High-fat or high-sugar diets as trigger inflammation in the microbiota-gut-brain axis

Abstract

Microbiota, intestine, and brain interact one with another through the afferent fibers of the vagus nerve, which is the major linkage of this one. It has been established that long-term dietary habits influence gut bacterial diversity and are capable of inducing changes in hypothalamic energy homeostasis. The biological effects are mediated by microglial activation, systemic inflammation, and vagal afferent nerve signaling, culminating in neuroinflammation. It has been emphasized the need for a further approach regarding the influence of the dietary factors as well as their direct impacts or outcomes on the gut dysbiosis. This review aimed to understand the role of some dietary triggers of neuroinflammation on changes in the gut microbiota. Each of the diets significantly altered the microbial composition in distinct ways, leading to neuroadaptations. Hyperlipidic diets (SFA and MUFA) can stimulate TLR4 inflammatory pathway by increased LPS translocation and LBP activation and modulate brain functions, mainly in the center of feeding. Overconsumption of sucrose seems to be more detrimental for metabolic alterations, whereas fructose has a more pronounced effect on gut barrier dysfunction and subclinical inflammation; nevertheless, sucrose absorption favors fructose bioavailability, contributing to adiposity and sugar addiction.

Keywords:

• overconsumption
• fatty acids
• simple sugar
• gut bacteria
• neuroinflammation

Acknowledgements

DAR and LPP are recipients of CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) fellowships.

Conflict of interest

There is no conflict interest.

Abbreviations

JNK: c-Jun N-terminal kinase

IL: interleukin

NAFLD: nonalcoholic fatty liver disease

NASH: nonalcoholic steatohepatitis

pIκB: phosphorylation of inhibitor of -κB

SCFA: short-chain fatty acids

TNF-α: tumor necrosis factor-alpha.