Abstract
Objective and methods: Metabolic viscera and their vasculature are richly innervated by peripheral sensory neurons. Here, we examined the metabolic and inflammatory profiles of mice with selective ablation of all Nav1.8-expressing primary afferent neurons. Results: While mice lacking sensory neurons displayed no differences in body weight, food intake, energy expenditure, or body composition compared to controls on chow diet, ablated mice developed an exaggerated inflammatory response to high-fat feeding characterized by bouts of weight loss, splenomegaly, elevated circulating interleukin-6 and hepatic serum amyloid A expression. This phenotype appeared to be directly mediated by the ingestion of saturated lipids. Conclusions: These data demonstrate that the Nav1.8-expressing afferent neurons are not essential for energy balance but are required for limiting the acute phase response caused by an obesogenic diet.
| Original language | English (US) |
|---|---|
| Journal | Molecular Metabolism |
| DOIs | |
| State | Accepted/In press - 2017 |
Fingerprint
Keywords
- Deafferentation
- Diphtheria toxin
- Energy homeostasis
- Inflammation
- Nodose ganglion
- Obesity
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology
Cite this
Nav1.8 neurons are involved in limiting acute phase responses to dietary fat. / Udit, Swalpa; Burton, Michael; Rutkowski, Joseph M.; Lee, Syann; Bookout, Angie L.; Scherer, Philipp E.; Elmquist, Joel K.; Gautron, Laurent.
In: Molecular Metabolism, 2017.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nav1.8 neurons are involved in limiting acute phase responses to dietary fat
AU - Udit, Swalpa
AU - Burton, Michael
AU - Rutkowski, Joseph M.
AU - Lee, Syann
AU - Bookout, Angie L.
AU - Scherer, Philipp E.
AU - Elmquist, Joel K.
AU - Gautron, Laurent
PY - 2017
Y1 - 2017
N2 - Objective and methods: Metabolic viscera and their vasculature are richly innervated by peripheral sensory neurons. Here, we examined the metabolic and inflammatory profiles of mice with selective ablation of all Nav1.8-expressing primary afferent neurons. Results: While mice lacking sensory neurons displayed no differences in body weight, food intake, energy expenditure, or body composition compared to controls on chow diet, ablated mice developed an exaggerated inflammatory response to high-fat feeding characterized by bouts of weight loss, splenomegaly, elevated circulating interleukin-6 and hepatic serum amyloid A expression. This phenotype appeared to be directly mediated by the ingestion of saturated lipids. Conclusions: These data demonstrate that the Nav1.8-expressing afferent neurons are not essential for energy balance but are required for limiting the acute phase response caused by an obesogenic diet.
AB - Objective and methods: Metabolic viscera and their vasculature are richly innervated by peripheral sensory neurons. Here, we examined the metabolic and inflammatory profiles of mice with selective ablation of all Nav1.8-expressing primary afferent neurons. Results: While mice lacking sensory neurons displayed no differences in body weight, food intake, energy expenditure, or body composition compared to controls on chow diet, ablated mice developed an exaggerated inflammatory response to high-fat feeding characterized by bouts of weight loss, splenomegaly, elevated circulating interleukin-6 and hepatic serum amyloid A expression. This phenotype appeared to be directly mediated by the ingestion of saturated lipids. Conclusions: These data demonstrate that the Nav1.8-expressing afferent neurons are not essential for energy balance but are required for limiting the acute phase response caused by an obesogenic diet.
KW - Deafferentation
KW - Diphtheria toxin
KW - Energy homeostasis
KW - Inflammation
KW - Nodose ganglion
KW - Obesity
UR - http://www.scopus.com/inward/record.url?scp=85028305622&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85028305622&partnerID=8YFLogxK
U2 - 10.1016/j.molmet.2017.07.012
DO - 10.1016/j.molmet.2017.07.012
M3 - Article
C2 - 29031710
AN - SCOPUS:85028305622
JO - Molecular Metabolism
JF - Molecular Metabolism
SN - 2212-8778
ER -