Metabolic Syndrome/Obesity

LXR agonist modifies neuronal lipid homeostasis and decreases... 12 October 2022

GW3965 decreased prostaglandin levels and decreased free fatty acid content, while increasing lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species in the sensory neurons of the dorsal root ganglia (DRG). These data suggest novel downstream interplaying mechanisms that modifies DRG neuronal lipid following GW3965 treatment.

 

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Short chain fatty acids: the messengers from down... 18 August 2025

Virginie Mansuy-Aubert and Yann Ravussin

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.

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C2CD5 in noradrenergic neurons regulates thermogenesis and lipid... 20 May 2026

This study highlights how our brains and nervous systems control body fat, specifically focusing on a newly discovered protein called C2CD5. [1, 2]
In simple terms, the text describes a biological chain reaction that controls how much energy we burn and how much fat we store. [1]
Here is a breakdown of the key findings in simple steps:
  • 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.

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