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Biomedical subjects

J Yudkin

Publications and source records attributed to J Yudkin.

At least 19 recordsLinked to original sources
PubMed1992

Diet as a source of phospholipid esterified 9,11-octadecadienoic acid in humans.

1. Diene-conjugated fatty acids are one of the products of free-radical attack upon lipids and therefore have been used as markers of such attack. The major diene-conjugated fatty acid in human tissue and serum is an isomer of linoleic acid (9,12-octadecadienoic acid), namely 9,11-octadecadienoic acid. Diet may be another source of this isomer, raising questions as to its value as a free-radical marker. The aim of this study was to determine the importance of diet as a source of 9,11-octadecadienoic acid in phospholipid esterified fatty acids in human serum. 2. Foodstuffs rich in 9,11-octadecadienoic acid were identified. Fourteen subjects volunteered to alter their diets, either increasing ('high diet') or decreasing ('low diet') their intake of these foodstuffs for 3 weeks. Where subjects undertook both diets, a washout period of at least 3 weeks was allowed between phases. 3. Seven-day diet histories were kept and scored with respect to their content of 9,11-octadecadienoic acid. The concentrations of 9,11-octadecadienoic acid and linoleic acid in serum phospholipids were measured by h.p.l.c. with u.v. detection. 4. The percentage molar ratio of 9,11-octadecadienoic acid to linoleic acid was calculated. The percentage molar ratio rose significantly on the 'high diet' [1.3(0.4) versus 1.9(0.7), P = 0.01, mean (SD)] and fell significantly on the 'low diet' [1.6(0.4) versus 1.1(0.4), P = 0.004, means (SD)]. There was a significant correlation between the change in dietary intake of 9,11-octadecadienoic acid and the change in the percentage molar ratio (r = 0.829, P = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Vitamins and IQ.

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Child↗
PubMed1979

Influence of different dietary carbohydrates on liver and plasma constituents in rats adapted to meal feeding.

Male Sprague-Dawley rats were given in one experiment diets with starch or sucrose and in a second experiment diets with glucose or fructose. In each experiment, one group of 5 rats was fed ad libitum and five other groups fed a 3-hour meal each day. After 36 days, one group of the meal-fed rats was killed when the meal was due, and the other groups at intervals after the beginning of the meal. The group fed ad libitum was killed the next day after 21 h fasting. Meal feeding led to a smaller food intake and a smaller gain in weight, and a lower blood concentration of triacylglycerol. The diets with sucrose or fructose produced heavier livers and kidneys than did those with starch or glucose. The consumption of the meal led also to a temporary increase in the weight of the liver. The weight of the kidney, however, did not change in rats given starch or gluocse, but fell in rats given sucrose or fructose. Meal consumption was also followed by an increase in the concentration of liver glycogen, irrespective of the nature of the dietary carbohydrate. The concentration of plasma fatty acids was affected differently by meals containing the different carbohydrates, the extremes being a continuing fall with starch and no change with fructose. The concentration of triacyglycerol was increased by sucrose or fructose after the presentation of the meal. The concentration of blood glucose rose and then fell when the meal contained starch or glucose, but fell and then rose when it contained sucrose, and especially when it contained fructose. The concentration of insulin in meal-fed rats receiving sucrose was higher than that of rats receiving starch, both before and after the meal. This difference was not seen in rats fed ad libitum. The results indicate that the effects of meal feeding, or of sucrose or fructose, are not additive.

Animals↗
PubMed1979

The avoidance of sucrose by thiamine-deficient rats.

Rats were fed carbohydrate-free diets without thiamine. Sucrose was offered separately, either before the thiamine was removed, or when it was removed, or at varying periods after it was removed. In the absence of dietary thiamine, sucrose consumption began at a high level, but was then reduced. Thereafter, death due to thiamine deficiency followed at intervals that varied from 4 weeks to 12 months. Survival was shortest in those rats that ate sucrose in largest amounts or at shortest intervals; survival was longest in those rats that avoided sucrose altogether for long periods. Sex or age did not appear to affect survival. The results are interpreted as demonstrating a conflict between the avoidance of sucrose so as to avoid the unpleasant symptoms of thiamine deficiency, and the consumption of sucrose so as to obtain the pleasure of its high palatability.

Age Factors↗