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Chronic intake of high-energy diets alters the physiological response to food and favors overconsumption. Feeding, especially of palatable food, leads to dopamine (DA) release in the Nucleus Accumbens (NAc, in the ventral striatum), prefrontal cortex (PFC) and dorsal striatum. The mesocortical (ventral tegmental area (VTA) projecting to NAc) DA system has been implicated in motivational drive and food seeking while the nigrostriatal DA (projections from the substantia nigra (SN) to the dorsal striatum) pathway plays a role in both food anticipatory behavior and reinforcement. In humans, hypersensitivity to food-associated reward may predispose to weight gain, however as obesity progresses deficit in reward signaling emerges. Individuals with obesity have reduced DRD2 availability in prefrontal brain regions compared to lean counterparts. 

Jiyoung S. Kim, Kevin C. Williams, Rebecca A. Kirkland, Ruth Schade, ... Claire B. de La Serre

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The gut-brain axis mediates bacterial driven modulation of reward signaling

Jiyoung S. Kim, Kevin C. Williams, Rebecca A. Kirkland, Ruth Schade, ... Claire B. de La Serre

The gut-brain axis mediates bacterial driven modulation of reward signaling

Objective

Our goal is to investigate if microbiota composition modulates reward signaling and assess the role of the vagus in mediating microbiota to brain communication.

Methods

Male germ-free Fisher rats were colonized with gastrointestinal contents from chow (low fat (LF) ConvLF) or HF (ConvHF) fed rats.

Results

Following colonization, ConvHF rats consumed significantly more food than ConvLF animals. ConvHF rats displayed lower feeding-induced extracellular DOPAC levels (a metabolite of dopamine) in the Nucleus Accumbens (NAc) as well as reduced motivation for HF foods compared to ConvLF rats. Dopamine receptor 2 (DDR2) expression levels in the NAc were also significantly lower in ConvHF animals. Similar deficits were observed in conventionally raised HF fed rats, showing that diet-driven alteration in reward can be initiated via microbiota. Selective gut to brain deafferentation restored DOPAC levels, DRD2 expression, and motivational drive in ConvHF rats.

Conclusions

We concluded from these data that a HF-type microbiota is sufficient to alter appetitive feeding behavior and that bacteria to reward communication is mediated by the vagus nerve.

Articles in Press

The gut-brain axis mediates bacterial driven modulation of reward signaling

Jiyoung S. Kim, Kevin C. Williams, Rebecca A. Kirkland, Ruth Schade, ... Claire B. de La Serre

The gut-brain axis mediates bacterial driven modulation of reward signaling

Objective

Our goal is to investigate if microbiota composition modulates reward signaling and assess the role of the vagus in mediating microbiota to brain communication.

Methods

Male germ-free Fisher rats were colonized with gastrointestinal contents from chow (low fat (LF) ConvLF) or HF (ConvHF) fed rats.

Results

Following colonization, ConvHF rats consumed significantly more food than ConvLF animals. ConvHF rats displayed lower feeding-induced extracellular DOPAC levels (a metabolite of dopamine) in the Nucleus Accumbens (NAc) as well as reduced motivation for HF foods compared to ConvLF rats. Dopamine receptor 2 (DDR2) expression levels in the NAc were also significantly lower in ConvHF animals. Similar deficits were observed in conventionally raised HF fed rats, showing that diet-driven alteration in reward can be initiated via microbiota. Selective gut to brain deafferentation restored DOPAC levels, DRD2 expression, and motivational drive in ConvHF rats.

Conclusions

We concluded from these data that a HF-type microbiota is sufficient to alter appetitive feeding behavior and that bacteria to reward communication is mediated by the vagus nerve.

2021 impact factor: 8.568

You are what you eat

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