Metabolic response to cottage cheese or egg white protein, with or without glucose, in type II diabetic subjects.

Test meals with 25 g protein in the form of cottage cheese or egg white were given with or without 50 g glucose to male subjects with mild to moderately severe, untreated, type II diabetes. Water was given as a control meal. The glucose, insulin, C-peptide, alpha amino nitrogen (AAN), glucagon, plasma urea nitrogen (PUN), nonesterified fatty acid (NEFA), and triglyceride area responses were determined using the water meal as a baseline. The glucose area responses following ingestion of cottage cheese or egg white were very small compared with those of the glucose meal, and were not significantly different from one another. The serum insulin area response was 3.6-fold greater following ingestion of cottage cheese compared with egg white (309 v 86 pmol/L.h). The simultaneous ingestion of glucose with cottage cheese or egg white protein decreased the glucose area response to glucose by 11% and 20%, respectively. When either protein was ingested with glucose, the insulin area response was greater than the sum of the individual responses, indicating a synergistic effect (glucose alone, 732 pmol/L.h; glucose with cottage cheese, 1,637 pmol/L.h; glucose with egg white, 1,213 pmol/L.h). The C-peptide area response was similar to the insulin area response. The AAN area response was approximately twofold greater following ingestion of cottage cheese compared with egg white. Following ingestion of glucose, it was negative. When protein was ingested with glucose, the AAN area responses were additive. The glucagon area response was similar following ingestion of cottage cheese or egg white protein. Following glucose ingestion, the glucagon area response was negative.(ABSTRACT TRUNCATED AT 250 WORDS)     

Leucine, when ingested with glucose, synergistically stimulates insulin secretion and lowers blood glucose

Our laboratory is interested in the metabolic effects of ingested proteins. As part of this research, we currently are investigating the metabolic effects of ingested individual amino acids. The objective of the current study was to determine whether leucine stimulates insulin and/or glucagon secretion and whether, when it is ingested with glucose, it modifies the glucose, insulin, or glucagon response. Thirteen healthy subjects (6 men and 7 women) were studied on 4 different occasions. Subjects were admitted to the special diagnostic and treatment unit after a 12-hour fast. They received test meals at 8:00 am. On the first occasion, they received water only. Thereafter, they received 25 g glucose or 1 mmol/kg lean body mass leucine or 1 mmol/kg lean body mass leucine plus 25 g glucose in random order. Serum leucine, glucose, insulin, glucagon, and α-amino nitrogen concentrations were measured at various times during a 2.5-hour period after ingestion of the test meal. The amount of leucine provided was equivalent to that present in a high-protein meal, that is, that approximately present in a 350-g steak. After leucine ingestion, the leucine concentration increased 7-fold; and the α-amino nitrogen concentration increased by 16%. Ingested leucine did not affect the serum glucose concentration. When leucine was ingested with glucose, it reduced the 2.5-hour glucose area response by 50%. Leucine, when ingested alone, increased the serum insulin area response modestly. However, it increased the insulin area response to glucose by an additional 66%; that is, it almost doubled the response. Ingested leucine stimulated an increase in glucagon. Ingested glucose decreased it. When ingested together, the net effect was essentially no change in glucagon area. In summary, leucine at a dose equivalent to that present in a high-protein meal, had little effect on serum glucose or insulin concentrations but did increase the glucagon concentration. When leucine was ingested with glucose, it attenuated the serum glucose response and strongly stimulated additional insulin secretion. Leucine also attenuated the decrease in glucagon expected when glucose alone is ingested. The data suggest that a rise in glucose concentration is necessary for leucine to stimulate significant insulin secretion. This in turn reduces the glucose response to ingested glucose.     

