In order to study the metabolic effects of dietary sucrose on Zucker rats, young male fatty and lean rats were fed ad libitum or in meals (2 hours/day) for 4 weeks. Diets contained 54% carbohydrate as either sucrose, invert sugar or cooked cornstarch. A genotype effect (fatty versus lean) occurred with the activities of liver and adipose tissue lipogenic enzymes, relative total fat pad size and soluble adipose tissue protein levels in both ad libitum- and meal-fed rats, whereas a genotype effect occurred with food intake and relative liver size only in meal-fed rats and with body weight gain only in ad libitum-fed rats. The significance of diet effects varied with genotype and feeding pattern. The sucrose effect (sucrose versus starch) occurred with food efficiency and body weight gain, activities of liver lipogenic and gluconeogenic enzymes, relative liver size, relative total fat pad size and soluble adipose tissue protein levels in both ad libitum- and meal-fed rats, and with adipose lipogenic enzyme activities in meal-fed rats. The disaccharide effect (sucrose versus invert sugar) occurred with the activities of liver lipogenic enzymes, relative total fat pad size and soluble adipose tissue protein levels in ad libitum-fed rats and was greater in lean than in fatty rats. The data demonstrate that the Zucker fatty and lean rat can be used as sensitive models to study differential effects of dietary carbohydrate.

Ten men and nine women ages 35 to 55 consumed two diets for 6 weeks each in a cross-over design. The diets were composed of identical natural foods and 30% of the calories as either sucrose or wheat starch. Carbohydrate, fat, and protein supplied 43, 42, and 15% of the calories, respectively. Of the calories 10% was eaten at breakfast (7:00 to 8:30 AM) and 90% at dinner (4:30 to 6:30 PM). Initial body weights were essentially maintained. Fasting serum insulin and glucose levels were significantly higher with the sucrose than with the starch diet. The insulin response and the insulin:glucose ratios after a sucrose load (2 g/kg body weight) were greater after the subjects consumed the sucrose diet. Sucrose feeding produced increases in fasting serum insulin, the insulin:glucose ratio and the insulin response to a sucrose load that were of greater magnitude in a subgroup of nine subjects classified as potentially carbohydrate-sensitive than in normal subjects. Glucose response to a sucrose load and fasting serum glucagon did not differ significantly with diet. Fasting insulin and glucose showed significant increases as a function of time on diet. These results indicate that sucrose feeding produces undesirable changes in several of the parameters associated with glucose tolerance.

A strain-specific, elevated serum free glycerol has been found in stock diet fed, carbohydrate-sensitive, hyperlipemic BHE rats. This suggests that considerably more peripheral lipolysis is taking place in the nonfasting BHE rat than in its Wistar counterpart. This observation further suggests that the BHE rat may exhibit metabolic changes in the fed state that are similar to those found in normal fasting rats. Individual, serum free glycerol levels were not correlated with individual serum insulin values. In the nonfasted BHE rats, serum free glycerol concentrations were found to be sufficiently high to initiate gluconeogenesis or to contribute to a maximal rate of triglyceride synthesis.

A glucagon-saline solution (0.1 ml, 10(7) mole/100 g body weight) was injected via the portal vein into nonfasted Wistar and carbohydrate-sensitive BHE rats. Levels of liver and epididymal fat pad cyclic-AMP were observed after 6 and 24 minutes. When compared to sham injected rats at 6 minutes, glucagon injected rats of both strains had twice the level of cyclie-AMP in liver and fat pad tissue. By 24 minutes, the cyclic-AMP levels of the Wistar rats had decreased to those observed in their sham injected counterparts, and the concentration of liver cyclic-AMP in both sham injected and glucagon injected BHE rats had decreased to levels significantly below those observed in the Wistar rats. This observation suggests that a lipolytic-lipogenic imbalance may reside in the livers of rats of the BHE strain.