Weanling male Sprague-Dawley rats were fed one of 10 purified, high fat (20% wt/wt) diets for 6 wk to determine if an in vivo relationship exists between dietary fat composition, plasma membrane composition and insulin binding to epididymal adipocytes. The diets fed provided ratios of polyunsaturated to saturated fatty acids (P/S ratios) representative of those consumed by the human population and ranging from 0.14 to 1.80. The dietary P/S ratio fed altered the essential and nonessential fatty acid composition of plasma membrane phospholipids. Diet-induced alterations in membrane phosphatidylcholine and phosphatidylethanolamine composition were found to be related in a dose-dependent manner to insulin binding at both physiological and supraphysiological insulin concentrations. This observation further supports in vivo a dietary mechanism for modulating insulin action. The present study establishes that the effect of diet on the relationship between membrane composition and insulin binding reaches a plateau within the physiological range of dietary P/S ratios.
Experiments have shown that the amount and source of dietary energy may alter protein metabolism. A high fat diet has resulted in greater nitrogen retention than a high carbohydrate (CHO) diet. To examine this question further, adult rats were fed diets providing ratios of CHO:FAT as a percentage of energy of 0.5, 1.0, 1.5, 2.0, 2.5 or 3.0 for 6 wk. Mean energy and protein intakes were 93.0 +/- 0.8 kcal/d and 5.3 +/- 0.1 g/d, respectively. Final body weight was lower in rats fed the high fat diet (CHO:FAT, 0.5) than in rats fed the high carbohydrate diet (CHO:FAT, 3.0) (P less than 0.05), and a linear response was observed over the entire range of treatments (r = 0.92). Rats fed the high fat diet had the highest nitrogen balance; values were significantly (P less than 0.05) different from those of rats fed high carbohydrate diets (CHO:FAT, 2.0 or 2.5) when expressed as mg nitrogen/kcal energy gain. Rats fed the high fat diet had the highest protein gain and the lowest fat gain as a function of energy gain. It is concluded that alterations in nonprotein energy source result in metabolic changes, which may be related to adaptations in energy expenditure and/or protein deposition.
The effect of dietary protein and fat levels on cardiac mitochondrial oxidative phosphorylation was assessed polarographically. Weanling rats were fed on semi-purified diets containing different protein levels (10, 30, 50 and 70%) on a gross energy basis (PGE) for 9, 23 and 58 d. Cardiac mitochondria isolated from rats fed on a 70% PGE diet for 23 d exhibited significantly reduced ADP:oxygen (ADP: 0) values compared with mitochondria from rats fed on a low-protein diet. Feeding low-protein diets for 58 d increased the ADP: 0 value. When the dietary fat level was altered to provide (% PGE: YO fat-energy): 30: 14,30:30,70: 14,70:30, feeding 70% PGE diets reduced the ADP:O value compared with the 30% P G E level, but no difference was observed between low-fat and high-fat groups, These results indicate that the impaired ADP:O value for rats fed on very-high-protein diets was not due to the dietary fat level but that the level of dietary protein is an important determinant of oxidative phosphorylation in rat heart mitochondria.Protein intake: Fat intake: Oxidative phosphorylation: Rat Treatment of morbid obesity often involves the use of high-protein, very-low-energy diets (Schemmel et al. 1983). Some biological responses to high-protein diets have been investigated. When animals were fed on a high-protein diet, fasting blood glucose and plasma insulin concentrations were significantly elevated in rats (Usami et ai. 1982) and the absolute rate of whole-body protein synthesis decreased in chicks (Kita et al. 1989). Stereological analysis of ultrathin sections illustrated that the high-protein diet induced a significant increment in the density and size of hepatocyte mitochondria (Zaragoza et al. 1987). However, little is known regarding the effect of high-protein diets on bioenergetic function or mitochondrial function. In the present study two experiments were undertaken : the first experiment involved clarifying the effect of dietary protein level on oxidative phosphorylation of cardiac mitochondria, while the second study was designed to determine whether or not the impaired oxidative phosphorylation of rats fed on highprotein diets would be improved by addition of dietary fat. MATERIALS A N D M E T H O D SAnimals and diets. Male Sprague-Dawley Weanling rats obtained from the University of Alberta at 3 weeks of age (52 (SE 3) g) were housed individually under a controlled 12 h lightdark cycle at 21 f 1". After a 6 d adaptation period, animals were fed on a semi-2 1, Japan.
Dietary lipids and evolution of the human brain I have been asked to comment on an interesting topic that as a nutritional biochemist I know almost nothing about. With this firm subject matter appreciation and conceptual starting point, I have read the publication by Broadhurst et al. (1988) with considerable interest. For me it was almost a new speciation event! Drs Broadhurst, Cunnane and Crawford have posed an intriguing hypothesis wherein they speculate that brain growth in early Homo occurred because of 'brain-specific' nutrition that had an enabling impact on the evolution of early man. The authors cite an association between 'precocious' cultures and the consumption of fish and shellfish. This association of the evolution of intelligent behaviours with consumption of polyunsaturated fatty acids has some merit, particularly as lack of consumption of these components reduces brain size and brain function. From recent research, it is likely that n-3 fatty acids may impact on human behaviours. Perhaps these behaviours were important to other cultural aspects of the speciation event?I find it attractive to agree with the notion posed by , but would suggest that the scavenging early hominid needed something more as a single speciation event: perhaps we should look to a change in a gene locus that favoured survival between meals and during different seasonal fortunes. On a metabolic basis, I would suggest that this enabling gene could be one that favoured an efficient conservation of a reserve of extra energy for use later when the 'fishing and clamming' was poor. Perhaps these same genes also represent the evolutionary origins of our present day problems with surplus energy. ReferencesBroadhurst CL, Cunnane SC & Crawford MA (1998) Rift Valley lake fish and shellfish provided brain-specific nutrition for early Homo. British Journal of Nutrition 79, 3-21.Dietary lipids and evolution of the human brain -Reply by Broadhurst et al.
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