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Obesity is the result of genetic, behavioral, environmental, physiological, social and cultural factors that result in energy imbalance and promote excessive fat deposition. In particular, in Western society, which is characterized by sedentary lifestyles combined with excess energy intake, many people often try to lose weight with caloric restriction. However it is well known that the weight regain after caloric restriction results in accelerated storage of adipose tissue (De Andrade et al. 2015). The high efficiency of the recovery of the energy depots of body fat probably evolved in ancient times, when the food availability was intermittent and it was necessary to face up to long periods of famine. Nowadays, this efficiency is the key factor causing higher body fat gain relative to lean tissue, and the preferential catch-up fat phenomenon has also been linked to the hyperinsulinemic state of catch-up growth and the associated risks for later development of metabolic syndrome (Crescenzo et al. 2003; Dulloo et al.2006). Several studies on refeeding after caloric restriction have been conducted on laboratory rats, a very good model for obesity studies, because energy intake, diet composition and the level of physical activity can be easily monitored, and also, considering the standard housing conditions, laboratory rats exhibit a sedentary behavior, similarly to what happens in humans (Aydin et al. 2014; Buettner et al. 2007; Spangenberg et al. 2005): it was observed that during the refeeding with low fat diet the rats showed a reduction in energy expenditure and an increase in metabolic efficiency, causing high body fat deposition, even in absence of hyperphagia (Dulloo et al. 2008). In addition it has been shown that this high metabolic efficiency that drives catch-up fat on a low fat diet is exacerbated by refeeding on HFD (Crescenzo et al. 2003; Dulloo & Gerardier, 1992), although in different ways depending on the type of fat included in the diet (Dulloo et al.

Obesity is the result of genetic, behavioral, environmental, physiological, social and cultural factors that result in energy imbalance and promote excessive fat deposition. In particular, in Western society, which is characterized by sedentary lifestyles combined with excess energy intake, many people often try to lose weight with caloric restriction. However it is well known that the weight regain after caloric restriction results in accelerated storage of adipose tissue (De Andrade et al. 2015). The high efficiency of the recovery of the energy depots of body fat probably evolved in ancient times, when the food availability was intermittent and it was necessary to face up to long periods of famine. Nowadays, this efficiency is the key factor causing higher body fat gain relative to lean tissue, and the preferential catch-up fat phenomenon has also been linked to the hyperinsulinemic state of catch-up growth and the associated risks for later development of metabolic syndrome (Crescenzo et al. 2003; Dulloo et al.2006). Several studies on refeeding after caloric restriction have been conducted on laboratory rats, a very good model for obesity studies, because energy intake, diet composition and the level of physical activity can be easily monitored, and also, considering the standard housing conditions, laboratory rats exhibit a sedentary behavior, similarly to what happens in humans (Aydin et al. 2014; Buettner et al. 2007; Spangenberg et al. 2005): it was observed that during the refeeding with low fat diet the rats showed a reduction in energy expenditure and an increase in metabolic efficiency, causing high body fat deposition, even in absence of hyperphagia (Dulloo et al. 2008). In addition it has been shown that this high metabolic efficiency that drives catch-up fat on a low fat diet is exacerbated by refeeding on HFD (Crescenzo et al. 2003; Dulloo & Gerardier, 1992), although in different ways depending on the type of fat included in the diet (Dulloo et al.

The recovery of body weight after a period of caloric restriction is accompanied by an enhanced efficiency of fat deposition and hyperinsulinemia—which are exacerbated by isocaloric refeeding on a high fat diet rich in saturated and monounsaturated fatty acids (SFA-MUFA), and poor in polyunsaturated fatty acids (PUFA), and associated with a blunting of de novo lipogenesis in adipose tissue and liver. As high fat diets rich in PUFA have been shown to limit the excess fat deposition and improve glucose homeostasis, we investigated here the extent to which de novo lipogenesis in liver and adipose tissues (white and brown), as well as hepatic oxidative stress, are influenced by refeeding on diets rich in PUFA.Design: In rats calorically restricted for 14 days and refed for 14 days on isocaloric amounts of a high fat diet rich in lard (i.e., high SFA- MUFA) or in safflower and linseed oils (rich in PUFA), we investigated energy balance, body composition, glycemic profile, and the regulation of fatty acid synthase (rate- limiting enzyme of de novo lipogenesis) in liver, white and brown adipose tissue. We also evaluated oxidative stress in liver and skeletal muscle and markers of hepatic inflammation.Results: Rats refed the PUFA diet gained less lipids and more proteins compared to rats refed SFA-MUFA diet and showed lower amount of visceral and epididymal white adipose tissue, but increased depots of interscapular brown adipose tissue, with higher expression of the uncoupling protein 1. A significant increase in non- protein respiratory quotient and carbohydrate utilization was found in rats refed PUFA diet. Rats refed PUFA diet showed improved glucose homeostasis, as well as lower triglycerides and cholesterol levels. Fatty acid synthase activity was significantly higher in liver, white and brown adipose tissue, while lipid peroxidation and the degree of inflammation in the liver were significantly lower, in rats refed PUFA diet.Conclusions: When considering the composit

The recovery of body weight after a period of caloric restriction is accompanied by an enhanced efficiency of fat deposition and hyperinsulinemia—which are exacerbated by isocaloric refeeding on a high fat diet rich in saturated and monounsaturated fatty acids (SFA-MUFA), and poor in polyunsaturated fatty acids (PUFA), and associated with a blunting of de novo lipogenesis in adipose tissue and liver. As high fat diets rich in PUFA have been shown to limit the excess fat deposition and improve glucose homeostasis, we investigated here the extent to which de novo lipogenesis in liver and adipose tissues (white and brown), as well as hepatic oxidative stress, are influenced by refeeding on diets rich in PUFA.Design: In rats calorically restricted for 14 days and refed for 14 days on isocaloric amounts of a high fat diet rich in lard (i.e., high SFA- MUFA) or in safflower and linseed oils (rich in PUFA), we investigated energy balance, body composition, glycemic profile, and the regulation of fatty acid synthase (rate- limiting enzyme of de novo lipogenesis) in liver, white and brown adipose tissue. We also evaluated oxidative stress in liver and skeletal muscle and markers of hepatic inflammation.Results: Rats refed the PUFA diet gained less lipids and more proteins compared to rats refed SFA-MUFA diet and showed lower amount of visceral and epididymal white adipose tissue, but increased depots of interscapular brown adipose tissue, with higher expression of the uncoupling protein 1. A significant increase in non- protein respiratory quotient and carbohydrate utilization was found in rats refed PUFA diet. Rats refed PUFA diet showed improved glucose homeostasis, as well as lower triglycerides and cholesterol levels. Fatty acid synthase activity was significantly higher in liver, white and brown adipose tissue, while lipid peroxidation and the degree of inflammation in the liver were significantly lower, in rats refed PUFA diet.Conclusions: When considering the composit