Gut· 2017Q1
Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit
- 669citations
- Q1SCImago
- 2017year
Short summary
Butyrate, when taken orally, reduces food intake by suppressing appetite-stimulating neurons and activating brown adipose tissue (BAT) through the gut-brain neural circuit, leading to improved energy metabolism.
AI-generated from the title and abstract; the full text is not read.
Key points
- Oral butyrate intake suppresses appetite by decreasing neuropeptide Y neuron activity in the hypothalamus and affecting brainstem satiety centers.
- Chronic butyrate supplementation prevents diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia, and hepatic steatosis, primarily by reducing food intake.
- Butyrate activates brown adipose tissue (BAT) and promotes fat oxidation through increased sympathetic outflow, independent of reduced food intake.
- The effects of butyrate on food intake and BAT activation are abolished by subdiaphragmatic vagotomy, indicating a crucial role for the gut-brain neural circuit.
AI-generated from the title and abstract; the full text is not read.
Abstract
OBJECTIVE: Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate. DESIGN: Acute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice. RESULTS: Acute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT. CONCLUSION: Butyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT.
The authors' abstract, as published at the source. Gut, 2017 · DOI ↗
Continue with a free account
Ask the paper: 3 free questions a day about this paper; save it, get its citation, new summaries every day for your field. Takeaways are Premium.
Continue free on the webSign in with Google or Apple; no card needed. You come back to this paper.
On your phone:
Field: Endocrine and Autonomic Systems
Endocrine and Autonomic SystemsNeuroscience