Methods available to estimate the energy values of sugar alcohols.

There is increased interest in the use of sugar alcohols as substitutes for sucrose in various food products. Part of this interest is derived from studies suggesting that sugar alcohols may have lower energy values because of the way they are metabolized. Contributing to the complexity is the fact that not all sugar alcohols are similarly metabolized. Indirect and direct methods used to assess the energy value of sugar alcohols have often yielded conflicting data. Energy values obtained using mathematical models have been adopted by some countries to account for metabolic processes associated with sugar alcohol digestion and absorption. I focus on two sugar alcohols, sorbitol and maltitol, and describe various methods that have been used to assess their energy value.

Marginal zinc status does not exacerbate pancreatic carcinogenesis associated with dietary soybean trypsin inhibitor concentrate in rats.

Although the etiology of pancreatic cancer is largely unknown, diet-associated factors may play a role. Male Sprague-Dawley rats (14 d of age) were given a single injection of either saline or azaserine and were weaned (21 d) to diets with either adequate (30 micrograms/g) or low (9 micrograms/g) zinc, with or without 1.0 g/100 g active trypsin inhibitor in the form of soybean trypsin inhibitor concentrate. Experimental diets were fed for 14 wk. Regardless of dietary zinc status, diets with soybean trypsin inhibitor concentrate caused hyperplasia and/or hypertrophy of the pancreas. Pancreatic zinc content was not different among groups. Low dietary zinc levels did not affect total body growth rate or serum zinc concentration. Tibia zinc was also used as an indicator of zinc status. Tibia zinc concentration was lower in rats fed diets low in zinc relative to adequate zinc diets. Azaserine-induced acidophilic foci were larger and more numerous when soybean trypsin inhibitor concentrate was present in the diet regardless of dietary zinc level. Thus, low zinc does not exacerbate the soybean trypsin inhibitor concentrate effects that promote pancreatic cancer.

Fructose utilization by the human intestinal epithelial cell line, Caco-2.

The potential use of Caco-2 cells as a model for the study of fructose metabolism and transport in the intestine was evaluated, since this human cell line exhibits many of the anatomical and biochemical characteristics of mature enterocytes. Pre- and postconfluent cultures converted [14C]fructose to CO2, lipid, and glycogen. Apparent utilization of [14C]fructose was less than that of [14C]glucose. This difference was due in part to the more rapid uptake of glucose from medium as compared with fructose. Addition of glucose, galactose, and mannose to medium markedly decreased the metabolism, while slightly inhibiting the uptake, of [14C]fructose. These data demonstrate that fructose can serve as a carbon and energy source for Caco-2 cells, and that common dietary monosaccharides affect the efficiency of fructose metabolism.

Lipoprotein status in Sprague-Dawley and LA/N-corpulent rats as affected by dietary carbohydrates.

1. To compare the impact of type of carbohydrate, genotype and phenotype on the synthesis and levels of plasma lipoprotein protein. Sprague-Dawley rats and carbohydrate-sensitive LA/N-corpulent (cp) rats were fasted (2 days) and then fed diets containing 54% carbohydrate as either sucrose, fructose or cooked cornstarch for 2 days. 2. The amount of 3H-protein present in the VLDL + chylomicron fraction of Sprague-Dawley rats 2 hr after injection of 3H-leucine was affected by type of dietary carbohydrate: sucrose greater than fructose greater than starch. 3. Obese and lean LA/N-cp rats fed diets containing sucrose or fructose had lower concentrations of HDL protein and higher levels of 3H-protein in VLDL + chylomicron fraction than those fed starch. 4. Obese LA/N-cp rats had more HDL protein and higher levels of 3H-protein in VLDL + chylomicron fraction than their lean littermates.

Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch.

Ten hyperinsulinemic and 11 nonhyperinsulinemic men consumed for 5 wk each in a cross-over design a diet, similar to one currently consumed in the United States, with 20% of the kilocalories from either fructose or high-amylose cornstarch to determine the effects of the two diets on various blood metabolites considered to be risk factors associated with heart disease. In the hyperinsulinemic men the intake of fructose as compared with cornstarch significantly increased total triglycerides and their lipoprotein distribution; total and very-low-density lipoprotein cholesterol; apoproteins B-100, C-II, C-III; and uric acid. In the nonhyperinsulinemic men total triglycerides, total and low-density lipoprotein cholesterol and uric acid were significantly greater after the consumption of fructose than after cornstarch. The results indicate that in a diet high in saturated fatty acids and cholesterol, fructose increases the levels of risk factors associated with heart disease, especially in hyperinsulinemic men.

