Short-term induced hyperinsulinaemia and dexamethasone challenge do not affect circulating total adiponectin concentrations in insulin-sensitive ponies.
Authors: Barnabé Marine A, Elliott Jonathan, Harris Patricia A, Menzies-Gow Nicola J
Journal: Equine veterinary journal
Summary
# Editorial Summary Understanding what drives adiponectin dysregulation in equine laminitis remains clinically important, particularly given the established association between low circulating adiponectin and endocrinopathic laminitis risk; however, whether insulin resistance causes low adiponectin or vice versa has remained unclear. Researchers administered either a dexamethasone challenge or a 9-hour euglycaemic-hyperinsulinaemic clamp to six insulin-sensitive native-breed ponies, measuring circulating adiponectin concentrations and whole blood expression of adiponectin and growth factor receptors via quantitative PCR at multiple timepoints. Neither acute glucocorticoid exposure nor induced hyperinsulinaemia altered total circulating adiponectin levels, though dexamethasone did upregulate adiponectin receptor 1 (AdipoR1) and insulin-like growth factor 1 receptor expression, suggesting a compensatory receptor response to the hormone's metabolic effects. The receptor upregulation without corresponding changes in adiponectin itself raises the possibility that short-term endocrine challenges may trigger signalling pathway adjustments independently of adiponectin availability, though the small sample size and measurement of total rather than high-molecular-weight adiponectin limit broader applicability. For equine practitioners, these findings suggest that simple acute insulin or steroid elevations may not directly suppress adiponectin production in metabolically healthy animals, implying that hypoadiponectinaemia associated with laminitis risk likely develops through different or longer-term metabolic perturbations worthy of further investigation.
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Practical Takeaways
- •Circulating total adiponectin may not be a reliable short-term biomarker for monitoring insulin dysregulation or dexamethasone effects in ponies; measurement of high-molecular-weight adiponectin or receptor expression patterns may be more informative
- •The disconnect between stable adiponectin levels and upregulated adiponectin signalling receptors during dexamethasone challenge suggests the relationship between adiponectin dysregulation and laminitis risk may be more complex than direct hormone concentration changes
- •Clinical monitoring of laminitis risk in insulin-sensitive ponies requiring dexamethasone therapy should not rely solely on adiponectin concentration changes to predict adverse metabolic effects
Key Findings
- •Short-term dexamethasone challenge (0.08 mg/kg i.v.) did not alter circulating total adiponectin concentrations in insulin-sensitive ponies despite upregulating AdipoR1 and IGF-1R expression at 150-180 minutes
- •Euglycaemic-hyperinsulinaemic clamp-induced hyperinsulinaemia for 9 hours produced no changes in circulating total adiponectin concentrations or receptor gene expression
- •Ex vivo incubation of whole blood with dexamethasone (10-1000 ng/mL for 3 hours) did not alter expression of adiponectin or insulin/IGF-1 receptors
- •Dexamethasone administration may trigger physiological compensatory responses via receptor upregulation to counteract insulin sensitivity changes, despite stable adiponectin levels