Glycaemic and insulinemic response to dietary carbohydrates in horses

Background

Dietary sugar and starch affect plasma glucose and insulin concentrations. Little information is available about the effect of dietary fibre on plasma glucose and insulin concentration. It is hypothesized that different dietary fibre compositions will alter post-prandial glycaemic- and insulinemic index of test meals. The objective was to measure postprandial glucose and insulin concentrations in horses fed meals of different fibre compositions.

Methods

Blood was drawn via jugular vein puncture and the glycaemic and insulinemic index were calculated.

Results

The meal effect on glycaemic and insulinemic response followed the expected pattern, where plasma concentrations increased after feeding and declined after peak concentration. Glycaemic index was 100 (H), 102 (OB), 102 (BB) and 106 (M) and did not differ significantly between meals. Insulinemic index was 100 (H), 140 (OB), 121 (BB) and 125 (M) and did not differ significantly between meals.

Conclusions

In conclusion, meals containing different fibre compositions did not affect the glycaemic- and insulinemic index in horses.

     

Wholemeal versus wholegrain breads: proportion of whole or cracked grain and the glycaemic response.

STUDY OBJECTIVE--To determine the effect on the glycaemic response to bread of the ratio of whole cereal grains to milled flour. DESIGN--Randomised assignment of groups of diabetic volunteers to test and control meals, taken after an overnight fast. Test foods were also analysed for in vitro digestion with human saliva. SETTING--Tertiary care centre. PATIENTS--Groups of six drawn from pool of 16 volunteers with diabetes mellitus (11 men, five women; mean age 64 (SE 3); 10 taking insulin, five taking oral agents, one controlled by diet; other characteristics comparable). INTERVENTIONS--All patients took standard white bread control meals on three occasions spanning the study and on different mornings took test meals containing varying ratios of whole cereal grains (barley or cracked wheat) to milled flour (75:25, 50:50, 0:100). All meals contained 50 g available carbohydrate and were eaten in 15 minutes. Capillary blood samples were taken for determination of glucose concentrations every 30 minutes for three hours. END POINT--Glycaemic index of foods (= increase in area under blood glucose concentration curve for test food divided by increase in area under curve for white bread control X 100). MEASUREMENTS AND MAIN RESULTS--Significant trend to lower glycaemic index with increasing proportion of whole cereal grains in test bread (p less than 0.05) and lower in vitro digestibility (p less than 0.001). Breads containing up to 75% whole grain were considered palatable. CONCLUSIONS--Breads containing a high proportion of whole cereal grains may be useful in reducing the postprandial blood glucose profile in diabetics because they are more slowly digested. These breads should be called "wholegrain" in distinction to "wholemeal" breads made from milled flour.     

Carbohydrates modulate opiate receptor mediated mechanisms during postprandial endocrine function

The present study was designed to determine the role of carbohydrates during naloxone-induced opiate receptor blockade upon the postprandial rise of plasma somatostatin (SLI), insulin and pancreatic polypeptide (PP) levels in response to protein and fat test meals in conscious dogs. Test meals consisting of 50 g liver extract + 50 g sucrose or 50 g corn oil + 50 g sucrose dissolved in 300 ml water were instilled intragastrically, respectively. Additionally, liver extract and fat meals were given with a concomitant intravenous infusion of glucose. To all test meals either naloxone (4 mg) or saline was added. The addition of sucrose to liver extract or the infusion of i.v. glucose during the liver meal abolished the inhibitory effect of naloxone on the rise of postprandial somatostatin levels which has been described recently. The addition of carbohydrate either orally or intravenously to the fat meal resulted in an even stimulatory effect of naloxone upon the rise of postprandial somatostatin levels. Insulin levels were not changed during liver extract + sucrose or i.v. glucose, respectively. When sucrose or i.v. glucose was administered together with the fat meal the addition of naloxone augmented postprandial insulin secretion. Pancreatic polypeptide (PP) release was augmented during the combination of sucrose or i.v. glucose with the fat and liver meal when naloxone was present in the meals. The present data demonstrate that the addition of carbohydrates either orally or intravenously to fat and protein meals modulates the effect of endogenous opiates in the regulation of postprandial somatostatin, insulin and pancreatic polypeptide release in dogs in a way that carbohydrates induce inhibitory mechanisms that are mediated via endogenous opiate receptors.     