Comparative hormonal profile of two newly developed obese congenic rat strains.

1. The effect of feeding diets containing either 54% sucrose or cooked corn starch for 12 weeks on levels of fasting plasma insulin, corticosterone, growth hormone and glucagon were compared in two newly developed genetically obese rat strains--the normoglycemic LA/N-cp and the diabetic SHR/N-cp. 2. In corpulent rats of either strain, levels of plasma insulin and corticosterone were greater when compared to the lean littermates. Corpulent LA/N-cp rats had lower levels of plasma glucagon and higher levels of plasma growth hormone than did lean LA/N-cp rats. 3. SHR/N-cp rats fed sucrose had greater levels of corticosterone and glucagon than did SHR/N-cp rats fed starch.

Genetic obesity and dietary sucrose decrease hepatic glucagon and insulin receptors in LA/N-corpulent rats.

A catabolic and hypolipemic effect of glucagon has been described in normal animals. We therefore studied the role of glucagon in genetically obese, hyperlipemic rats. Twelve genetically obese hyperlipemic LA/N-cp/cp (corpulent) rats and 12 lean littermates were fed either 54% starch or 54% sucrose for 12 weeks. Plasma glucagon and insulin levels and glucagon and insulin binding to liver membranes were measured. Comparing all corpulent and lean animals regardless of diet, a significant (P less than 0.0001) phenotypical effect (cp/cp greater than lean) was observed in plasma insulin levels (464 +/- 54 vs 70.3 +/- 7.6 muu/ml, mean +/- SEM). Insulin binding (2.68 vs 16.1%/50 micrograms protein) and glucagon binding (25.6 vs 47.3%/50 micrograms protein) were both significantly lower (P less than 0.0001) in corpulent rats as compared to their lean littermates. Sucrose feeding had marginal effect on plasma insulin or insulin binding. It, however, decreased glucagon binding in corpulent rats but not in their controls. A significant negative correlation was observed between plasma insulin and insulin binding, while a positive correlation was seen for plasma glucagon and glucagon binding. A significant negative correlation was observed between plasma glucagon and lipogenic enzymes (glucose-6-phosphate dehydrogenase and malic enzyme) in liver and between glucagon binding and these enzymes. We propose that in these genetically obese rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target cells may be an important contributor to the hyperlipemia and obesity. A further decrease in glucagon binding in rats fed sucrose indicates that sucrose, per se, may be an additional contributory factor.

Hormonal and lipogenic and gluconeogenic enzymatic responses in LA/N-corpulent rats.

Genetically obese normotensive rats, LA/N-corpulent (cp), were fed ad libitum diets containing either 54% sucrose or cooked corn starch for 12 weeks. Twenty-four rats were used for the study; half were corpulent (cp/cp) and half were lean (cp/+ or +/+). Fasting levels of plasma insulin, glucose, corticosterone, glucagon and growth hormone, and activities of liver and epididymal fat pad glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME), and liver and kidney glucose-6-phosphatase (G6Pase), fructose 1,6-diphosphatase (FDPase), and phosphoenolpyruvate carboxykinase (PEPCK) were measured. A significant phenotype effect was observed in insulin, corticosterone, growth hormone, and liver G6PD, ME, FDPase, and kidney PEPCK, G6Pase, FDPase, and epididymal fat pad G6PD and ME (corpulent greater than lean), and glucagon (lean greater than corpulent). Diet effect (sucrose greater than starch) was significant for plasma glucose, liver ME, and kidney G6Pase. Although not significant at the P less than 0.05 level, insulin, corticosterone, liver G6PD and FDPase and kidney FDPase tended to be higher in sucrose-fed rats. This study suggests that the corpulent rat is more lipogenic and gluconeogenic than the lean, and that the hormones responsible are effective in keeping both the lipogenic and gluconeogenic enzyme activity elevated.

Effect of dietary sucrose on the SHR/N-corpulent rat: a new model for insulin-independent diabetes.