The insulin and glucose responses to meals of glucose plus various proteins in type II diabetic subjects

We previously have shown that ingested beef protein is just as potent as glucose in stimulating a rise in insulin concentration in type II diabetic patients. A synergistic effect was seen when given with glucose. Therefore, we considered it important to determine if other common dietary proteins also strongly stimulate an increase in insulin concentration when given with glucose. Seventeen type II (non-insulin-dependent) untreated diabetic subjects were given single breakfast meals consisting of 50 g glucose, or 50 g glucose plus 25 g protein in the form of lean beef, turkey, gelatin, egg white, cottage cheese, fish, or soy. The peripheral plasma concentrations of glucose, insulin, glucagon, alpha amino nitrogen, urea nitrogen, free fatty acids, and triglycerides were measured. Following ingestion of the meals containing protein, the plasma insulin concentration was increased further and remained elevated longer compared with the meal containing glucose alone. The relative area under the insulin response curve was greatest following ingestion of the meal containing cottage cheese (360%) and was least with egg white (190%) compared with that following glucose alone (100%). The glucose response was diminished following ingestion of the meals containing protein with the exception of the egg white meals. The peripheral glucagon concentration was decreased following ingestion of glucose alone and increased following all the meals containing protein. The alpha amino nitrogen concentration varied considerably. It was decreased after glucose alone, was unchanged after egg white ingestion, and was greatest after ingestion of gelatin. The free fatty acid concentration decrease was 4- to 8-fold greater after the ingestion of protein with glucose compared with ingestion of glucose alone.     

The metabolic response to ingestion of proline with and without glucose

Ingested protein results in an increase in circulating insulin and glucagon concentrations and no change, or a slight decrease, in circulating glucose. In subjects with type 2 diabetes, when protein is ingested with glucose, insulin is further increased and the glucose rise is less than when glucose is ingested alone. Presumably these effects are due to the amino acids present in the proteins. The effects of individual amino acids, ingested in physiologic amounts, with or without glucose, have not been determined. Therefore, we have begun a systematic study of the response to ingested amino acids. Eight young, non-obese, subjects (4 men, 4 women) ingested 1 mmol proline/kg lean body mass, 25 g glucose, 25 g glucose + 1 mmol proline/kg lean body mass or water only on 4 separate occasions at 8 am. Blood was obtained before and after ingestion of the test meal over the following 150 minutes. Proline ingestion resulted in a 13-fold increase in the plasma proline concentration. This was decreased by 50% when glucose was ingested with proline. Proline alone had little effect on glucose, insulin, or glucagon concentrations. However, ingestion of proline with glucose resulted in a 23% attenuation of the glucose area response and no change in insulin response compared with the response to that of glucose alone. A glucose-stimulated decrease in glucagon was further facilitated by proline. Ingested proline is readily absorbed. It reduces the glucose-induced increase in glucose concentration in the presence of an unchanged insulin and a decreased glucagon response.     

The serum insulin and plasma glucose responses to milk and fruit products in Type 2 (non-insulin-dependent) diabetic patients

Summary The plasma glucose and serum insulin responses were determined in untreated Type 2 (non-insulin-dependent) diabetic patients following the ingestion of foods containing sucrose, glucose, fructose or lactose in portions that contained 50 g of carbohydrate. The results were compared to those obtained following the ingestion of pure fructose, sucrose, glucose, +fructose and lactose. The objectives were to determine 1) if the glucose response to naturally occurring foods could be explained by the known carbohydrate content, and 2) whether the insulin response could be explained by the glucose response. The glucose response was essentially the same whether the carbohydrate was given as a pure substance, or in the form of a naturally occurring food. The glucose response to each type of carbohydrate was that expected from the known metabolism of the constituent monosaccharides. The glucose areas following the ingestion of the foods were: Study 1: glucose 11.7, orange juice 7.3, sucrose 5.2, glucose+fructose 6.3, and fructose 0.7 mmol · h/1; Study 2: glucose 14.6, orange juice 7.3, apples 5.5, and apple juice 4.7 mmol · h/1; Study 3 : glucose 12.6, ice cream 8.1, milk 3.7, and lactose 4.1 mmol · h/1. The insulin response was greater than could be explained by the glucose response for all meals except apples. Milk was a particularly potent insulin secretagogue; the observed insulin response was approximately 5-fold greater than would be anticipated from the glucose response. In summary, the plasma glucose response to ingestion of fruits and milk products can be predicted from the constituent carbohydrate present. The serum insulin response cannot.     