Salt and the glycaemic response.

The possibility that salt increases plasma glucose and insulin responses to starchy foods was investigated. Six healthy adults took four morning test meals randomly: 50 g carbohydrate as cooked lentils or white bread, with or without 4.25 g of added salt (an amount within the range of salt found in a meal). When salt was added to the lentils the incremental area under the three hour plasma glucose curve was significantly greater than that for lentils alone (43.2 mmol.min/l v 11.1 mmol.min/l (778 mg.min/100 ml v 200 mg.min/100 ml]. When salt was added to bread the peak glucose concentration was significantly higher than that for unsalted bread (6.96 mmol/l v 6.35 mmol/l (125 mg/100 ml v 114 mg/100 ml], and this was followed by relative hypoglycaemia. Plasma insulin concentrations at 45 minutes were higher after a meal of salted lentils and salted bread than after the unsalted foods (p less than 0.05). The high insulin concentration after salted bread was sustained for one hour after the meal, thus the mean area under the three hour curve was 39% greater than that for unsalted bread (p less than 0.05). Salt may increase the postprandial plasma glucose and insulin responses to lentils and bread by accelerating the digestion of starch by stimulating amylase activity or accelerating small intestinal absorption of the liberated glucose, or both. The findings of this preliminary study, if confirmed by others, would support the recommendation that diabetics, as well as the general population, should reduce their intake of salt.     

Glycaemic effects of incretins in Type 1 diabetes mellitus: a concise review, with emphasis on studies in humans

The remission phase of Type 1 diabetes mellitus is associated with substantial recovery of beta-cell function and with marked improvement of endogenous insulin responses to meals in the early months after diagnosis, accompanied by little or no improvement in the insulin response to parenteral glucose, suggesting that the incretin function may be important in glycaemic regulation in this phase of diabetes. Preservation of the insulin response to parenteral glucagon-like peptide-1 (GLP-1), contrasting with lack of stimulation of insulin secretion by the other known incretin gastric inhibitory polypeptide (GIP), prompted studies with exogenous GLP-1 in recent-onset Type 1 diabetes. These studies showed substantial reduction of glycaemic excursions after ingestion of mixed nutrients during intravenous infusion of GLP-1 without administration of insulin, in subjects with a range of endogenous secretion of insulin in response to meals as demonstrated by blood levels of the insulin-connecting peptide (CP). These effects were independent of stimulation of blood levels of CP and were reproduced in volunteers with no endogenous release of CP in response to meals. The glycaemic effects were associated with inhibition of abnormal rises of blood levels of glucagon, and with suppression of endogenous release of human pancreatic polypeptide (HPP), by GLP-1. It was hypothesized that a major component of the glycaemic effect is attributable to the known action of GLP-1 to inhibit gastric emptying and to inhibit glucagon secretion. Studies of the effects of GLP-1 agonists (GLP-1 and exendin-4) given together with established insulin doses before a meal supported the hypothesis. The more prolonged actions of exendin-4 were accompanied by greater and more prolonged reduction of glycaemic effects of ingestion of meals in volunteers with CP-negative Type 1 diabetes mellitus, during intensive insulin therapy, in whom delay of gastric emptying was confirmed by studies of blood levels of acetaminophen ingested with the meals. Side effect-free doses of exendin-4 given together with insulin in volunteers with CP-negative Type 1 diabetes receiving continuing intensive insulin therapy demonstrated the capacity of this combination therapy to normalize blood glucose levels after ingestion of meals that were consistent with the dietary program of the volunteers, without apparent increased risk of hypoglycaemia within a normal between-meals interval. It is suggested that further and more prolonged studies of the use of long-acting GLP-1 agonists as congeners with insulin in Type 1 diabetes mellitus are indicated.     

