Abstract
Objective—To evaluate postprandial changes in the leptin concentration of CSF in dogs during development of obesity.
Animals—4 male Beagles.
Procedures—Weight gain was induced and assessments were made when the dogs were in thin, optimal, and obese body conditions (BCs). The fat area at the level of the L3 vertebra was measured via computed tomography to assess the degree of obesity. Dogs were evaluated in fed and unfed states. Dogs in the fed state received food at 9 AM. Blood and CSF samples were collected at 8 AM, 4 PM, and 10 PM.
Results—Baseline CSF leptin concentrations in the thin, optimal, and obese dogs were 24.3 ± 2.7 pg/mL, 86.1 ± 14.7 pg/mL, and 116.2 ± 47.3 pg/mL, respectively. In the thin BC, CSF leptin concentration transiently increased at 4 PM. In the optimal BC, baseline CSF leptin concentration was maintained until 10 PM. In the obese BC, CSF leptin concentration increased from baseline value at 4 PM and 10 PM. Correlation between CSF leptin concentration and fat area was good at all time points. There was a significant negative correlation between the CSF leptin concentration–to–serum leptin concentration ratio and fat area at 4 PM; this correlation was not significant at 8 AM and 10 PM.
Conclusions and Clinical Relevance—Decreased transport of leptin at the blood-brain barrier may be 1 mechanism of leptin resistance in dogs. However, leptin resistance at the blood-brain barrier may not be important in development of obesity in dogs.