Glucose and insulin responses to meals containing milk, lactose, glucose or fructose in subjects with non-insulin-dependent diabetes

The postprandial blood glucose and serum insulin responses to liquid test meals containing 40 g carbohydrate from milk, lactose, glucose or fructose and equal amounts of energy were compared in 10 non-insulin-dependent (type 2) diabetic patients. The meals were consumed in random order on consecutive days after an overnight fast. Significant differences (p less than 0.001, ANOVA) were observed between the glucose and insulin responses to the meals. The glucose response was significantly higher after the glucose containing meal and lower after the fructose meal as compared with the other meals. The insulin response was significantly higher after the lactose and glucose meals than after the milk and fructose meals. After the milk and lactose meals the blood glucose responses were similar whereas the insulin response was significantly lower after the milk meal. As lactose apparently was similarly absorbed from the two meals the difference in the insulin response was probably due to different insulinogenic effects of the protein components or to differences in the physical properties of the respective meals.     

Effect of intermittent physiologic hyperglucagonemia on postprandial plasma glucose levels in normal man

The ability of glucagon to impair glucose tolerance has been questioned by studies involving infusion of exogenous glucagon during a glucose load. Since such hormone administration may not reflect the physiologic pattern of glucagon secretion and may result in hepatic downregulation to glucagon, the present experiments have examined the effects of intermittent andogenous hyperglucagonemia (induced by episodic infusion of arginine) on plasma glucose profiles of normal man following ingestion of mixed meals. In control studies following meal ingestion, plasma glucose, insulin and glucagon increased respectively 15–30 mg/dl, 30–60 uU/ml and 25–50 pg/ml. When meals were accompanied by arginine infusions, plasma glucagon responses were augmented three to fourfold (p < 0.05). Amplitudes of glycemic excursions during infusion of arginine (345 ± 40 mg/dl) were significantly augmented compared to those observed in control studies (286 ± 34 mg/dl, p < 0.02). These results indicate that intermittent increases in plasma glucagon within the physiologic range can adversely affect postprandial glucose profiles in normal man despite concomitant hyperinsulinemia and suggest that such hyperglucagonemia may contribute to impaired postprandial glucose tolerance in diabetic individuals in whom insulin secretion is deficient.     

The metabolic response to various doses of fructose in type II diabetic subjects.

Eight men with untreated type II diabetes were given 480 mL water containing 15 g, 25 g, 35 g, and 50 g fructose orally, in random sequence. The same subjects were given the same volume of water as a control. They also were given 50 g glucose on two occasions for comparative purposes. Plasma glucose, urea nitrogen, and glucagon, and serum insulin, C-peptide, alpha-amino-nitrogen (AAN), nonesterified fatty acids (NEFA), and triglycerides were determined over the subsequent 5-hour period. The area responses to each dose of fructose were calculated and compared with the water control. The integrated glucose area dose-response was curvilinear, with little increase in glucose until 50 g fructose was ingested. With the 50-g dose, the area response was 25% of the response to 50 g glucose. The insulin response also was curvilinear, but the curve was opposite to that of the glucose curve. Even the smallest dose of fructose resulted in a relatively large increase in insulin, and a near-maximal response occurred with 35 g. The area response to 50 g fructose was 39% of that to 50 g glucose. The C-peptide data were similar to the insulin data. The AAN area response to fructose ingestion was negative. However, the response was progressively less negative with increasing doses. The glucagon area response was positive, but a dose-response relationship was not apparent. The glucagon area response was negative after glucose ingestion, as expected. The urea nitrogen area response was negative, but again, a dose-response relationship to fructose ingestion was not present.(ABSTRACT TRUNCATED AT 250 WORDS)     

