The responses of glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) were studied in liver and adipose tissue of rats fed for 2 days a high glucose diet containing levels of synthetic trilinolein ranging from 0 to 25% (w/w) of the diet (trilinolein was substituted for glucose). One group of rats was starved for 2 days before the trilinolein-containing diets were fed (starved-refed); a second group of rats was fed a fat-free diet for 7 days before the trilinolein-containing diets were fed (ad libitum). Liver G6PD activity decreased exponentially and liver ME activity decreased linearly with increasing dietary trilinolein in starved-refed rats, but did not decrease significantly in ad libitum fed rats. Total liver lipid decreased exponentially with increasing trilinolein in starved-refed rats, but increased exponentially in ad libitum fed rats. Adipose tissue G6PD and ME activities decreased slightly with increasing trilinolein in starved-refed rats, but did not decrease in ad libitum fed rats. When the data were adjusted by analysis of covariance for differences in glucose intake, the liver responses in starved-refed rats were still significant but the adipose tissue responses were not, indicating that the responses of adipose tissue (but not of liver) may have resulted from decreased glucose intake rather than from increased trilinolein intake. The results suggest that dietary trilinolein inhibits the characteristic increase in liver G6PD, ME and total lipids upon starvation-refeeding. However, after the levels of these parameters have been increased by feeding a fat-free diet they cannot be decreased by dietary trilinolein in 2 days.

Male Wistar rats were either starved for 2 days and refed for 2 days or meal-fed (2 hours/day) for 2 or 6 weeks. Diets contained 45% carbohydrate as either disaccharides (maltose, sucrose) or the monosaccharide equivalents (glucose, invert sugar). Changes in the activities of glucose-6-phosphate dehydrogenase (G6PD) and malic enzyme (ME) in the liver and epididymal adipose tissue, relative liver and epididymal fat pad sizes, fasting serum insulin levels, and food efficiencies were determined. The response to the diets containing the monosaccharide equivalents (glucose or invert sugar) was used as the basal response. With starvation-refeeding or 6 weeks of meal-feeding, the activities of G6PD and ME in the liver were greater with maltose than with glucose (disaccharide effect), but with sucrose only starvation-refeeding induced the effect. The disac-charide effect increased the activities of G6PD and ME in the liver and decreased the activities in the adipose tissue. Rats meal-fed the disaccharide diets for 2 weeks had greater fasting insulin levels and relative liver and epididymal fat pad sizes than did rats fed the equivalent monosaccharide diets. The disaccharide effect increased food efficiency significantly after both 2 and 6 weeks of meal-feeding. In rats starved and refed carbohydrates containing fructose, activities of G6PD and ME were higher in liver and lower in adipose tissue than in rats refed carbohydrates containing only glucose (fructose effect); with meal-feeding only the liver showed a fructose effect. These findings support the hypothesis that dietary disaccharides produce metabolic effects which are different in magnitude than those produced by their equivalent monosaccharides.

1. Responses of hepatic glucose-6-phosphate dehydrogenase (EC 1.1.1.49; G6PD), malic enzyme (EC 1.1.1.40; ME), acetyl-CoA carboxylase (EC 6.4.1.2; ACAC), and fatty acid synthetase (FAS) were studied in male Wistar rats after a period of starvation and refeeding of diets containing 400 g glucose, or raw or cooked starches as the source of carbohydrate/kg. Starches fed included maize, potato, wheat, rice, and tapioca. 2. When compared to the responses of rats given the glucose-containing diet, rats given raw maize- or rice-starch-containing diets had a significantly lower ME response, and rats given raw potato starch had significantly lower responses of G6PD, ME, ACAC, and FAS. The enzyme responses of rats given cooked starches were similar to those of glucose-fed rats, except that rats given cooked wheat starch had significantly lower G6PD and ME responses than did glucose-fed rats. 3. When the enzyme responses to refeeding of the same starch source in either raw or cooked form were compared, it was found that (a) the FAS response was significantly higher to cooked than to raw maize starch, (b) the G6PD and ACAC responses were significantly higher to cooked than to raw tapioca starch, (c) the G6PD, ME, ACAC, and FAS responses were significantly higher to cooked than to raw potato starch. 4. The results suggest that reported differences in the lipogenic enzyme responses between simple sugars and starch may in some instances be magnified because of the use of uncooked starches in experimental diets.

