Abstract

Plant-based nutritional supplementation has been shown to attenuate and reduce mortality in the processes of both acute and chronic disorders, including diabetes, obesity, cardiovascular disease, cancer, inflammatory diseases, and neurological and neurodegenerative disorders. Low-level systemic inflammation is an important contributor to these afflictions and diets enriched in phytochemicals can slow the progression. The goal of this study was to determine the impact of lipopolysaccharide (LPS)-induced inflammation on changes in glucose and insulin tolerance, performance enhancement, levels of urinary neopterin and concentrations of neurotransmitters in the striatum in mouse models. Both acute and chronic injections of LPS (2 mg/kg or 0.33 mg/kg/day, respectively) reduced glucose and insulin tolerance and elevated neopterin levels, which are indicative of systemic inflammatory responses. In addition, there were significant decreases in striatal neurotransmitter levels (dopamine and DOPAC), while serotonin (5-HT) levels were essentially unchanged. LPS resulted in impaired execution in the incremental loading test, which was reversed in mice on a supplemental plant-based diet, improving their immune function and maintaining skeletal muscle mitochondrial activity. In conclusion, plant-based nutritional supplementation attenuated the metabolic changes elicited by LPS injections, causing systemic inflammatory activity that contributed to both systemic and neurological alterations.

Highlights

  • Poor eating habits and diets enriched in high cholesterol or fats have become a major health issue and represent a significant cause of disability and mortality in the United States and around the world [1,2,3]

  • LPS elevated the glucose clearance and reduced the area under the curve (AUC), suggesting a greater nutrient requirement during the time of acute inflammation when compared to the control group (Figure 1A,B)

  • We found that that consumption of this particular diet for at least a 2-month period helped to reduce the outcomes of both acute and chronic inflammation induced by LPS

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Summary

Introduction

Poor eating habits and diets enriched in high cholesterol or fats have become a major health issue and represent a significant cause of disability and mortality in the United States and around the world [1,2,3]. Neuroinflammation involves the triggering of glial cell activation and the release of inflammatory cytokines such as tumor necrosis factor-α (TNF-α), as well as interleukins-1β (IL-1β) and IL-6 [22,23,24]. These cytokines function in various ways to promote neuronal cell death in disorders like Parkinson’s disease (PD) or Alzheimer’s disease (AD), and in so doing contribute to pathologenesis [25,26]. We and others have shown that, in a number of neurodegenerative diseases, in addition to neuroinflammation, there is a systemic component that exacerbates these diseases and promotes the progression to neurodegeneration [27]

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