Oral Gavage Palmitic Acid Administration
Objective: Assess CNS effects of palmitic acid on PKC-θ localization and hypothalamic insulin resistance via oral gavage administration in rodents
This is a Oral Gavage Palmitic Acid Administration protocol using rats and mice as the model organism. The procedure involves 3 procedural steps, 2 materials. Extracted from a 2009 paper published in Journal of Clinical Investigation.
Model and subjects
rats and mice • Not specified in provided text • unknown • Not specified in provided text • Not specified in provided text
Study window
Estimated timing pending
Core workflow
Oral gavage administration of palmitic acid • Assessment of PKC-θ subcellular localization • Control treatment with oleic acid
Primary readouts
- PKC-θ subcellular localization to cell membranes in hypothalamus
- Hypothalamic insulin signaling
- Hypothalamic leptin signaling
- Insulin resistance development
Key equipment and reagents
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Protocol Steps
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Oral gavage administration of palmitic acid
Administer palmitic acid to rodents via oral gavage to assess CNS effects on PKC-θ localization and insulin resistance
Note: This method was used as an alternative to direct infusion to deliver palmitic acid to the CNS
View evidence from paper
“CNS exposure to palmitic acid via direct infusion or by oral gavage increased the localization of PKC-θ to cell membranes in the hypothalamus”
Assessment of PKC-θ subcellular localization
Evaluate PKC-θ localization to cell membranes in hypothalamic regions following palmitic acid exposure
Note: Localization changes were associated with impaired hypothalamic insulin and leptin signaling
View evidence from paper
“CNS exposure to palmitic acid via direct infusion or by oral gavage increased the localization of PKC-θ to cell membranes in the hypothalamus, which was associated with impaired hypothalamic insulin and leptin signaling”
Control treatment with oleic acid
Administer oleic acid (monounsaturated fatty acid) as control to demonstrate specificity of palmitic acid effects
Note: Oleic acid did not increase membrane localization of PKC-θ or induce insulin resistance, confirming specificity
View evidence from paper
“the monounsaturated fatty acid, oleic acid, neither increased membrane localization of PKC-θ nor induced insulin resistance”