Insulin sensitivity predicts glycemia after a protein load

Protein ingestion results in small but distinct changes in plasma glucose and insulin. We hypothesized that the glycemic and/or insulin response to protein might be related to the degree of insulin sensitivity. Our aim was to determine the relationships between insulin sensitivity (assessed by euglycemic-hyperinsulinemic clamp) and postprandial glucose, insulin, C-peptide, and glucagon responses to a 75-g protein meal and a 75-g glucose load. Sixteen lean healthy Caucasian subjects (mean +/- SD age, 25 +/- 6 years; body mass index [BMI], 23.1 +/- 1.7 kg/m2) participated in the study. After the protein meal, the mean plasma glucose declined gradually below fasting levels to a nadir of -0.36 +/- 0.46 mmol/L from 60 to 120 minutes, showing wide intraindividual variation. Insulin sensitivity (M value) was 1.1 to 3.9 mmol/L/m2 min in the subjects and correlated inversely with the plasma glucose response to the protein meal (r = -.58, P = .03), ie, the most insulin-sensitive subjects showed the greatest decline in plasma glucose. In contrast, there was no correlation between insulin sensitivity and the insulin or glucagon response to the protein load, or between the M value and the metabolic responses (glucose, insulin, C-peptide, and glucagon) to the glucose load. Our study suggests that the net effect of insulin and glucagon secretion on postprandial glucose levels after a protein meal might depend on the individual's degree of insulin sensitivity. Gluconeogenesis in the liver may be less susceptible to inhibition by insulin in the more highly resistant subjects, thereby counteracting a decline in plasma glucose.     

The influence of glucose on serum galactose levels in man

To investigate the effect of simultaneous glucose and galactose administration on serum galactose levels in man, volunteers were given a standard galactose meal of 0.5 g galactose/kg BW alone and with various body weight related glucose loads and with fructose; lactose was also given to a group of volunteers. Two groups of subjects received the standard galactose meal alone and with a simultaneous intravenous infusion of glucose or insulin. There was a marked individual variation in the serum galactose response to the standard galactose meal, the maximum galactosemia ranged from 0.23 to 4.56 mmole/L. Peroral glucose suppressed the serum galactose response to galactose producing significant reductions in the mean area under the serum galactose response curves. At a glucose intake of 0.15 g/kg by-32 +/- 14.3%, 0.50 g/kg BW -69 +/- 5.93% and at 0.75 g/kg BW -75 +/- 4.93%. Ingestion of glucose with galactose did not increase galactose loss in the urine. Lactose produced similar serum galactose, glucose and insulin responses to those seen after administration of equal quantities of galactose and glucose as monosaccharides. Fructose did not affect serum galactose levels when given with the standard galactose meal. Intravenous glucose produced a significant reduction of 56 +/- 14.1% in the mean area under the galactose response curve [p less than 0.01], whereas intravenous insulin did not affect the serum galactose response to peroral galactose.     

Blood glucose and plasma insulin responses to various carbohydrates in Type 2 (non-insulin-dependent) diabetes

The blood glucose and plasma insulin responses to some simple carbohydrates (glucose, fructose, lactose) and some complex ones (apples, potatoes, bread, rice, carrots and honey) were studied in 32 Type 2 (non-insulin-dependent) diabetic patients. Blood glucose and plasma insulin were measured at zero time and then at 15, 30, 60, 90 and 120 min after ingestion of 25 g glucose, fructose or lactose, or 30 g honey, 50 g white bread, 125 g white rice or potatoes, 150 g apples or 260 g carrots. Maximum blood glucose and plasma insulin responses were recorded 60 min after ingestion of each test meal. At this time the increases in blood glucose and in plasma insulin were significantly higher after the more refined carbohydrates (glucose, fructose and lactose) than after the more complex ones (apples, potatoes, rice, carrots and honey, -p less than 0.01). Counting the blood glucose increase after glucose as 100%, the corresponding increases in glycaemia for other carbohydrates were: fructose, 81.3%; lactose, 68.6%; apples, 46.9%; potatoes, 41.4%; bread, 36.3%; rice, 33.8%; honey, 32.4% and carrots, 16.1%.     