Postprandial glucose, insulin and glucagon responses to meals with different nutrient compositions in non-insulin-dependent diabetes mellitus

Postprandial glycaemic and hormone responses to meals with different nutrient compositions and their heterogeneity were evaluated in 16 non-insulin-dependent diabetic patients and 5 healthy volunteers. Five kinds of nutrient stimulation--75 g glucose, a Japanese mixed meal (400 kcal, carbohydrate 60%, protein 14%, fat 26%), a high protein meal (300 kcal, C 26%, P 64%, F 10%), a high fat meal (300 kcal, C 23%, P 5%, F 72%) and 20 g iv glucose--was given to each subject. On the average, in both normal and diabetic subjects, the increases in plasma glucose (PG) and insulin (IRI) were the largest with the oral glucose load and the smallest with the high protein meal. The ratio of increase in IRI and PG (sigma delta IRI/sigma delta PG) was the highest with the high protein meal and the lowest with the oral glucose load. sigma delta IRI with the high protein meal and the high fat meal were the same in normal and diabetic subjects. However, each of the 16 NIDDM patients and 5 normal volunteers exhibited a different pattern of response to the nutrient stimuli and no definite subgroup could be classified. There was no correlation between metabolic responses and family history of diabetes mellitus, duration of diabetes, body mass index and fasting plasma glucose. The present results suggest the nearly intact capacity of insulin secretion in NIDDM in response to a high protein or high fat meal and the difficulty of subclassification in NIDDM according to the glycaemic and hormone responses to the different nutrient stimuli.     

Lipogenic activation after nibbling and gorging in mice

Lipogenic activation was studied in mice that had been restricted to a single large meal once a day rather than being allowed to eat at frequent intervals throughout the night. Mice were injected intravenously with [U-(14)C]glucose, and the flux of glucose C to total lipid fatty acids (TLFA) and to all "end products" was estimated from serial plasma glucose specific activities and measurements of incorporation of (14)C into TLFA of hepatic and extrahepatic tissues. Tracer studies were carried out in mice fasted for 1 day and at various times after the mice ate one or two small test meals or a single large test meal. Test meals consisted of a fat-free, 58% glucose diet. The flux of glucose C to TLFA increased by an order of magnitude within an hour after mice nibbled a test meal for several minutes. After ingestion of two small test meals or a single large test meal, the flux of glucose C to TLFA increased from a fasting rate of 0.5 to 35 and 87 micro g of glucose C/min/20 g body wt, respectively. Although trained meal eaters are thought to have abnormally increased lipogenesis, their lipogenic response to a single test meal was the same as that previously reported for untrained nibbling mice. Most of the newly synthesized fatty acids were found in extrahepatic tissues. Ingestion of a first test meal completely prevented the expected hyperglycemic response following ingestion of a second test meal even though the latter contained over 10 times more glucose than that in the total body glucose pool.     

Digestion of starch and glycaemic response to mixed meals in pigs.

The digestion in the proximal intestine of mixed meals (5,160 kJ) containing either native (NS) or pregelatinized (PS) maize starches (approximately 200 g), and the postprandial glycaemic responses they induced were compared in pigs. For both meals, approximately 25% of the ingested starch was assimilated above the duodenal cannula (positioned 75 cm beyond the pylorus). Larger amounts of starch were collected for NS than for PS during the first 30 min. The glycaemic responses, however, indicated a higher rate of glucose absorption for PS during the first 30 min, which could be explained by the higher susceptibility of PS to hydrolysis, as we observed in vivo. Indeed, malto-oligosaccharides (G1-G3) represented almost 80% of the total alpha-glucans collected at 150 min in the duodenum after the PS meal. At that time, after the NS meal, only 30% of the alpha-glucans were malto-oligosaccharides. Thus, even after a mixed meal, the starch digestion rate can alter the observed postprandial glycaemic response.     

