1. In growing rats, the time-course effects of giving a normal-protein diet (200 g casein/kg; NP) for 52 d, a lowprotein diet (20 g casein/kg; LP) for 52 d and a LP diet for 26 d followed by balanced refeeding (200 g casein/ kg; BR) for 26d, on the fatty acid composition of liver total lipids and microsomal phospholipids were investigated together with 66-and A5-microsomal desaturase activities.2. The oleic acid content (mg/g tissue) of liver total lipids increased progressively with the LP diet, while linoleic acid was increased only at days 7 and 52. 20:306, 20:4w6,22:5w6 and 22:6w3 fatty acids decreased during the period on the LP diet. BR for 7 d was sufficient to restore the fatty acid composition of total lipids to control values. Changes in the fatty acid composition of liver microsomal L-a-phosphatidylcholines were observed only after 52 d on the LP diet; the proportions (% w/w total fatty acids) of 18:0, 20:3w6 and 20:406 fatty acids decreased while oleic acid increased. The fatty acid composition of L-or-phosphatidylethanolamines was less affected.3. A6-and A5-desaturase activities decreased to 2&30 % of their original values after 2 d on the LP diet; a smaller deficit prevailed after 14 d but disappeared after 25 d, to appear again after 52 d. As early as day 2 of BR, desaturase activities were greatly recovered and returned to control values at day 13.4. The present work shows that modifications in microsomal A6-and A5-desaturase activities are not strictly paralleled by the changes in the composition of fatty acids of liver total lipids and microsomal phospholipids.Linoleic acid (1 8 : 2w6) and a-linolenic acid (1 8 : 3w3) are the main dietary forms of essential fatty acids (EFA). In the body, especially in the liver, linoleic acid is converted mainly into arachidonic acid (20: 4w6) and a-linolenic acid into eicosapentaenoic acid (20: 5w3) and docosahexaenoic acid (22:6w3). Williams & Hurlebaus (1966) showed in the rat that a dietary protein insufficiency may lead to changes in lipid composition and suggested this to be due to an impairment of the enzyme systems converting linoleic acid into arachidonic acid. These authors found that, in rats maintained on a protein-free diet for 2 months, there was a progressive decrease in 20:406 in liver phospholipids (PL) and an accumulation of 18:2w6 in neutral lipids. Plasma 20:4w6 was also reduced. Gerson (1974) has shown that protein deficiency leads to a decrease in PL C,, and C,, fatty acids. Particularly, 20 : 4w6 was decreased in rat liver outer mitochondria1 membranes and microsomes, accompanied by an accumulation of 18 : 2w6. It was postulated that 18 : 2w6 accumulation was due to impaired chain elongation or desaturation, or both, in protein-deficient rats. However, Gerson & Wong (1 978) also showed that the incubation in vitro of liver microsomes of adult rats fed on a protein-free diet for 7 weeks, with labelled palmitate or linoleate, revealed unchanged chain elongation and desaturation enzyme activities. De Gomez Dumm et al. (1970), Mercuri et al....

The effects of protein restriction on A9 desaturase (EC 1.14.99.5) activity were studied in growing rats. A control group was fed on a balanced diet (200 g caseinlkg; BD) for 28 d. The experimental group was fed on the low-protein diet (20 g caseinlkg; LP) for 26 d, then refed the balanced diet (BD-R) for 2 d. Rats were born to and suckled from normally fed dams. The enzyme activity was measured after 2 and 14 d of LP, and 26 d of L P plus 2 d of BD-R, by incubations in vitro of hepatic microsomal pellets with [ l-'4Cjstearic acid. The results indicated a decreased A9 desaturase activity after 2 and 14 d of LP of -33 and -43 YO respectively. Refeeding for 2 d was sufficient to super-repair this activity ( + 66 YO). The fatty acid composition of total liver lipids and microsomal phosphatidylethanolamines (PE) and phosphatidylcholines (PC) were also investigated; 18:O decreased in total liver lipids at 14 d of LP, when 18:ln-9 increased. Stearic acid (18:O) increased in PC at 2 d of L P and in P E a t 14 d of L P ; oleic acid (18:ln-9) did not change. Therefore, it is concluded that a defect occurred in the bioconversion of 18:O into 18:ln-9 by A9 desaturation during protein depletion. As oleic acid is accumulated in total liver lipids during LP, we speculate that this is due to a decreased oxidation or transport of this fatty acid. Microsomal desaturation: Protein restriction: Liver lipidsProtein restriction alters the metabolism of polyunsaturated fatty acids (Waterlow et al. 1960; Williams & Hurlebaus, 1965a, b, 1966 Truswell et al. 1969;Flores et al. 1970;Naismith, 1973;Anthony & Edozien, 1975; Brenner, 1981;Holman et al. 1981;Leat, 1983). Rogers (1971Rogers ( , 1972 has shown that liver mitochondria1 and microsomal polyunsaturated fatty acid compositions were altered by such a diet. All these findings suggested an impairment of the bioconversion of linoleic acid into arachidonic acid, via a decrease in desaturase activities. Mercuri et al. (1979) showed that A6 and A5 desaturase activities were diminished in pregnant rats fed on a low-protein diet (50 g casein/kg, LP). Then De Tomas et al. (1980Tomas et al. ( , 1983 reported decreased liver A6 and A5 desaturase activities in the early developing rat related to a maternal protein restriction. These authors also showed the negative effect of protein depletion on the supply of polyunsaturated fatty acids for normal development and metabolic adaptations. But Gerson & Wong (1978) indicated that, in the adult rat, if the liver fatty acid composition was affected by protein restriction, the A6 and A5 desaturase activities were not.We have demonstrated, by a time-course study using a low-protein diet (50 g gluten/kg), the impairment of A6 and A5 desaturase activities in growing rats (Narce et al.

Rat liver microsomal delta 6 and delta 5 desaturation are defective in experimental diabetes, but this defect is correctable with insulin treatment. Rat liver fatty acid composition and delta 6 and delta 5 desaturation were studied in the spontaneously diabetic adult female Bio-Breeding (BB) rat. Control Wistar rats and BB rats (4 weeks of diabetes), that received insulin (1 IU.100 g body weight-1.day-1), were killed 20 h after the last insulin injection. delta 6 and delta 5 desaturase activities were estimated from the incubation of liver microsomes with (1-14C) 18:2, n-6 or (2-14C) 20:3, n-6, respectively, and the fatty acid composition of the liver and microsomal liver lipids were investigated. Under experimental conditions delta 6 and delta 5 desaturase activities were unchanged in the BB rats when compared to the control rats. Impairment of the liver fatty acid composition of diabetic BB rats is not consistent with normal desaturase activity and may be explained by factors other than desaturation disturbance.

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