Login now to access Regular content available to all registered users.
Abstract
Discussion Forum (0)
LXR synthetic agonist GW3965 modifies neuronal lipid homeostasis and decreases prostaglandin production in the dorsal root ganglia of obese mice
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
LXR synthetic agonist GW3965 modifies neuronal lipid homeostasis and decreases prostaglandin production in the dorsal root ganglia of obese mice
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
LXR synthetic agonist GW3965 modifies neuronal lipid homeostasis and decreases prostaglandin production in the dorsal root ganglia of obese mice
Nadia Elshareif
Abstract
Discussion Forum (0)
LXR synthetic agonist GW3965 modifies neuronal lipid homeostasis and decreases prostaglandin production in the dorsal root ganglia of obese mice
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
LXR synthetic agonist GW3965 modifies neuronal lipid homeostasis and decreases prostaglandin production in the dorsal root ganglia of obese mice
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
Poster No: 1084
Presenter: Nadia Elshareif
Institution: Loyola University Chicago
Introduction: The prevalence of peripheral neuropathy is owed to the increasing diabetic and overweight population. Chronic neuropathic pain as a result of peripheral neuropathy is a major disabling symptom in obese individuals. Neuropathic pain management is limited and ineffective, as glucose management for diabetic and prediabetic individuals fails to reduce or improve pain symptoms. It is necessary to understand the mechanisms behind neuropathic pain and associated neuronal dysfunction to identify potential therapeutic options. Recent studies focus on lipid dysfunction associated with excess fat intake and obesity as a target for neuropathic pain management. We assessed the role of Liver X Receptors (LXRs), which are nuclear transcription factors that regulate lipid homeostasis, phospholipid remodeling, and inflammation. We have previously observed that the activation of LXRs using the synthetic agonist GW3965, protects mice from Western diet (WD)-induced mechanical allodynia.
Methods: To further understand the mechanisms of LXR-activation on obesity-induced pain, we used translating ribosome affinity purification (TRAP) to evaluate the WD-induced translatomic and lipidomic changes in sensory neurons of WD-fed mice treated with the LXR agonist GW3965.
Results: We observed that GW3965 treatment may regulate and maintain lipid homeostasis in sensory neurons of the dorsal root ganglia. Interestingly, treatment with GW3965 decreased prostaglandin D2 levels in the dorsal root ganglia of obese mice, which suggests downstream mechanisms to attenuate obesity-induced neuronal dysfunction and inflammation. We observed a decrease in neuronal free fatty acid content, accompanied by an increase in lysophosphatidylcholine, phosphatidylcholine, and cholesterol ester species, which may have interplaying mechanisms upon LXR activation.
Conclusions: Given our observations, LXR activation may protect neurons from metabolic insults that contribute to neuropathic pain. Future studies are required to understand these interplaying mechanisms behind LXR activation and lipid homeostasis in the peripheral nervous system to downstream inflammatory pain pathways, which may help identify effective therapeutic options.
References: No
References 1:
References 2:
References 3:
References 4:
Grant Support:
Keywords: Liver X Receptors, GW3965, Peripheral Neuropathy, Lipids, Inflammation
{{ help_message }}
{{filter}}