Carbohydrate metabolism in pregnancy. XIV. Relationships between circulating glucagon,insulin, glucose and amino acids in response to a “mixed meal” in late pregnancy

Gestational influences upon the changes in circulating glucose, amino acids, insulin, and glucagon after the ingestion of a “mixed meal” containing carbohydrate (50 g), protein (25 g), and fat (10 g) were examined. Nine subjects were tested during weeks 30–40 of gestation and again 6–8 wk postpartum. The “mixed meal” elicited greater and more prolonged increases in plasma glucose antepartum, whereas the increments in total serum amino acids were blunted at all time points. In the face of greater glycemic but lesser aminogenic stimulation, the integrated increase in plasma insulin was 60% greater antepartum than post partum, whereas the increment in glucagon was not significantly altered. Thus, integrated insulin/glucagon response was increased during antepartum studies. The insulin preponderance following alimentary challenge with mixed nutrients would suggest that the anabolism of ingested amino acids is “facilitated” during late human pregnancy.     

Blood glucose and serum insulin responses to breakfast including guar gum and cooked or uncooked milk in Type 2 (non-insulin-dependent) diabetic patients

Summary The post-prandial blood glucose and serum insulin responses to test meals, each including 300 ml fat-free milk taken separately with the meal or premixed before cooking into the meal consisting of oatmeal porridge, were studied in 10 diet-treated Type 2 (non-insulin-dependent) diabetic subjects. The modifying effect of guar gum on the responses was also studied by supplementing both types of test meals with 5 g granulated guar gum taken at the beginning of the meal. The blood glucose response was higher after the meal which contained cooked milk than after the respective meal with milk taken separately. The guar gum supplementation attenuated the blood glucose response after the meals, but the effect was more pronounced after the meal containing cooked milk. Post-prandial serum insulin responses were similar after all test meals. The results suggest that cooking may facilitate the absorption of lactose from milk-containing foods, and that supplementation with guar gum may counteract this response.     

Prandial insulin requirements in insulin-dependent diabetics: effects of size, time of day, and sequence of meals

To assess the effects of size, time of day, and sequence of meals on insulin requirements determined by an artificial endocrine pancreas, eight insulin-dependent diabetics ate meals of 12.5%, 25%, and 50% of total calories (30 Kcal/kg) at 0800, 1300, and 1800 on each of 3 separate days in a randomized order in one of two sequences in a three by three Latin square design. Plasma glucose and free insulin concentrations and amounts of insulin infused by the artificial endocrine pancreas were associated with meal size (P less than 0.001) but not with time of day of meal ingestion (analysis of variance). The sequence of meal ingestion did not alter integrated plasma glucose responses, but did influence the meal-related amounts of insulin infused. Thus, consideration should be given to meal size and sequence of meal ingestion but not time of day of meal ingestion when determining prandial iv insulin requirements.     

Postprandial plasma glucose,insulin, glucagon and triglyceride responses to a standard diet in normal subjects

