Abstract

As a kind of metabolically triggered inflammation, obesity influences the interplay between the central nervous system and the enteral environment. The present study showed that β-elemene, which is contained in various plant substances, had effects on recovering the changes in metabolites occurring in high-fat diet (HFD)-induced obese C57BL/6 male mice brains, especially in the prefrontal cortex (PFC) and hippocampus (HIP). β-elemene also partially reversed HFD-induced changes in the composition and contents of mouse gut bacteria. Furthermore, we evaluated the interaction between cerebral metabolites and intestinal microbiota via Pearson correlations. The prediction results suggested that Firmicutes were possibly controlled by neuron integrity, cerebral inflammation, and neurotransmitters, and Bacteroidetes in mouse intestines might be related to cerebral aerobic respiration and the glucose cycle. Such results also implied that Actinobacteria probably affected cerebral energy metabolism. These findings suggested that β-elemene has regulatory effects on the imbalanced microbiota-gut-brain axis caused by obesity and, therefore, would contribute to the future study in on the interplay between cerebral metabolites from different brain regions and the intestinal microbiota of mice.

Highlights

  • Obesity is characterized as a kind of low-grade systematic inflammation with the potential to cause deficits in memory, behavior, or learning ability compared with a healthy state [1]

  • For the obese mouse model (Figure S1), we found that β-elemene did not influence mouse body weight but alleviated the inflammation in the mice white adipose tissue [14]

  • The principal component analysis (PCA) results showed that CON and ELE groups were characterized by higher amounts of GABA, Cr*, and Glx than the high-fat diet (HFD) group in the prefrontal cortex (PFC)

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Summary

Introduction

Obesity is characterized as a kind of low-grade systematic inflammation with the potential to cause deficits in memory, behavior, or learning ability compared with a healthy state [1]. Substantial neural circuitry and neuroendocrine activity disorders, impaired cortisol feedback, imbalanced neurotransmitter metabolism, alternating dopamine systems, and defective cognition are derived from obesity-related inflammatory processes in adipose tissue [3]. One of the intrinsic factors underlying obesity-related brain dysfunction is the gut microbiota, which seems to represent a link between environmental pressures, such as lifestyle and diet, and the host physiology that regulates neural pathways [4]. The microbiota-gut-brain axis contributes greatly to treating obesity-induced diseases in the central nervous system (CNS), including the prefrontal cortex (PFC), HIP, and hypothalamus (HYP). The PFC is the implementation center of the CNS, and damage to the PFC influences cognitive function, behavioral ability, and mental conditions in humans [5].

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