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Rats fed ad libitum were given insulin alone (4 U/kg), glucagon alone (25 micrograms/kg), or insulin and glucagon sequentially. Phosphorylase a and synthase R activities, hepatic glycogen, uridine diphosphoglucose, inorganic phosphate (Pi), and plasma glucose, lactate, glucagon, and insulin concentrations were determined over the subsequent 40 min. In separate animals, muscle extraction of 2-deoxy-D-[3H]glucose also was determined. After glucagon administration, glycogen phosphorylase a and plasma glucose were increased within 5 min. However, the glycogen concentration did not decrease for 20 min. Glucagon administration to rats pretreated with insulin stimulated a similar increase in phosphorylase a activity. Again, glycogen was not degraded for 20 min. After insulin only, glycogen concentration remained unchanged. Plasma glucose decreased as expected. In each group, muscle extraction of 2-deoxy-D-[3H]glucose increased compared with the controls (P < 0.05). In summary, glucagon and/or insulin administration did not stimulate significant glycogen degradation for 20 min, even though phosphorylase was activated. The mechanism remains to be determined.

OBJECTIVE In normal subjects, ingestion of fat with potato in a morning meal resulted in a decrease in the glucose response. Therefore, we wished to determine whether a fat-induced decrease in blood glucose also would be observed after a second identical meal. In addition, we were interested in determining if fat ingestion with a morning meal would have an effect on the blood glucose and insulin responses to a second meal not containing fat. RESEARCH DESIGN AND METHODS Nine healthy male subjects ingested two meals consisting of an amount of potato containing 50 g carbohydrate, either alone or with 50 g fat as butter. The meals were served in four combinations as follows: 1) potato for the first meal, potato for the second meal; 2) potato for the first meal, potato with fat for the second meal; 3) potato with fat for the first meal, potato for the second meal; and 4) potato with fat for the first meal, potato with fat for the second meal. Meals were ingested at 8:00 A.M. and noon. Plasma glucose and C-peptide, serum insulin, triglyceride, and free fatty acid (FFA) concentrations were determined over an 8-h period. The integrated area responses to the meals were quantified over the subsequent 4-h period using the fasting value or the noon value as baseline for the first and second meals, respectively. RESULTS When the first meal contained potato only, the glucose area response to the second meal was significantly less when the second meal contained fat. However, fat ingestion had no effect on the glucose area response to the second meal when fat was present in the first meal. The insulin area responses to the first and second meals were similar after ingestion of potato or potato with fat. However, the insulin response to the second meal always was less that to the first meal. The C-peptide area responses after ingestion of the second meal also were all higher than those after the first meal. The triglyceride area responses were slightly negative after ingestion of potato alone in the first meal. When fat was ingested, they were positive. When the first meal contained fat but the second meal did not, there was a rise in triglyceride concentration after the second meal as well as after the first meal. That is, a rise occurred without ingestion of fat with the second meal. If fat was present in the second meal the rise was even greater. The FFA area responses were similar to the triglyceride area responses. CONCLUSIONS When fat was ingested with carbohydrate in either the first or second meal, the glucose area response was decreased. However, when both meals contained fat, a decrease in the glucose area response did not occur with the second meal. The glucose area responses all were greater after the second meal compared with those after the first meal, i.e., the opposite of a Staub-Traugott effect was observed. The insulin area responses to the first and second meals were similar whether fat was ingested or not.

Fasted rats were given 4 g/kg glucose orally. Synthase R (active forms), total synthase, and phosphorylase a activities, and hepatic glycogen, glucose B-phosphate (glucose-6-P), uridine diphosphoglucose (UDP-glucose), glucose, and plasma glucose concentrations were determined over the subsequent 24 h. The resulting glycogen concentration changes could be divided into three distinct phases. A glycogen synthetic phase (between 0 and 4 h), a stability phase (between 4 and 12 h), and a degradation phase (between 12 and 24 h). Synthase R activity increased rapidly and reached a maximum at 20 min. With the onset of glycogen synthesis it gradually decreased below the control values, reaching a nadir by 4 h. During the glycogen stability phase it gradually increased again up to the control value. It then remained stable during the subsequent glycogen degradation phase. Phosphorylase a activity did not change throughout the entire 24-h period. Glucose-6-P concentration increased almost twofold at 20 min. It then decreased but was above the control values at the 24 th h. The plasma and hepatic glucose concentrations increased as expected after the glucose load. They then decreased but remained above the control value at all subsequent time points. In summary, the synthase R, phosphorylase a activities, or changes in the known allosteric modifiers of these enzymes could not explain the changes in glycogen concentration. The reasons for these discrepancies remain to be determined.

With progressive ripeness there is a decrease in starch and an increase in free sugar content of bananas. The starch also is considered to be poorly digestible. Therefore, we decided to study plasma glucose, serum insulin, C-peptide, and plasma glucagon responses to bananas with increasing degrees of ripeness. Seven male subjects with untreated noninsulin-dependent diabetes mellitus ingested 50 g carbohydrate as bananas of stage 4 (more yellow than green), 5 (yellow with green tip), 6 (all yellow), and 7 (yellow flecked with brown) ripeness. They also received 50 glucose on two occasions for comparative purposes. On a separate occasion water only was given as a control. The area responses were quantified by determining incremental areas using the water control as baseline. The mean glucose area following the 50 g glucose meals was 15.1 +/- 1.9 mM.h. After the ingestion of bananas of 4, 5, 6 and 7 ripeness the glucose area response was 42, 41, 51 and 48% of that after glucose ingestion, respectively. The insulin area response following glucose meals was 888 pM.h. Responses to 4, 5, 6 and 7 bananas were 85, 70, 61, 85%, respectively, of that following glucose ingestion. C-peptide data were similar to the insulin data. The glucagon area response was negative after glucose ingestion but was positive following banana ingestion. In summary, the glucose, insulin, C-peptide, and glucagon area responses varied little with ripeness of the bananas.

