production rates (LPR) were measured using a biochemical analyzer. A finite element model was developed to simulate nutrient transport and adenosine triphosphate (ATP) synthesis in the IVD under experimental conditions.</p> Results <p>Both CSE and low-nutrient conditions significantly reduced GCR and LPR in AF and NP, where NP cells exhibited the greatest metabolic activity. Low-nutrient conditions increased the LPR:GCR ratio, indicating an increase in glycolysis. CEP metabolism was marginally impacted by treatments. Computational modeling revealed that CSE conserved oxygen but reduced ATP synthesis, while low-nutrient conditions severely depleted glucose, oxygen, and ATP. Combined effects of CSE and nutrient deprivation exacerbated the reduction in ATP availability.</p> Conclusions <p>Cigarette smoking impairs IVD cellular energy metabolism through both direct toxic exposure and indirect nutrient deprivation mechanisms, with the modeled low-nutrient conditions having a more pronounced effect. The NP is the most metabolically sensitive region in the IVD, while the CEP is more resilient to fluctuations with its environment. These findings provide insights into IVD metabolic adaptations to smoking.</p>

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A Comparison of Cigarette Smoking Effects on Intervertebral Disc Cell Metabolism in a Rat Tissue Model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Nathan Buchweitz,
  • Avery Madden,
  • Joshua Kelley,
  • Hui Li,
  • Zhaoxu Meng,
  • Michael Kern,
  • Danyelle M. Townsend,
  • Hai Yao,
  • Yongren Wu

摘要

Purpose

This study investigated the direct (cigarette smoke extract, CSE) and indirect (low nutrient) effects of cigarette smoking on intervertebral disc cell energy metabolism, with a focus on glucose consumption and lactate production in lumbar discs.

Methods

Lumbar IVDs from Sprague–Dawley rats were harvested and dissected into nucleus pulposus (NP), annulus fibrosus (AF), and cartilaginous endplate (CEP) regions. Minced tissue cultures from each region were exposed to physiological control (5.5 mM glucose, 5% oxygen), CSE-treated (physiological + 10% CSE), or low-nutrient conditions (1.5 mM glucose, 1% oxygen). Glucose consumption rates (GCR) and lactate production rates (LPR) were measured using a biochemical analyzer. A finite element model was developed to simulate nutrient transport and adenosine triphosphate (ATP) synthesis in the IVD under experimental conditions.

Results

Both CSE and low-nutrient conditions significantly reduced GCR and LPR in AF and NP, where NP cells exhibited the greatest metabolic activity. Low-nutrient conditions increased the LPR:GCR ratio, indicating an increase in glycolysis. CEP metabolism was marginally impacted by treatments. Computational modeling revealed that CSE conserved oxygen but reduced ATP synthesis, while low-nutrient conditions severely depleted glucose, oxygen, and ATP. Combined effects of CSE and nutrient deprivation exacerbated the reduction in ATP availability.

Conclusions

Cigarette smoking impairs IVD cellular energy metabolism through both direct toxic exposure and indirect nutrient deprivation mechanisms, with the modeled low-nutrient conditions having a more pronounced effect. The NP is the most metabolically sensitive region in the IVD, while the CEP is more resilient to fluctuations with its environment. These findings provide insights into IVD metabolic adaptations to smoking.