A new congenic strain of genetically obese rat, SHR/N-corpulent (cp), was studied. Young male corpulent (cp/cp) and lean (cp/+ or +/+) rats approximately 5 wk of age were fed a diet containing 54% carbohydrate as either sucrose or cooked cornstarch for 9 wk. A phenotype effect was observed with body weight, fasting levels of serum insulin, triglyceride and total cholesterol, levels of serum insulin and glucose after an oral glucose load, and level of urine glucose (corpulent greater than lean), and with systolic blood pressure (corpulent less than lean). Only lean rats were hypertensive. Corpulent rats were hyperinsulinemic, hyperlipidemic, exhibited glycosuria, and were hyperglycemic after an oral glucose load. Lean rats were hyperinsulinemic, but normoglycemic. A diet effect (sucrose greater than starch) was observed with body weight, level of serum glucose after an oral glucose load, and urine volume in both corpulent and lean rats, and with levels of serum insulin and total urine glucose in corpulent rats. Corpulent rats fed sucrose had 20 to 40% higher levels of serum glucose and insulin after an oral glucose load, and twice the amount of total urine glucose, than did corpulent rats fed starch. The data demonstrate that corpulent rats have metabolic characteristics associated with insulin-independent diabetes in humans and that sucrose is more diabetogenic than starch. Manifestation of hyperglycemia in this model may be the result of superimposing obesity on an insulin-resistant genetic background.

Blood insulin, glucose, fructose and gastric inhibitory polypeptide levels in carbohydrate-sensitive and normal men given a sucrose or invert sugar tolerance test.

Twelve carbohydrate-sensitive and 12 normal men were selected for the study. Carbohydrate-sensitivity was based on an abnormal insulin response to a sucrose load. The subjects were fed a diet consisting of 45% of the calories as carbohydrate, 40% fat and 15% protein for 5 days prior to a sucrose or invert sugar tolerance test. In a crossover design, subjects were given 2 g/kg body weight of sucrose or invert sugar, and responses of insulin, glucose, fructose and gastric inhibitory polypeptide (GIP) were determined. Blood samples were taken at 0, 0.5, 1, 2 and 3 hours after being given the test loads. Insulin and glucose levels were significantly higher in carbohydrate-sensitive as compared to normal men. Glucose and GIP did not show any significant differences between the two carbohydrate loads. At 1 hour, the carbohydrate-sensitive men given sucrose had significantly higher insulin levels than carbohydrate-sensitive men given invert sugar (disaccharide effect). At 1, 2 and 3 hours, the disaccharide effect was shown in the fructose levels of the carbohydrate-sensitive men. In normal men, the disaccharide effect with levels of fructose was seen at 0.5 and 3 hours. This study indicates that the disaccharide effect on blood insulin cannot be explained by differences in gastric inhibitory polypeptide in unadapted human subjects.

Effects of dietary fructose on plasma glucose and hormone responses in normal and hyperinsulinemic men.

Twelve men with abnormally high insulin responses to a sucrose load and 12 normal men were fed diets containing 0, 7.5, or 15% of the calories as fructose for 5 weeks each. The diets contained approximately 43% of the calories as total carbohydrate, 42% as fat and 15% as protein. Mean insulin responses of the hyperinsulinemic men were initially 235% of control responses. Plasma glucose concentrations 1 hour after the sucrose load were significantly higher in hyperinsulinemic men than in controls. There were no initial differences between the two groups in glucagon or gastric inhibitory polypeptide (GIP) responses. Consumption of 7.5 and 15% Fructose diets increased fasting plasma glucose and GIP responses in both groups. Consumption of the 15% fructose diet resulted in significantly higher insulin and glucose responses than consumption of the other two diets. These results indicate that moderate levels of dietary fructose can produce undesirable changes in glucose metabolism of both normal and hyperinsulinemic men.

Effect of dietary sucrose in humans on blood uric acid, phosphorus, fructose, and lactic acid responses to a sucrose load.

10 men and 9 women consumed diets that were identical, except for the 30% of the calories derived from either starch or sucrose, for 6 weeks in a crossover design. Of the total calories, 10% were given at breakfast and 90% at dinner. A sucrose load of 2 g/kg body weight was administered 1 week before and during the last week of both dietary periods. Blood was drawn before (fasting) and 0.5, 1, 2 and 3 h after the sucrose load. Serum uric acid was significantly higher (p < 0.01) and blood fructose significantly lower (p < 0.05) before and at all times after the sucrose load when subjects consumed the sucrose versus the starch diet. Levels of serum inorganic phosphorus and blood lactic acid were not affected by kind of carbohydrate in the diet.