Summary The liver plays a key role in lipid metabolism. Depending on species it is, more or less, the hub of fatty acid synthesis and lipid circulation through lipoprotein synthesis. Eventually the accumulation of lipid droplets into the hepatocytes results in hepatic steatosis, which may develop as a consequence of multiple dysfunctions such as alterations in β‐oxidation, very low density lipoprotein secretion, and pathways involved in the synthesis of fatty acids. In addition an increased circulating pool of non‐esterified fatty acid may also to be a major determinant in the pathogenesis fatty liver disease. This review also focuses on transcription factors such as sterol‐regulatory‐element‐binding protein‐1c and peroxisome proliferator‐activated receptor alpha, which promote either hepatic fatty acid synthesis or oxidation.

Weight gain in neutered cats was decreased by feeding an LF, low energy-dense diet. To prevent weight gain in cats after neutering, a suitable LF diet should be fed in carefully controlled meals rather than ad libitum.

Butyrate is recognised as efficient in healing colonic inflammation, but cannot be used as a long-term treatment. Dietary fibre that produces a high-butyrate level when fermented represents a promising alternative. We hypothesised that different types of dietary fibre do not have the same efficiency of healing and that this could be correlated to their fermentation characteristics. We compared short-chain fructo-oligosaccharides (FOS) and type 3 resistant starch (RS) in a previously described dextran sulfate sodium (DSS)-induced colitis model. Seventytwo Sprague -Dawley rats received water (control rats) or DSS (50 g DSS/l for 7 d then 30 g DSS/l for 7 (day 7) or 14 (day 14) d). The rats were fed a basal diet (BD), or a FOS or RS diet creating six groups: BD-control, BD-DSS, FOS-control, FOS-DSS, RS-control and RS-DSS. Caeco-colonic inflammatory injuries were assessed macroscopically and histologically. Short-chain fatty acids (SCFA) were quantified in caeco-colon, portal vein and abdominal aorta. At days 7 and 14, caecal and distal macroscopic and histological observations were improved in RS-DSS compared with BD-DSS and also with FOS-DSS rats. Caeco-colonic SCFA were reduced in FOS-DSS and RS-DSS groups compared with healthy controls. The amount of butyrate was higher in the caecum of the RS-DSS rats than in the BD-DSS and FOS-DSS rats, whereas distal butyrate was higher in FOS-DSS rats. Partially explained by higher luminal levels of SCFA, especially butyrate, the healing effect of RS confirms the involvement of some types of dietary fibre in inflammatory bowel disease. Moreover, the ineffectiveness of FOS underlines the importance of the type of dietary substrate.

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The present study was conducted to assess the body composition, leptin, and energy expenditure changes following gonadectomy in cats. Twenty-one females (12 intact and nine spayed) and 21 males (11 intact and 10 castrated) were used. Body weight was recorded. Serum plasma leptin was measured by radioimmunoassay and body composition and energy expenditure were assessed after injection of doubly labelled water. These results confirmed the gain in body weight and body fat following neutering and demonstrated a strong linear relationship between body fat and serum level of leptin. Energy expenditure decreased in castrated cats in comparison with intact ones. This study underlined the effect of gonadectomy as a major factor of obesity in cats and showed that the increase in circulating leptin reflected the amount of body fat. The present results provide further evidence that the regimen of gonadectomized cats should be carefully controlled to avoid excessive weight gain.

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Obesity-induced insulin resistance (IR) is a common problem in humans as well as domestic dogs. It is well-known that this syndrome is associated with many modifications but it is still unclear if the changes are alterations or adaptations. The purpose of this study was to develop obesity-induced IR in dogs, through a long-term overfeeding period, and to explore hormonal and metabolic disturbances associated with the development of this syndrome. Dogs were overfed for 7 months. Body weight increased by 43 +/- 5%, and insulin sensitivity decreased by 44 +/- 5%. Plasma insulin-like growth factor 1 (IGF1), tumour necrosis factor alpha (TNFalpha), and non-esterified fatty acids (NEFA) concentrations progressively increased during the overfeeding period (IGF1: 111 +/- 13 to 266 +/- 32 ng/ml, p < 0.001; TNFalpha: 5 +/- 5 to 134 +/- 41 pg/ml; NEFA: 0.974 +/- 0.094 to 1.590 +/- 0.127 mmol/l, p < 0.05). These metabolic and hormonal impairments are associated with IR, in obese dogs, and could explain, at least in part, the outbreak of this syndrome.

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