Haemolymph glucose concentrations of juvenile rock lobsters, Jasus edwardsii, feeding on different carbohydrate diets

Postprandial changes in haemolymph glucose concentration ([Glc]H) were measured in 4-day-fasted juvenile intermoult spiny lobsters, Jasus edwardsii, provided with meals composed of glycogen, maltose, sucrose, glucose, or fructose in a gelatine base, or with gels of the algal glycans agar, alginate and carrageenan. Baseline [Glc]H was 0.61+/-0.02 mmol L(-1). After consumption of glycogen, maltose or sucrose, [Glc]H approximately doubled, peaked after 3 h and returned to baseline between 12 and 24 h. Glucose and fructose meals were followed by periods of sustained hyperglycaemia lasting more than 24 h (peaking at approximately 2.5 times baseline at 6 and 3 h respectively). Suggested explanations for augmented hyperglycaemic responses to glucose and fructose are: 1) these monosaccharides by-passed contact digestion and absorption in the R-cells of the digestive gland, directing them away from storage and toward transepithelial scavenging routes; or 2) glucose and fructose directly elicited release of crustacean hyperglycaemic hormone via a chemosensory reflex. Agar and alginate induced significant postprandial glycaemic responses, consistent with reports of carbohydrases in this species and indicating their potential for inclusion in artificial diets as both binders and energy sources. Carrageenan, a highly sulphated galactan, did not produce a glycaemic response. The measurement of glycaemic responses is a quick method of obtaining nutritional information on carbohydrates considered for inclusion in formulated diets prior to lengthy growth trials.     

Effects of glucose ingestion on postprandial lipemia and triglyceride clearance in humans

To determine whether the metabolism of diet-derived triglycerides (TG) is acutely regulated by the consumption of insulinogenic carbohydrates, we measured the effects of glucose ingestion on oral and intravenous fat tolerance, and on serum triglyceride concentrations obtained during duodenal fat perfusion. Postprandial lipemia was diminished by the ingestion of 50 g (148 +/- 121 mg.dl-1 x 7 h-1 vs 192 +/- 124 mg.dl-1 x 7 h-1, P less than 0.05) and 100 g (104 +/- 106 mg.dl-1 x 7 h-1 vs 171 +/- 104 mg.dl-1 x 7 h-1, P less than 0.05) glucose. Peak postprandial TG concentrations occurred later after meals containing glucose and fat than after meals containing fat alone. This effect could be reproduced when an iso-osmotic quantity of urea was substituted for glucose in the test meal. Starch ingestion had no discernible effect on postprandial lipemia. Intravenous fat tolerance was similar before (4.9 +/- 1.2%.min-1) and 2 h (4.4 +/- 1.3%.min-1) and 4 h (4.8 +/- 1.5%.min-1) after 50 g glucose ingestion. During duodenal fat perfusion, glucose ingestion caused a progressive decrease in plasma triglyceride concentrations. These data suggest that glucose ingestion diminishes postprandial lipemia in a dose-dependent manner, but that this effect is not due to increased clearance of triglyceride from the circulation. The hypotriglyceridemic effects of glucose appear to reflect delayed gastric emptying and decreased hepatic secretion of triglyceride.     

Plasma C-peptide concentration in women with Type 1 diabetes during early and late pregnancy

