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.     

The effects of carbohydrate-enriched meals on glucose turnover and metabolic clearance rates of glucose in Type 2 diabetic patients

Summary The addition of fructose to natural meals elicits lower serum glucose and immunoreactive insulin responses when compared with that of sucrose and starch meals. Differences in rates of splanchnic glucose appearance and peripheral glucose disposal may be partly responsible. To evaluate the role of both parameters after different carbohydrate-enriched meals, we measured the arterialized venous blood glucose, immunoreactive insulin and gastric inhibitory polypeptide concentrations in seven Type 2 diabetic patients after ingestion of isocaloric test meals. Measurements were made in a random manner on three separate occasions. Fructose, sucrose, and bread supplementation constituted 68% of the total carbohydrate content of each meal. Rates of total glucose appearance, glucose utilization and metabolic clearance rates of glucose were determined by the D³-H-3glucose prime-continuous infusion technique. The mean fasting glucose levels were similar in the three groups. Mean peak glucose concentrations and integrated incremental areas were significantly lower (p < 0.02) after the fructose-enriched meals compared with that of either sucrose or bread. The basal arterialized venous blood glucose levels were similar in all three groups. The mean incremental integrated arterialized venous blood glucose area was significantly lower in the fructose group when compared with the sucrose (p < 0.05) and bread (p < 0.02) groups. The mean fasting gastric inhibitory polypeptide levels were similar in the three groups. However, the mean incremental integrated gastric inhibitory polypeptide areas were significantly lower in the fructose group compared with the sucrose and bread groups (p < 0.01 and p < 0.05 respectively). Basal hepatic glucose outputs were not significantly different in the three groups. After each test meal ingestion, the rate of total glucose appearance was lowest for the fructose group, intermediate for the bread group and highest for the sucrose group. However, the metabolic clearance rate did not change from the baseline despite variable arterialized venous blood glucose responses after each test meal. We conclude that the differences in glycaemic responses after carbohydrate-enriched meals cannot be ascribed solely to differences in peripheral glucose disposal in Type 2 diabetic patients. Rather, the rates of total splanchnic glucose output appear to determine the ultimate glycaemic responses after different carbohydrate-enriched meals in Type 2 diabetic patients.     

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.     

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%.     

Effects of glucose, galactose, and lactose ingestion on the plasma glucose and insulin response in persons with non-insulin-dependent diabetes mellitus

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, α-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. That following ingestion of 25 g glucose + 25 g galactose or following the 50-g lactose meal was 0.17 ± 0.07 and 0.13 ± 0.05 mmol · h/L, respectively. Following ingestion of 25-g or 50-g glucose meals, the galactose area responses increased only slightly. The mean glucose area response following the 50-g glucose meals was 14.8 ± 2.5 mmol · h/L. Glucose area responses following ingestion of 25 g galactose, 25 g glucose, 25 g glucose + 25 g galactose, and 50 g lactose were 11%, 49%, 54%, and 60% of that observed following ingestion of 50 g glucose, respectively. The mean insulin area response following ingestion of the 50-g glucose meals was 965 ± 162 pmol · h/L. The insulin area responses observed with 25 g galactose, 25 g glucose, 25 g glucose + 25 g galactose, and 50 g lactose were 24%, 51%, 81%, and 85% of that observed with the 50-g glucose meals, respectively. The C-peptide data confirmed the insulin data. The glucagon concentration was unchanged after galactose ingestion and decreased after glucose ingestion. However, the decrease in the glucagon area response observed with 25 g galactose + 25 g glucose or 50 g lactose was less than that with ingestion of 25 g glucose alone. The latter suggests inhibition of the glucagon response to glucose by the added galactose. In conclusion, ingested galactose results in only a modest increase in plasma glucose concentration. The glucose area responses to galactose and glucose are additive. Oral galactose is a relatively potent insulin secretagogue, and the insulin response is also additive to that following glucose ingestion. Ingestion of glucose with galactose markedly reduces the increase in plasma galactose concentration. The mechanism of this effect remains to be defined.     

Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women

Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Because fructose, unlike glucose, does not stimulate insulin secretion, we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose. Blood samples were collected every 30-60 min for 24 h from 12 normal-weight women on 2 randomized days during which the subjects consumed three meals containing 55, 30, and 15% of total kilocalories as carbohydrate, fat, and protein, respectively, with 30% of kilocalories as either a fructose-sweetened [high fructose (HFr)] or glucose-sweetened [high glucose (HGl)] beverage. Meals were isocaloric in the two treatments. Postprandial glycemic excursions were reduced by 66 +/- 12%, and insulin responses were 65 +/- 5% lower (both P < 0.001) during HFr consumption. The area under the curve for leptin during the first 12 h (-33 +/- 7%; P < 0.005), the entire 24 h (-21 +/- 8%; P < 0.02), and the diurnal amplitude (peak - nadir) (24 +/- 6%; P < 0.0025) were reduced on the HFr day compared with the HGl day. In addition, circulating levels of the orexigenic gastroenteric hormone, ghrelin, were suppressed by approximately 30% 1-2 h after ingestion of each HGl meal (P < 0.01), but postprandial suppression of ghrelin was significantly less pronounced after HFr meals (P < 0.05 vs. HGl). Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day (P < 0.005). Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.     

Effects of meal size and composition on incretin, α-cell, and β-cell responses

The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate postprandial insulin release from the β-cells. We investigated the effects of 3 standardized meals with different caloric and nutritional content in terms of postprandial glucose, insulin, glucagon, and incretin responses. In a randomized crossover study, 18 subjects with type 2 diabetes mellitus and 6 healthy volunteers underwent three 4-hour meal tolerance tests (small carbohydrate [CH]-rich meal, large CH-rich meal, and fat-rich meal). Non-model-based and model-based estimates of β-cell function and incremental areas under the curve of glucose, insulin, C-peptide, glucagon, GLP-1, and GIP were calculated. Mixed models and Friedman tests were used to test for differences in meal responses. The large CH-rich meal and fat-rich meal resulted in a slightly larger insulin response as compared with the small CH-rich meal and led to a slightly shorter period of hyperglycemia, but only in healthy subjects. Model-based insulin secretion estimates did not show pronounced differences between meals. Both in healthy individuals and in those with diabetes, more CH resulted in higher GLP-1 release. In contrast with the other meals, GIP release was still rising 2 hours after the fat-rich meal. The initial glucagon response was stimulated by the large CH-rich meal, whereas the fat-rich meal induced a late glucagon response. Fat preferentially stimulates GIP secretion, whereas CH stimulates GLP-1 secretion. Differences in meal size and composition led to differences in insulin and incretin responses but not to differences in postprandial glucose levels of the well-controlled patients with diabetes.     

Influence of non-carbohydrate foods on glucose and insulin responses to carbohydrates of different glycaemic index in type 2 diabetic patients.

In order to study the influence of non-carbohydrate foods on responses to carbohydrates during mixed meals, 30 Type 2 (non-insulin-dependent) diabetic patients followed a standardized diet for 5 consecutive days. On days 2, 3, 4, and 5, four different lunches were eaten in a randomized order. Lunches consisted of rice or glucose (50 g carbohydrate) eaten either alone, or as part of a mixed meal (32 g protein, 20 g fat). Glucose and insulin levels prior to the lunches did not differ significantly. Glucose and insulin responses differed (p less than 0.001), responses to rice being lower than responses to glucose, and responses to the meal plus rice lower than responses to the meal plus glucose. The ratios of glucose responses to rice and glucose (glycaemic index) were similar (alone, 47 +/- 4%; meal, 47 +/- 4%; NS). The ratios of the insulin responses did not differ (78 +/- 8 vs 96 +/- 7%; NS). The blood glucose responses to mixed meals were lower than responses to the carbohydrates eaten alone, the ratios being similar (rice, 52 +/- 3%; glucose, 58 +/- 5%; NS). Serum insulin responses were however higher, and the ratios differed (172 +/- 13 vs 138 +/- 14%; p = 0.05). These results suggest that the glycaemic index of isolated carbohydrate foods can predict the relative response to mixed meals in the same individuals with Type 2 diabetes. They also support the insulin secretagogue effect of non-carbohydrate foods, which may vary according to the source of carbohydrate in the meal.     