The responses of glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) in liver and adipose tissue and of total liver lipid were studied in rats fed a fat-free diet for 2 days, then fed diets containing 12% synthetic triglyceride for 3 days, or fed a fat-free diet for 5 days. Triglycerides of the following fatty acids were used: caprylic (8:0), capric (10:0), palmitic (16:0), stearic (18:0), oleic (18:1) or linoleic (18:2). Enzyme activities and total liver lipids were statistically adjusted for differences in fat absorption to determine the theoretical effects of the different triglycerides if they all had been absorbed equally. Liver G6PD activity was highest in the group fed the 8:0 diet and lowest in the group fed the 18:2 diet; the response of liver ME was similar, but the differences were smaller among groups. The levels of both G6PD and ME in liver were greater in the groups fed saturated triglycerides (8:0, 10:0, 16:0, 18:0) than in the groups fed unsaturated triglycerides (18:1, 18:2). Total liver lipids were highest in the group fed the 8:0 diet, intermediate in the groups fed the 10:0, 18:2 and fat-free diets, and lowest in the groups fed the 16:0, 18:0 and 18:1 diets. When adjusted for differences in fat absorption, however, total liver lipids were generally highest in the groups fed saturated triglycerides (8:0, 10:0, 16:0, 18:0) or the fat-free diet, and lowest in the groups fed unsaturated triglycerides (18:1, 18:2). Adipose tissue G6PD and ME levels varied among the groups fed different triglycerides, but adjusted values for G6PD were greater in the groups fed the long-chain saturated triglycerides (16:0, 18:0) than in any other group.

The responses of liver glycogen and glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) to a high glucose, adequate protein diet were compared between rats previously starved 2 days, then refed a high protein, carbohydrate-free diet for 2 days, and rats previously fed the high protein diet for 4 days. Glycogen levels increased dramatically during the first day the high carbohydrate diet was fed, then decreased gradually on the second day. The response was the same regardless of whether the rats had been starved more before the high protein diet was fed. Liver G6PD activity also increased when the high carbohydrate diet was fed, and continued to increase on the second day. The increase in G6PD, however, was significantly greater in the rats which had been starved before the high protein diet was fed. It is suggested that some process occurs during starvation that predisposes the induction of G6PD upon refeeding a high carbohydrate diet, over and above any effect of glycogen accumulation and breakdown. Glucose or glucose-6-phosphate derived from glycogen does not appear to be the primary inducer of G6PD in rat liver.

The role of dietary unsaturated fat in the control of hepatic glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) was studied in rats subjected to one or two cycles of starvation-refeeding. Rats starved and refed a control (5% corn oil) diet showed a threefold increase in G6PD activity and a twofold increase in ME activity compared to ad libitum-fed rats. After a second cycle of starvation-refeeding G6PD and ME activities showed fourfold and threefold increases, respectively, as compared to ad libitum-fed rats. Feeding rats diets containing 8% linoleic acid (as triglycerides) prevented the increase in G6PD and ME activities upon starvation-refeeding, diets with oleic, palmitic, and stearic acis when fed did not prevent this increase. Feeding rats various combinations of linoleic, linolenic and oleic acids following starvation prevented the additional increase in G6PD and ME activities after a second starvation-refeeding cycle; however, linoleic acid fed alone during the first refeeding prevented the additional increase in ME activity but not in G6PD activity. It is suggested that the dietary control of these enzymes involves one or more specific polyunsaturated fatty acids.

Male Wistar rats were starved and refed diets containing either 40% carbohydrate as monosaccharides (glucose, fructose, invert sugar) or disaccharides (maltose, sucrose), or 42.2% carbohydrate as glucose. Induction of various liver enzymes and changes in total liver lipid levels by the different dietary sugars were studied. Liver enzymes measured included glucose-6-phosphate dehydrogenase (g6pd), 6-phosphogluconate dehydrogenase (6PGD), malic enzyme (ME), phosphofructokinase (PFK), L-alpha-glycerol phosphate dehydrogenase (LalphaGPD), pyruvate kinase (PK), citrate cleavage enzyme (CCE), acetyl CoA carboxylase (AcCoAC), and fatty acid synthetase (FAS). The responses in enzyme activity to diets containing glucose or invert sugar were used as the basal response. Enzyme responses to refeeding the carbohydrate diets fell into three categories: (1) enzyme activity increased both by the disaccharide configuration of the carbohydrate and by fructose (G6PD, PK, CCE, AcCoAC, FAS); (2) enzyme activity increased only by the disaccharide configuration of the carbohydrate (6PGD, ME); and (3) enzyme activity increased only by fructose (PFK, LalphaGPD). Total liver lipid level was increased both by the disaccharide configuration of the carbohydrate and by fructose. Refeeding diets containing equal molar amounts of glucose or maltose did not abolish the disaccharide effect. The data indicate that the disaccharide configuration of maltose and sucrose may have an effect at the gastrointestinal level, which causes an increased induction of certain enzymes in the liver.