Theoretical and Experimental Contributions to Characterising the Adipokine-Inflammation Axis in Obese Companion Dogs in Lagos State, South West Nigeria

The adipokine-inflammation axis, in which excess adipose tissue drives chronic low-grade inflammation through dysregulated adipokine secretion, is well characterised in humans and rodents but remains poorly understood in obese companion dogs, particularly in African clinical populations. This doctoral study made original theoretical and experimental contributions to characterising this axis in obese client-owned dogs in Lagos State, South West Nigeria. One hundred dogs classified as obese by dual-energy X-ray absorptiometry body fat percentage above 35% and fifty lean-weight controls were enrolled. A theoretical model proposing adipose tissue hypoxia as the upstream driver of adipokine dysregulation and systemic inflammation was constructed and tested. Serum leptin, adiponectin, resistin, interleukin-6, tumour necrosis factor-alpha, monocyte chemoattractant protein-1, and C-reactive protein were quantified by canine-specific immunoassays. Adipose tissue biopsies from obese dogs were analysed for hypoxia-inducible factor-1-alpha and adiponectin receptor expression by real-time PCR. Obese dogs demonstrated a fourfold elevation in leptin and a 68% reduction in adiponectin relative to lean controls, alongside significantly elevated interleukin-6, tumour necrosis factor-alpha, and C-reactive protein. Adipose hypoxia-inducible factor-1-alpha was upregulated twofold in obese dogs, confirming the adipose tissue hypoxia hypothesis. Adiponectin-to-leptin ratio was the strongest single predictor of systemic inflammatory marker elevation in regression modelling. This doctoral study establishes the adipokine-inflammation axis as a clinically important molecular framework for understanding obesity comorbidities in Lagos companion dogs. Keywords: canine obesity, adipokines, leptin, adiponectin, inflammation.