The predisposition of cats to gain weight following neutering is well established; however, there is little information about the distribution and range of post-neutering weight gains observed in cats under a controlled environment. This retrospective study investigated 6-month post-castration weight gain and distribution of percentage body weight (BW) change in a cohort of twenty, male domestic shorthair cats relative to a control group of intact cats. Cats were matched in age (2·0-2·6 years), husbandry conditions and consumed ad libitum the same dry maintenance diet for at least 3 months prior to and 6 months following castration. All cats were castrated within 48 h of each other. All cats gained weight after castration. Mean BW was 4·67 (sd 0·70) kg at the start of the study and 5·93 (sd 1·38) kg at the end of the study, with individual weight gain ranging 3-53 % at 6 months post-neutering. The pre-conception BW of the queens of each cat was compared with the pre- and post-neutering BW of their offspring. The pre-conception BW of the queens was significantly correlated with the offspring's initial BW (ρ = 0·65, P = 0·01), final BW (ρ = 0·67, P = 0·01) and percentage BW change (ρ = 0·54, P = 0·04). A wide range of post-castration weight gains was observed among cats of similar backgrounds and housing conditions. Implementation of effective methods to control food consumption pre-conception and post-neutering may be a strategy for preventing obesity and obesity-related disorders in cats.

The initial cause of post-neutering weight gain in male cats is not entirely known. There is evidence that energy intake (EI) increases rapidly post-neutering, but it is not clear if neutering also decreases energy expenditure (EE) prior to weight gain. Thus, the purpose of this study was to determine if a decrease in EE contributes to the initial shift toward positive energy balance in neutered male cats. To determine the influence of neutering on EE independent of changes in EI and body weight (BW), male cats were fed at their pre-neutering maintenance EI and EE was measured at 4 days pre-neutering, 3-4 days post-neutering, and 9 days post- neutering. Ad libitum food access was then provided for 6 months. Body composition was measured and blood samples collected for serum chemistry at pre-neutering and 7 days, 13 days and 6 months post-neutering. Total energy expenditure (TEE) adjusted for lean body mass (LBM) did not change in cats from pre-neutering to 9 days post-neutering. However, TEE adjusted for BW and resting energy expenditure adjusted for either LBM or BW showed a small, but significant (P<0.05) increase from pre-neutering to 9 days post-neutering. When allowed free choice food access, cats showed significant increases of food intake (FI) and BW. Circulating concentrations of ghrelin increased, while adiponectin levels decreased following neutering. The results of this study indicate that initial post-neutering weight gain in male cats results from increased FI and not decreased EE. Long-term control of FI should be initiated after neutering to prevent hyperphagia and weight gain in male cats.

The polyunsaturated nature of n-3 fatty acids makes them prone to oxidative damage. However, it is not clear if n-3 fatty acids are simply a passive site for oxidative attack or if they also modulate mitochondrial reactive oxygen species (ROS) production. The present study used fat-1 transgenic mice, that are capable of synthesizing n-3 fatty acids, to investigate the influence of increases in n-3 fatty acids and resultant decreases in the n-6:n-3 ratio on liver mitochondrial H(2)O(2) production and electron transport chain (ETC) activity. There was an increase in n-3 fatty acids and a decrease in the n-6:n-3 ratio in liver mitochondria from the fat-1 compared to control mice. This change was largely due to alterations in the fatty acid composition of phosphatidylcholine and phosphatidylethanolamine, with only a small percentage of fatty acids in cardiolipin being altered in the fat-1 animals. The lipid changes in the fat-1 mice were associated with a decrease (p<0.05) in the activity of ETC complex I and increases (p<0.05) in the activities of complexes III and IV. Mitochondrial H(2)O(2) production with either succinate or succinate/glutamate/malate substrates was also decreased (p<0.05) in the fat-1 mice. This change in H(2)O(2) production was due to a decrease in ROS production from ETC complex I in the fat-1 animals. These results indicate that the fatty acid changes in fat-1 liver mitochondria may at least partially oppose oxidative stress by limiting ROS production from ETC complex I.