Diabet. Med. 29, e361-e364 (2012) ABSTRACT: Aims There are previous suggestions of increased C-peptide concentration in women with Type?1 diabetes during pregnancy. Our aim was to re-evaluate the hypothesis of a pregnancy-induced increase by measuring plasma C-peptide concentration in women with stable blood glucose control under standardized fasting and meal-stimulated conditions. Methods Ten women with Type 1 diabetes; median age 31.1?years, median diabetes duration 19?years, median HbA(1c) 52?mmol/mol (6.9%) were admitted to a clinical research facility for two 24-h visits in early (12-16?weeks) and late (28-32?weeks) pregnancy. Women They ate standardized study meals - 80-g carbohydrate dinner, 60-g carbohydrate breakfast, and fasted between meals and overnight. Closed-loop insulin delivery maintained stable and comparable glycaemic conditions. Paired samples for plasma glucose and C-peptide were obtained. Results Plasma glucose levels were comparable in early (median 6.5?mmol/l; interquartile range 5.6-8.6) and late pregnancy (median 7.0?mmol/l; interquartile range 6.1-7.8; P?=?0.72). There was no change in fasting or meal-stimulated plasma C-peptide concentration from early to late pregnancy; mean difference 4.0?pmol/l (95%?CI -6.0 to 7.0; P?=?0.9). Four women had detectable C-peptide; peak (range) early vs. late pregnancy 48.5 (10-115) vs. 40.0?pmol/l (80-105); P?=?0.5, which was weakly associated with plasma glucose; R(2) =?0.15, P?相似文献   

Oxidative DNA damage and plasma antioxidant capacity in type 2 diabetic patients with good and poor glycaemic control

Diabetes mellitus is a complex metabolic disorder characterized by a disturbance in glucose metabolism. Recent evidence suggests that increased oxidative damage as well as reduction in antioxidant capacity could be related to the complications in patients with type 2 diabetes. The aim of this study was to measure plasma antioxidant status in type 2 diabetic patients with good and poor glycaemic control and its relationship with oxidative DNA damage. Thirty-nine type 2 diabetic patients and eighteen healthy subjects were recruited for this study. We found that diabetic patients had slightly, but not significantly lower antioxidant capacity, measured with the "ferric reducing ability of plasma" (FRAP) assay, than healthy subjects. On the contrary, oxidative DNA damage (measured by the Comet assay) in leukocytes obtained from diabetic patients was significantly higher compared to healthy subjects. Taking into account glucose control, we found that the FRAP level was significantly (p<0.05) lower in diabetic subjects with poor glycaemic control than healthy subjects, while patients with good glycaemic control had FRAP values similar to controls. We also observed an unexpected positive correlation between FRAP values and oxidative DNA damage in diabetic patients; moreover, a positive correlation was found between FRAP and glucose level or HbA(1c) in patients with poor glycaemic control. In conclusion, our results confirm that patients with type 2 diabetes have a higher oxidative DNA damage than healthy subjects and that plasma antioxidant capacity is significantly lower only in patients with poor glycaemic control, moreover, in these patients FRAP values are positively correlated with glycaemic levels and HbA(1c). These observations indicate that a compensatory increase of the antioxidant status is induced as a response to free radical overproduction in type 2 diabetes. Therefore, the addition of antioxidant supplements to the current pharmacological treatment could have potentially beneficial effects in diabetic patients with poor glycaemic control.     

Chlorogenic acid reduces the plasma glucose peak in the oral glucose tolerance test: effects on hepatic glucose release and glycaemia

The effects of chlorogenic acid (CA) on hepatic glucose output, blood glucose levels and on glucose tolerance were analysed. Hepatic uptake of CA and its effects on hepatic catabolism of L-alanine and glucose-6-phosphatase (G-6-Pase) activity were also evaluated. CA (1 mM) inhibited about 40% of G-6-Pase activity (p < 0.05) in the microsomal fraction of hepatocytes, but no effect was observed on production of glucose from gluconeogenesis or on L-alanine catabolism, at various concentrations of CA (0.33, 0.5 and 1 mM), in liver perfusion experiments. Since there were indications of a lack of uptake of CA by the liver, it is possible that this compound did not reach sufficiently high intracellular levels to inhibit the target enzyme. Accordingly, intravenous administration of CA also failed to provoke a reduction in blood glucose levels. However, CA did promote a significant reduction (p < 0.05) in the plasma glucose peak at 10 and 15 min during the oral glucose tolerance test, probably by attenuating intestinal glucose absorption, suggesting a possible role for it as a glycaemic index lowering agent and highlighting it as a compound of interest for reducing the risk of developing type 2 diabetes.     

