peripheral nerve system Archives

Neuronal LXR Regulates Neuregulin 1 Expression and Sciatic... 17 April 2020

Gavini CK, Bonomo R, Mansuy-Aubert V

Neuronal LXRs may regulate non-neuronal cell function via a Nrg1-dependent mechanism. The decrease in Nrg1 expression in DRG neurons of WD-fed mice may suggest an altered Nrg1-dependent neuron-SC communication in Obesity. The communication between neurons and non-neuronal cells such as SC could be a new biological pathway to study and understand the molecular and cellular mechanism underlying Obesity-associated neuropathy and PNS dysfunction.

The lipid sensor LXRs protect small sensory neurons... 29 September 2018

Chaitanya Gavini, Raiza Bonomo, Laurent Gautron, Angie Bookout, Syann Lee and Virginie Mansuy-Aubert

Our findings suggest that lipid-binding nuclear receptors expressed in the sensory neurons of the DRG play a role in the onset of obesity-induced hypersensitivity. The LXR and lipid-sensor pathways represent a research avenue to identify targets to prevent debilitating complications affecting the peripheral nerve system in obesity.

Obesity-Associated Neuropathy: Recent Preclinical Studies and Proposed Mechanisms 26 February 2022

In this review, we focus on interventions and their mechanisms that are shown to ameliorate neuropathy in MetS obese models including: (i) inhibition of a sensory neuron population, (ii), modification of dietary components, (iii) activation of nuclear and mitochondrial lipid pathways, (iv) exercise, (v) modulation of gut microbiome composition and their metabolites.

Fecal Transplantation and Butyrate Improve Neuropathic Pain, Modify... 15 October 2020

Raiza R. Bonomo, Tyler M. Cook, Chaitanya K. Gavini, Chelsea R. White, Jacob R. Jones, Elisa Bovo, Chelsea White,Raiza R. Bonomo, Tyler M. Cook, aiza R. Bonomo, Tyler M. Cook, Chaitanya K. Gavini, Chelsea R. White, Jacob R. Jones, Elisa Bovo, Chelsea White,Raiza R. Bonomo, Tyler M. Cook

Circulating butyrate, a metabolite secreted by gut microbiome and absorbed in the blood stream, may be involved by acting directly on peripheral nerve system immune cells and gene expression or pain channels.

Communication between the gut microbiota and peripheral nervous... 1 May 2022

Tyler Cook, Virginie M. Aubert

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.

Fecal microbiome transplantation and tributyrin improves early cardiac... 2 March 2023

Fecal microbiome transplantation and tributyrin improves early cardiac dysfunction and modifies the BCAA metabolic pathway in a diet induced pre-HFpEF mouse model

More than 50% of patients with heart failure present with heart failure with preserved ejection fraction (HFpEF), and 80% of them are overweight or obese. In this study we developed an obesity associated pre-HFpEF mouse model and showed an improvement in both systolic and diastolic early dysfunction following fecal microbiome transplant (FMT). Our study suggests that the gut microbiome-derived short-chain fatty acid butyrate plays a significant role in this improvement.

Comparison of western diet-induced obesity and streptozotocin mouse... 4 June 2024

Elshareif N, Gornick E, Gavini CK, Aubert G, Mansuy-Aubert V.

Front Physiol. 2023 Oct 11;14:1238120. doi: 10.3389/fphys.2023.1238120. PMID: 37885804; PMCID: PMC10598778.

Elshareif N, Gornick E, Gavini CK, Aubert G, Mansuy-Aubert V.

In our research, we thoroughly characterized energy balance and glucose homeostasis, as well as allodynia and cardiac function, all of which have been previously shown to be altered by WD feeding. Notably, our findings revealed that the treatment of WD-fed mice with STZ exacerbated dysfunction in glucose homeostasis via reduced insulin secretion in addition to impaired peripheral insulin signaling. Furthermore, both WD and WD + STZ mice exhibited the same degree of cardiac autonomic neuropathy, such as reduced heart rate variability and decreased protein levels of cardiac autonomic markers. Furthermore, both groups developed the same symptoms of neuropathic pain, accompanied by elevated levels of activating transcription factor 3 (Atf3) in the dorsal root ganglia. These discoveries enhance our understanding of metabolic activity, insulin resistance, neuropathy, and cardiac dysfunction of diet-induced models of obesity and diabetes.

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.

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.

A gut-adipose-nerve axis mediates inulin protection against Western... 20 May 2026

Western diets—high in fat and sugar but low in fiber—often cause chronic nerve pain and hypersensitivity. Researchers discovered that adding a type of dietary fiber called inulin to the diet can reverse this damage. Inulin feeds beneficial gut bacteria, which then produce short-chain fatty acids (SCFAs). These SCFAs travel to fatty tissues, reduce inflammation, and help the nervous system recover.

The study highlights how targeted fiber intake can act as an effective alternative to fecal transplants to protect nerve health.

Key takeaways from the research:

The Problem: Western diets lack fermentable fibers, which leads to nerve-related pain and hypersensitivity.
The Solution: Adding inulin (a complex carbohydrate fiber) to the diet remodels gut bacteria and produces beneficial short-chain fatty acids.
How It Works: The SCFAs improve overall metabolic health and reduce inflammation around nerves

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