The Effects of Dietary Fibre on Glucose Tolerance in Healthy Males

Summary: Previous studies have shown that the addition of non-absorbable carbohydrate (NAC) to test meals decreases the glucose and insulin response both in normal and diabetic subjects. However, these studies appear to have used bran in the basic test meal without a knowledge of the effect of bran itself or of the added NAC alone. In the present investigation bran alone, pectin alone, guar alone and pectin with guar have been studied. Guar alone added to the test meal significantly lowered blood glucose at 90 minutes. Pectin alone did not have a significant effect. Pectin and guar together resulted in a blood glucose lower at 30 minutes and greater at 120 minutes. No significant changes in insulin response were noted to our study. It appears that NAC alters the glucose response to a given meal, but the extent to which this occurred in the present study was less than in previous studies. The differences may reflect synergism between bran and other NAC's to lower blood glucose response after a meal.     

Pancreatobiliary responses to an intragastric amino acid meal: comparison to albumin, dextrose, and a maximal cholecystokinin stimulus

Little is known about how gastric and pancreatobiliary responses differ after intake of elemental diets from responses to polymeric food. We therefore compared pancreatic and biliary secretions after gastric instillation of albumin (7 g%, with dextrose 21 g%) with an elemental diet in 6 healthy volunteers. The elemental diet contained amino acids (7 g%, with dextrose 21 g%) in the same molar composition as the albumin. Furthermore, we studied the effect of a pure intragastric dextrose solution (21 g%) on pancreatobiliary secretions, as glucose constitutes a major component of elemental diet formulas. The various pancreatobiliary responses were tested against a maximal i.v. cholecystokinin stimulus. The dextrose, amino acid, and albumin meals emptied at similar rates, and gastric emptying was completed within 3 h. Similar pancreatobiliary responses were observed after the albumin and amino acid meals, but response to both the amino acid and albumin meals was smaller than to the intravenous cholecystokinin stimulus. The glucose meal caused a marked and sustained stimulation of pancreatobiliary outputs, which did not differ significantly from the other test meals. However, lower cholecystokinin levels were observed after the glucose meal compared with distinct cholecystokinin release after the albumin and amino acid meals. We conclude first that there are no major differences in secretory responses between elemental (amino acid) and polymeric (protein) meals and second, that intragastric pure glucose meals strongly stimulate pancreatobiliary secretions. The marked pancreatic and biliary responses to intragastric dextrose cannot be fully explained on the basis of cholecystokinin release, suggesting that this response is probably mediated by neural mechanisms.     

Postprandial glucose and insulin responses to rolled oats ingested raw, cooked or as a mixture with raisins in normal subjects and type 2 diabetic patients

Cooking and processing of food may account for differences in blood glucose and insulin responses to food with similar contents of carbohydrate, fat, and protein. The present study was carried out to see if short-term cooking of rolled oats caused an increase in blood glucose. Furthermore, we wanted to see if dried fruit could substitute for some of the starch without deterioration of the postprandial blood glucose response. We therefore compared the blood glucose and insulin responses to three isocaloric, carbohydrate equivalent meals in 11 normal subjects and 9 Type 2 diabetic patients. Meals composed either of raw rolled oats, oatmeal porridge or a mixture of raw rolled oats with raisins were served. In normal subjects, the three meals produced similar glucose (75 +/- 22, 51 +/- 16 and 71 +/- 23 (+/- SE) mmol l-1 180 min, respectively) and insulin response curves (3160 +/- 507, 2985 +/- 632 and 2775 +/- 398 mU l-1 180 min, respectively). Type 2 diabetic patients also showed similar postprandial blood glucose (515 +/- 95, 531 +/- 83 and 409 +/- 46 mmol l-1 180 min, respectively) and insulin (5121 +/- 850, 6434 +/- 927 and 6021 +/- 974 mU l-1 180 min, respectively) responses to the three meals. Thus short-term cooking of rolled oats has no deleterious effect on blood glucose and insulin responses, and substitution of 25% of the starch meal with simple sugars (raisins) did not affect the blood glucose or insulin responses.     

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.     

Glycaemic and insulin responses of six traditional Sudanese carbohydrate-rich meals in subjects with Type 2 diabetes mellitus.