Early post-prandial hyperglycemic response: from case reports of insulin-dependent diabetics evaluated with an artificial pancreas

In order to define the after-meal glycaemic response in diabetic subjects, we studied it in 20 insulin-dependent diabetic patients by automatic control using artificial beta-cell. We observed a different behaviour of blood glucose and of the consequent insulin requirement at the meals: in two subjects an early and excessive rise of blood glucose values at the meal was shown, not rapidly normalizable by artificial beta-cell. It should support, in our opinion, in these subjects, an increased neuro-entero-hormonal activity on endocrine pancreas production and a subsequent enhancement of hepatic glucose output.     

The human amylin analog, pramlintide, reduces postprandial hyperglucagonemia in patients with type 2 diabetes mellitus.

AIMS: Amylin is a second beta-cell hormone that is normally co-secreted with insulin in response to meals; it complements the effects of insulin in postprandial glucose control, in part by suppressing glucagon secretion. In patients with type 2 diabetes, mealtime administration of the human amylin analog pramlintide markedly improves postprandial glucose excursions. The aim of this study was to examine whether pramlintide reduces the postprandial hyperglucagonemia that is often seen in this patient population. METHODS: Utilizing a single-blind, placebo-controlled crossover design, 24 patients with type 2 diabetes, 12 insulin-treated and 12 non-insulin-treated, underwent a standardized mixed meal test on 2 occasions during which they received, in randomized order, a five-hour intravenous infusion of placebo or pramlintide (100 microg/h). RESULTS: During the placebo infusion, plasma glucose and plasma glucagon concentrations increased substantially after the meal. During the pramlintide infusion, postprandial plasma glucose and plasma glucagon responses were significantly (p < 0.05, all) reduced following ingestion of the same meal, both in the insulin-treated and non-insulin-treated subgroups. CONCLUSION: Supplementation of mealtime amylin with pramlintide reduces postprandial hyperglucagonemia in patients with type 2 diabetes, a mechanism that likely contributes to pramlintide's postprandial glucose-lowering effect.     

Reduction of postprandial triglyceridemia in humans by dietary n-3 fatty acids

Long chain n-3 fatty acids present in fish oils have been shown to reduce fasting plasma triglyceride and very low density lipoprotein levels in normal and hyperlipidemic human subjects. The present studies were designed to examine whether dietary n-3 fatty acids influence chylomicron formation and metabolism in healthy volunteers. In the first study seven subjects were fed either saturated fat, vegetable oil, or fish oil-based diets for 4 weeks each, and test meals containing 50 g of the background fat were administered after the second week of each diet. The postprandial rise in triglyceride levels was significantly lower following the fish oil test meal as compared to the saturated fat or vegetable oil test meals. In the second study, six subjects eating their usual home diets were given two fat tolerance tests. The first contained saturated fat and the second, given 1 week later, contained fish oil. There was no difference in the postprandial triglyceride response between the fish oil and the saturated fat meals. A third study was then conducted with eight volunteers in which saturated fat and fish oil test meals were administered during saturated fat and fish oil background diets in a crossover design. The presence of fish oil in the background diet reduced postprandial lipemia regardless of the type of fat in the test meal. Although there was no effect of the fish oil diet on the lipoprotein lipase and hepatic lipase activity of postheparin plasma measured in vitro, stimulation of in vivo lipolysis was not ruled out. Our results suggest that chronic (but not acute) intake of fish oil may inhibit the synthesis or secretion of chylomicrons from the gut. However, accelerated clearance due to decreased VLDL competition cannot be excluded.     

Dietary Myoinositol Results in Lower Urine Glucose and in Lower Postprandial Plasma Glucose in Obese Insulin Resistant Rhesus Monkeys.