Galactose usually is ingested as lactose, which is composed of equimolar amounts of glucose and galactose. The contribution of galactose to the increase in glucose and insulin levels following ingestion of equimolar amounts of galactose and glucose, or lactose, has not been reported in people with non-insulin-dependent diabetes mellitus (NIDDM). Therefore, we studied the effects of galactose ingestion alone, as well as with glucose either independently or in the form of lactose, in subjects with untreated NIDDM. Eight male subjects with untreated NIDDM ingested 25 g glucose, 25 g galactose with or without 25 g glucose, or 50 g lactose as a breakfast meal in random sequence. They also received 50 g glucose on two occasions as a reference. Water only was given as a control meal. Plasma galactose, glucose, glucagon, alpha-amino nitrogen (AAN), nonesterified fatty acids (NEFA), and serum insulin and C-peptide concentrations were determined over a 5-hour period. The integrated area responses were quantified over the 5-hour period using the water control as a baseline. Following ingestion of 25 g galactose, the maximal increase in plasma galactose concentration was 1 mmol/L. The mean maximal increases in plasma galactose concentration following ingestion of 25 g galactose + 25 g glucose or following 50-g lactose meals were similar and were only 12% of that following ingestion of galactose alone (P < .05). The mean galactose area response over the water control for the 25-g galactose meal was 0.95 +/- 0.31 mmol.h/L.(ABSTRACT TRUNCATED AT 250 WORDS)

OBJECTIVE— In normal subjects, ingestion of butter with potato resulted in considerably lower blood glucose levels but similar or higher insulin concentrations compared with those observed in the same subjects after potato ingestion alone. We determined whether butter ingested with potato would result in a greater stimulation in insulin secretion than ingestion of potato alone in subjects with NIDDM. RESEARCH DESIGN AND METHODS— Seven male subjects with untreated NIDDM ingested 50 g CHO alone or 50 g CHO with 5, 15, 30, or 50 g fat as a breakfast meal. Fat was ingested in the form of butter, and CHO was given in the form of potato. Subjects received 50 g glucose on two separate occasions for comparative purposes. The subjects also were given only water and were studied over the same time period (water control). Plasma glucose, glucagon, alpha-amino nitrogen, nonesterified fatty acids, serum insulin, C-peptide, and triglyceride concentrations were determined over 5 h. The integrated area responses were quantified over the 5-h period using the water control as a baseline. RESULTS— The mean plasma glucose area response after ingestion of potato with or without the various amounts of butter were all similar and were 82% of that observed after ingestion of 50 g glucose. The mean insulin area response to potato alone was 532 pmol · h · L−1. The mean insulin area responses to potato plus 5,15,30, and 50 g of fat meals were 660,774,750, and 756 pmol · h · L−1, respectively. Thus, the mean insulin areas were all greater than for ingestion of potato alone, and a maximal response was observed with addition of 15 g fat (1.4-fold). The C-peptide data did not confirm an increase in insulin secretion. Overall the area responses after ingestion of meals containing fat were not different from the response to potato ingestion alone, although the responses were erratic. The glucagon area response was positive after ingestion of all fat containing meals except for that containing only 5 g fat, and there was a dose-response relationship. The plasma alpha-amino nitrogen and nonesterified fatty acid area responses were negative after potato ingestion and were not significantly different when fat was added. The serum triglyceride concentration increase was greater after the ingestion of butter with the potato as expected. CONCLUSIONS— In contrast to the results in normal subjects after ingestion of butter with potato, the glucose response was not smaller in subjects with NIDDM. The insulin response was greater. The insulin area response data indicated the presence of a dose-response relationship. Whether similar responses will be observed with other dietary fat and CHO sources remains to be determined.

Glycogenin is a 37-kDa protein upon which new glycogen molecules are considered to be constructed. Therefore, we were interested in determining its role in liver glycogen synthesis following glucose administration. Twenty-four-hour fasted rats were given 4 g/kg glucose orally. Glycogenin and synthase R activities and glycogen were determined over the subsequent 24 h. In fasted rats given just water, glycogenin activity was present and did not change over the subsequent 24 h. Following glucose, glycogenin activity also was not different for 1 h, i.e. the glycogenin was not incorporated into glycogen even though the glycogen concentration had increased. Subsequently, the glycogenin activity became unmeasurable. Presumably, the glycogenin was incorporated into a proteoglycan product since after amylase treatment, glycogenin activity was again present and was quantitatively unchanged. Free glycogenin activity remained unmeasurable until after 12 h. At this time, glycogen began to decrease, and, by 15 h, free glycogenin activity again appeared. The results indicate that in fasted rats, essentially all of the glycogenin was free. Following administration of oral glucose, glycogenin was incorporated into a proteoglycan product but only 60 min after glycogen synthesis had begun. Free glycogenin did not reappear until the 15th h after glucose was given and after the glycogen concentration had decreased by approximately 60%.