AIMS: The objective of this study was to investigate the influence of six Sudanese traditional carbohydrate-rich meals on glucose and insulin responses and to formulate appropriate dietary guidelines based on glycaemic excursions of traditional foods. METHODS: On six occasions with 1-week intervals, 10 Type 2 diabetic subjects consumed six Sudanese traditional carbohydrate-rich meals. The following meals were tested and also analysed for their composition: wheat gorasa (pancakes), sorghum kisra (flat bread) and sorghum acida (porridge), millet kisra and millet acida and maize acida. Blood samples were collected before and after meal ingestion at 0, 30, 60, 120 and 240 min and analysed for plasma glucose and plasma insulin and incremental areas under the curves (AUC) were calculated. RESULTS: A significant variation in AUC for glucose and insulin responses were found between meals, the over all differences in incremental AUCs between the six meals were significant for both plasma glucose (P = 0.0092) and insulin (P = 0.0001). The 2-h glucose values were 10.5 +/- 2.7 for sorghum flatbread, 9.5 +/- 3.1 for sorghum porridge, 10.3 +/- 3.4 for millet flatbread, 10.6 +/- 3.6 for millet porridge, 11.4 +/- 2.7 for maize porridge and 8.7 +/- 2.4 for the wheat pancakes. The comparison between the AUCs of the meals showed that millet acida (porridge) followed by wheat gorasa (pancakes) displayed significantly lower post-prandial glucose and insulin responses, whereas maize acida induced a higher post-prandial glucose and insulin response. CONCLUSIONS: The comparison of glycaemic and insulin responses to six traditional Sudanese meals show differences of clinical importance, and could form a basis for dietary advice to diabetic subjects in Sudan and countries sharing similar food traditions.     

Sorbitol as a Sweetener in the Diet of Insulin-dependent Diabetes

ABSTRACT. We compared sorbitol given alone and as part of a mixed meal to nine insulin-dependent diabetics (IDD's) during continuous subcutaneous insulin infusion (CSII). Blood glucose, sorbitol and breath hydrogen+methane were measured following six test meals: Pure glucose, sorbitol and lactulose, a mixed meal alone, and sweetened with sorbitol and sucrose. Blood glucose increase was very small after lactulose and sorbitol, significantly larger after glucose. A considerable increase in breath hydrogen+methane appeared after sorbitol and lactulose, but not after glucose. No differences in blood glucose responses were found after the mixed meal alone or sweetened with sorbitol and sucrose. A sustained low level increase in breath hydrogen+methane occurred after all solid meals. Sorbitol was not detected in serum after any meal. Conclusion: Sorbitol ingested by IDD's during CSII in watery solution is not absorbed in the small intestine and causes osmotic diarrhoea. Ingested in a composite meal it does not affect blood glucose and does not cause osmotic diarrhoea.     

Glycemic responses of patients with type 2 diabetes to individual carbohydrate-rich foods and mixed meals

Aims: Our purpose was to determine whether the glycemic index (GI) of individual foods applies to mixed meals. Methods: The glycemic responses elicited by portions of 4 individual foods with 25 g of available carbohydrate when served alone (rice, lacy pancake, flatbread and noodles) and when made into typical Malaysian mixed meals (coconut milk rice, lacy pancake with chicken curry, flatbread with dhal curry and fried noodles) were measured in 10 subjects with type 2 diabetes. To allow calculation of the GI of the foods and the relative glycemic responses of the mixed meals, each subject also tested 25 g of glucose 3 times. Capillary blood glucose was measured at 30-min intervals for 180 min after consuming each test meal. Results: The mean ± SEM incremental area under the curve (AUC) after flatbread (345 ± 26 mmol × min/l) was significantly greater than after rice (238 ± 35) and lacy pancake (235 ± 31, p < 0.05), with noodles being intermediate (294 ± 35). The AUC after the flatbread with dhal curry (341 ± 49), coconut milk rice (238 ± 39) and fried noodle (272 ± 42) mixed meals were similar to those after the individual foods, but the AUC after the lacy pancake with chicken curry mixed meal (388 ± 52) was significantly greater than after the individual food item (p < 0.01). Conclusions: The results support the utility of the GI of individual foods such as rice, flatbread and noodles when applied to mixed meals. The reason for the higher response after the lacy pancake mixed meal compared to the individual food is not clear and may warrant further research.     