Summary Postprandial plasma glucose, insulin and triglyceride responses were determined in 12 normal subjects (7 male and 5 female) fed a standard diet composed of typical American foods; the three meals were identical for each subject. A significant post-prandial rise in glucose and insulin was observed. They were closely related temporally in the early post-absorptive period. However, in the late post-absorptive phase insulin decline was generally slower than the glucose decline. A considerable difference in the glucose and insulin response was observed between males and females. Fasting plasma glucose and insulin concentrations were lower in the women. Following each meal the peak plasma glucose was lower in the women, but the difference was significant only following breakfast (p < 0.02). The area under the glucose curve following breakfast was also lower (p < 0.01) in the women. In the men the maximal postprandial glucose concentration and the postprandial glucose area remained stable throughout the day, but there was an increase in peak insulin concentration and insulin area after dinner. In contrast, in the women the maximal postprandial glucose concentration and the postprandial glucose area increased throughout the day, but the peak insulin concentration and insulin area did not change. Plasma triglycerides increased with breakfast and remained elevated throughout the day. Both fasting and postprandial mean triglycerides were higher in the men, but this did not reach statistical significance. The circulating pancreatic glucagon concentration, determined in 4 subjects, was unaffected by meals and remained stable throughout the day.     

The effect of oral galactose on GIP and insulin secretion in man

Summary The insulinotropic effect of 50 g galactose given orally to 5 normal volunteers on two occasions — once with and once without a period of hyperglycaemia produced by an intravenous glucose infusion — was studied. Oral galactose caused a rise in plasma GIP from fasting levels of 260±50 ng/l (mean ± S. E. M.) to a maximum of 900±65 ng/l 30 min after ingestion, but in the presence of induced hyperglycaemia the GIP response was significantly diminished and delayed (maximum plasma GIP levels 595+110 ng/l at 45 min, p<0.05). The insulin response to galactose was greatly enhanced by IV glucose (mean area under plasma insulin curve with galactose alone 236.5±66.0, with galactose + IV glucose 451.9+81.6, p<0.025). The mean rise in plasma galactose was significantly lower in the presence of IV glucose (mean peak level 1.97±0.28 mmol/l with galactose alone, 0.69±0.16 mmol/l galactose + IV glucose, p <0.025). Oral galactose caused the release of GIP, which is powerfully insulinotropic in the presence of moderate hyperglycaemia. The lower plasma GIP and galactose levels observed following oral galactose in the presence of IV glucose may be accounted for either by postulating that insulin inhibits the absorption of oral galactose, or that insulin exerts a negative feed-back control on GIP release and accelerates galactose disposition in the body.     

Influence of glucose, alcohol and glycerol on galactose tolerance in man

Six volunteers were given 0.5 g galactose/kg body weight alone (A) or with 0.5 g glucose/kg (B) or with 0.5 g glycerol/kg body weight (C). Meals A and B were also given 15 min after ingestion of 300 mg ethanol/kg body weight. Glycerol did not influence the serum galactose response to galactose. Glucose reduced the serum galactose response as was expected. Administration of alcohol prior to a galactose test meal increased the mean area under the serum galactose response curve (p less than 0.01); when glucose was given with galactose after alcohol ingestion, the serum galactose response was significantly reduced (p less than 0.01) when compared to the serum galactose response to galactose after alcohol, but remained higher than after the galactose and glucose test meal. Glucose, therefore, can reduce the effect of alcohol on galactose levels but alcohol can abolish the effect of glucose on galactose metabolism.     

Blood glucose and hormonal responses to small and large meals in healthy young and older women

Blood glucose regulation in the fasting and fed states has important implications for health. In addition, the ability to maintain normal blood glucose homeostasis may be an important determinant of an individual's capacity to regulate food intake. We tested the hypothesis that aging is associated with an impairment in the ability to maintain normal blood glucose homeostasis following the consumption of large meals but not small ones, a factor that could help to explain age-related impairments in the control of food intake and energy regulation. The subjects were eight healthy younger women (25 +/- 2 years, SD) and eight healthy older women (72 +/- 2 years) with normal body weight and glucose tolerance. Following a 36-h period when diet and physical activity were controlled, subjects consumed test meals containing 0, 1046, 2092, and 4184 kJ (simulating extended fasting, and consumption of a snack, a small meal, and a moderately large meal), with 35% of energy from fat, 48% from carbohydrate, and 17% from protein. Each subject consumed each of the test meals on a separate occasion. Serial blood samples were collected at baseline and during 5 h after consumption of the meals. Measurements were made of circulating glucose, insulin, glucagon, free fatty acids, and triglycerides. There was no significant difference between young and older women in their hormone and metabolite responses to fasting and consumption of the 1046-kJ meal. However, following consumption of 2092 and 4148 kJ, older individuals showed exaggerated responses and a delayed return to premeal values for glucose (p = .023), insulin (p = .010), triglycerides (p = .023), and the ratio of insulin to glucagon (p = .026). In conclusion, these results suggest an impairment in the hormonal and metabolite responses to large meals in older women.     

