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Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens, Georgia 30602, USA

(Requests for offprints should be addressed to M Hoenig; Email: mhoenig{at}uga.edu)

(D C Ferguson is now at Department of Veterinary Biosciences, The University of Illinois at Urbana-Champaign, Urbana, Illinois 61802, USA)

The obese cat is a model for the study of the progression toward type 2 diabetes. In this study, the impact of obesity on the hypothalamic–pituitary–thyroid axis was examined in 21 domestic shorthair cats before and after the development of obesity, which significantly increased body mass index (BMI), % body fat (BF), and girth (P<0.0001 for all). Serum total thyroxine (TT₄), tri-iodothyronine, free T₄ (FT₄) by direct dialysis, nonesterified fatty acids (NEFA), and leptin were measured, and FT₄ fraction (FFT₄) was calculated. Serum thyrotropin (TSH) concentrations were measured in nine animals by validating a heterologous canine TSH assay with recombinant feline TSH as a standard. FT₄, FFT₄, NEFAs, and leptin were significantly higher in obese cats. FT₄ had the strongest positive correlation with obesity indices BF, BMI, girth, NEFA, and leptin. Fatty acids oleate and palmitate were shown to inhibit T₄ binding to pooled cat serum in vitro, suggesting the possibility that this mechanism was also relevant in vivo. Serum TT₄ and TSH did not rise significantly. The implications for thyroid hormone (TH) action are not yet clear, but fatty acids have been proposed to inhibit the cellular uptake of TH and/or pituitary TH receptor binding, leading to TH resistance. Increased leptin may also alter sensitivity to negative feedback of TH. In conclusion, feline obesity is associated with a significant increase in FT₄ within the normal range; future investigation into the cellular thyroid status will be necessary to establish cause and effect in this obesity model.