Comment: response of the hypothalamic-pituitary-adrenocortical axis to high-protein/fat and high-carbohydrate meals in women with different obesity phenotypes

Subjects with abdominal obesity are characterized by hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis. Food intake, particularly at noon, is a well-known inducer of HPA axis activation. Whether obese subjects present an abnormal response to meals containing different macronutrient proportions is at present unknown. Therefore, this study was carried out to investigate the effect of a high-lipid/protein meal (HLP-meal) and a high-carbohydrate meal (HCHO-meal) on the HPA axis activity in women with different obesity phenotypes. Nondepressed, noncomplicated obese (body mass index greater than 28 kg/m(2)) women with abdominal (A-BFD) (n = 10) and peripheral body fat distribution (P-BFD) (n = 9) and a group of 11 normal-weight controls were investigated in the follicular phase of the menstrual cycle. They were randomly given an 800-kcal HCHO-meal (containing 89% carbohydrates, 11% proteins, 0% lipids), and an 800-kcal HLP-meal (containing 53% lipids, 43% proteins, 4% carbohydrates), which were eaten within 15 min at noon, with an interval of 2 d between each meal. Blood samples for ACTH, cortisol, glucose, and insulin were obtained at 15-min intervals before and after each meal. Baseline hormone and glucose concentrations in the three groups were similar. After the HLP-meal, ACTH tended to similarly but insignificantly increase in all groups, whereas cortisol increased significantly (P < 0.05) in the P-BFD group and insignificantly in the other groups. Conversely, both ACTH and cortisol significantly (P < 0.05) increased only in the A-BFD group, without any significant changes in both controls and P-BFD women. The analysis of the interaction between meals and groups clearly indicated that the cortisol response to the HLP-meal and the HCHO-meal was significantly different (P < 0.025) between the two obese groups, the A-BFD group being characterized by a significantly lower response to the HLP-meal and a significantly higher response to the HCHO-meal, compared with the P-BFD group. Considering all groups together and after adjusting for body mass index, a highly significant relationship was found between cortisol-area under the curve and ACTH-area under the curve after each meal test. However, no relationships were found between changes in ACTH and cortisol and those of glucose, insulin, and the glucose:insulin ratio after each meal. Therefore, our data demonstrate that the response of the HPA axis to meals containing different macronutrient proportions may depend on the pattern of body fat distribution. We also suggest that the activation of the HPA axis following the ingestion of large amounts of carbohydrates may have some pathophysiological relevance, specifically in women with the abdominal obesity phenotype.     

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)     

Guar by-product improves carbohydrate tolerance in healthy human subjects

Guar gum possesses distinct hypoglycemic properties. The other fraction of the guar bean, guar by-product (GBP), was studied to determine if it possesses any hypoglycemic properties. When 25 g GBP or wheat bran were consumed with a carbohydrate test meal by 10 healthy subjects, at 15 and 30 min after the GBP test meal significantly lower normalized plasma glucose responses were measured. Postprandial plasma insulin responses were similar after both test meals. During the first 60 min postprandially, the mean integrated plasma glucose response area was significantly lower after the GBP test meal. These data indicate that GBP, like guar gum, possesses hypoglycemic properties; because of the different chemical characteristics of these 2 guar bean fractions, it seems that their hypoglycemic properties are due probably to different mechanisms.     

Comparative study of the gastric emptying of disaccharides and their respective monosaccharides in rats with ontogenic lactase deficiency]

In order to evaluate the gastric emptying of disaccharides and their monosaccharides, 64 male, Wistar rats weighing approximately 180 g, were divided into the following eight groups containing eight animals each: maltose, sucrose, lactose, and lactulose, and their correspondent group of monosaccharides: glucose, fructose plus glucose, galactose plus glucose and galactose plus fructose. Each animal received, after a 20 hours fast, 2 ml/100 g weight of a test meal containing a 10% solution of the correspondent sugar and phenol red (6 mg/dl) as a marker. Gastric retention was determined at 10 minutes after orogastric infusion and expressed as a percentage of the infused volume. The observed values (mean +/- SE) of gastric retention (%) of sucrose (35.0 +/- 1.8), lactose (30.4 +/- 1.5), and lactulose (29.5 +/- 1.6) were significantly lower (t test alpha = 0.05), than those observed with their respective monosaccharides, i.e. glucose plus fructose (46.9 +/- 2.6), glucose plus galactose (48.3 +/- 2.4), galactose plus fructose (43.5 +/- 1.5). No difference was noted between gastric retention of maltose (49.9 +/- 4.7) and that of glucose (53.0 +/- 3.0). As far the disaccharides are concerned, statistical analysis (ANOVA followed by Tukey test alpha = 0.05) revealed no differences among the values of gastric retention of sucrose, lactose and lactulose. Gastric retention of maltose was significantly greater than that of the other disaccharides. No differences were found among the gastric retention of monosaccharides.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.