Autonomic function
Vagal free fatty acid receptor (FFAR3), is necessary... 30 September 2021
Our data demonstrate that FFAR3 expressed in vagal neurons regulates feeding behavior and mediates propionate-induced decrease in food intake.
Read more >Communication between the gut microbiota and peripheral nervous... 1 May 2022
 In this review, we cover the general anatomy and function of the PNS, and then we discuss how the molecules secreted or stimulated by gut microbes signal through the PNS to alter host development and physiology.
Short chain fatty acids: the messengers from down... 18 August 2025
Short-chain fatty acids (SCFAs), produced by the metabolism of dietary fibers in the gut, have wide-ranging effects locally and throughout the body. They modulate the enteric and central nervous systems, benefit anti-inflammatory pathways, and serve as energy sources. Recent research reveals SCFAs as crucial communicators between the gut and brain, forming the gut-brain axis. This perspective highlights key findings and discusses signaling mechanisms connecting SCFAs to the brain. By shedding light on this link, the perspective aims to inspire innovative research in this rapidly developing field.
Read more >C2CD5 in noradrenergic neurons regulates thermogenesis and lipid... 20 May 2026
- The Chain of Events: Your sympathetic nervous system releases a chemical messenger called Norepinephrine (NE). This messenger tells your body to burn fat and produce heat (a process known as thermogenesis).
- The Role of C2CD5: RC2CD5 protein acts like a traffic controller. It is located in the specific nerve cells that release Norepinephrine, and it helps ensure that enough of this chemical is secreted.
- The Effect of a Poor Diet: When mice were fed an obesogenic (unhealthy/high-fat) diet, the production of the C2CD5 protein in their nerve cells was heavily suppressed.
- What Happens Without C2CD5: When scientists genetically removed the C2CD5 protein from these nerve cells in mice, the chain reaction broke. The nerves couldn’t release enough Norepinephrine, which lowered the mice’s energy expenditure and caused them to gain excess fat (adiposity).
- The Solution: When the researchers gave these C2CD5-deficient mice a Norepinephrine supplement, it fixed the problem—restoring their ability to burn fat and energy normally.