Contribution of galactose and fructose to glucose homeostasis

To determine the contributions of galactose and fructose to glucose formation, 6 subjects (26 ± 2 years old; body mass index, 22.4 ± 0.2 kg/m²) (mean ± SE) were studied during fasting conditions. Three subjects received a primed constant intravenous infusion of [6,6-²H₂]glucose for 3 hours followed by oral bolus ingestion of galactose labeled to 2% with [U-¹³C]galactose (0.72 g/kg); the other 3 subjects received a primed constant intravenous infusion of [6,6-²H₂]glucose followed by either a bolus ingestion of fructose alone (0.72 g/kg) (labeled to 2% with [U-¹³C]fructose) or coingestion of fructose (labeled with [U-¹³C]fructose) (0.72 g/kg) and unlabeled glucose (0.72 g/kg). Four hours after ingestion, subjects received 1 mg of glucagon intravenously to stimulate glycogenolysis. When galactose was ingested alone, the area under the curve (AUC) of [¹³C₆]glucose and [¹³C₃]glucose was 7.28 ± 0.39 and 3.52 ± 0.05 mmol/L per 4 hours, respectively. When [U-¹³C]fructose was ingested with unlabeled fructose or unlabeled fructose plus glucose, no [¹³C₆]glucose was detected in plasma. The AUC of [¹³C₃]glucose after fructose and fructose plus glucose ingestion was 20.21 ± 2.41 and 6.25 ± 0.34 mmol/L per 4 hours, respectively. Comparing the AUC for the ¹³C₃ vs ¹³C₆ enrichments, 67% of oral galactose enters the systemic circulation via a direct route and 33% via an indirect route. In contrast, fructose only enters the systemic circulation via the indirect route. Finally, when ingested alone, fructose and galactose contribute little to glycogen synthesis. After the coingestion of fructose and glucose with the resultant insulin response from the glucose, fructose is a significant contributor to glycogen synthesis.     

Comparative insulinogenic effects of glucose,arginine and glucagon in patients with diabetes mellitus,endocrine disorders and liver disease

Summary In order to compare the insulinogenic effects of glucose, arginine and glucagon, plasma immunoreactive insulin levels following oral glucose loading (50 g), intravenous arginine infusion (30 g for 45 min) and intravenous glucagon injection (1 mg) were determined in patients with diabetes mellitus, various endocrine diseases and chronic hepatitis. In patients with Cushing’s syndrome, plasma insulin responses to all three stimuli were exaggerated, whereas they were low in patients with pheochromocytoma. In other diseases, certain disparities were observed in plasma insulin responses. In patients with mild diabetes mellitus, insulin secretion elicited by glucose seems to be selectively impaired, because arginine and glucagon caused a rise in plasma insulin not significantly different from that in normal subjects. In patients with hyperthyroidism, plasma insulin responses to arginine and glucagon were either absent or limited, although rather a exaggerated response was noted following oral glucose loading. On the contrary, exaggerated responses to arginine and glucagon, and limited response to glucose were observed in hypothyroidism. In patients with chronic hepatitis, the responses of plasma insulin to glucose and arginine were both exaggerated, whereas the response to glucagon was comparable to that in normal subjects. These disparate responses suggest that glucose, arginine and glucagon act on the B-cell via different mechanisms.