Time-course effects of protein malnutrition on hepatic fatty acids Δ6 and Δ5 desaturation in the growing rat

Abstract

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....

Maternal low protein diet in rats programmes fatty acid desaturase activities in the offspring

“…This may at first seem surprising given the difference in measured D5 desaturase activity. Apparent discrepancies between desaturase activities and phospholipid composition have also been reported previously [14,15]. This is not unexpected as membrane incorporated arachidonic acid could arise from two sources.…”

“…The activity of D6 and D5 desaturases were assayed according to a published method [9] using [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C] labelled linoleic acid (18:2n-6) and eicosatrienoic acid (20:3n-6) fatty acids as their respective substrates. After reaction, fatty acids were saponified, transmethylated and spotted onto 10 % silver nitrate-impregnated silica gel thin-layer chromatography plates (Merck, Darmstadt, Germany) with known standards.…”

Fatty acid desaturases in human adipose tissue: relationships between gene expression, desaturation indexes and insulin resistance

“…The inherent difficulty of measuring desaturase activities directly has led to the use of fatty acid product/substrate ratios as surrogate estimates of desaturase activities. This approach is supported to some degree by results from animal studies [21][22][23][24], but compelling evidence is lacking. Importantly, the absence of human data on the validity of these relationships is of concern, since mice, in contrast to humans, express various isoforms of SCD with different affinities for the precursor fatty acids [4].…”

Cystic Fibrosis Presenting With Dermatitis

“…Numerous studies have supported the importance of zinc in the metabolism of EFAs, as reviewed by Cunnane et al 35,36 Finally, decreased protein (more specifically, deficiencies in certain amino acids) may alter EFA metabolism. 37 PEM is frequently associated with EFA deficiency, and it has been suggested that many of the clinical symptoms-including skin changes-seen in these malnourished individuals may be at least partially attributed to EFA deficiency. 38 In conclusion, the dermatitis seen in infants with CF is likely multifactorial, with deficiencies in zinc, EFAs, and protein contributing to its development.…”