In a previous study, D-chiroinositol added to a meal (0.5 g/kg) resulted in significantly lower postprandial plasma glucose concentrations without an increase in insulin concentrations in obese insulin-resistant monkeys. The present report describes the effects of another isomer of inositol, myoinositol, on postprandial plasma glucose and insulin concentrations and on urine glucose concentrations in 6 similarly insulin-resistant monkeys. The three 5 day study periods included a control period (liquid diet ad libitum) and 2 experimental periods (liquid diet ad libitum with either 1.5 g/kg/day myoinositol or D-chiroinositol added). Twenty-four hour urine samples were collected during each 5 day period. On the sixth day of each period the monkeys were anesthetized 110 min after completing either the control meal (15 ml/kg) or the experimental meals (1.5 g/kg myoinositol or D-chiroinositol) and plasma samples were obtained at 120, 150,180, 210, 240, 270 and 300 min. The plasma glucose concentration was lower after the meal with myoinositol compared to the control meal at 120, 150 and 180 min (p's<0.05). The plasma insulin concentration was lower after the meal with myoinositol compared to the control meal at 150 and 180 min (p's<0.05). In addition, 24 hour urine glucose concentrations were lower during the myoinositol diet compared to the control diet (p<0.001). The plasma glucose concentration was lower after the meal with D-chiroinositol compared to the control meal at 150, 240, 270 and 300 min (p's≥0.05). In obese insulin-resistant monkeys, myoinositol added to the diet lowers urine glucose concentrations and both myoinositol and D-chiroinositol added to a meal lower postprandial plasma glucose concentrations without increasing postprandial insulin concentrations. Therefore, myoinositol, like D-chiroinositol, may be a useful agent for reducing meal-induced hyperglycemia without inducing hyperinsulinemia in insulin-resistant subjects.     

Adding fat calories to meals after exercise does not alter glucose tolerance.

A single session of exercise increases insulin sensitivity for hours and even days, and dietary carbohydrate ingested after exercise alters the magnitude and duration of this effect. Although increasing systemic fatty acid availability is associated with insulin resistance, it is uncertain whether increasing dietary fat availability after exercise alters the exercise-induced increase in insulin sensitivity. The purpose of this study was to determine whether adding fat calories to meals after exercise alters glucose tolerance the next day. Seven healthy men cycled 90 min at 66 +/- 2% peak oxygen uptake followed by a maximum of five high-intensity intervals. During the hours after exercise, subjects ingested three meals containing either low-fat (5% energy from fat) or high-fat (45% energy from fat) foods (Low-Fat and High-Fat groups, respectively). Each diet contained the same amount of carbohydrate and protein. An oral glucose tolerance test was performed the next morning. Muscle glycogen and intramuscular triglyceride (IMTG) concentrations were measured in muscle biopsy samples obtained immediately before exercise and the next morning. The day after exercise, muscle glycogen concentration was identical in High-Fat and Low-Fat (393 +/- 70 and 379 +/- 38 mmol/kg dry wt). At the same time, IMTG concentration was approximately 20% greater during High-Fat compared with Low-Fat (42.5 +/- 3.4 and 36.3 +/- 3.3 mmol/kg dry wt; P < 0.05). Despite the addition of approximately 165 g of fat to meals after exercise ( approximately 1,500 kcal) and a resultant elevation in IMTG concentration, glucose tolerance was identical in High-Fat and Low-Fat (composite index: 8.7 +/- 1.0 and 8.4 +/- 1.0). In summary, as long as meals ingested in the hours after exercise contain the same carbohydrate content, the addition of approximately 1500 kcal from fat to these meals did not alter muscle glycogen resynthesis or glucose tolerance the next day.     

A comparison of metformin versus guar in combination with sulphonylureas in the treatment of non insulin dependent diabetes

Twelve non-obese non insulin dependent diabetics whose mean +/- SE fasting blood glucose was 12.9 +/- 0.9 mmol/l despite maximal doses of sulphonylureas, received 8 weeks of guar (5 g tid before meals) and 8 weeks of metformin (0.5 g tid) following a six week washout period, in a cross-over design. Guar significantly lowered fasting cholesterol and triglyceride concentrations but did not alter glucose concentrations. Conversely, metformin significantly reduced fasting and post-prandial glucose concentrations but had no influence on plasma lipids.     

Release of vasoactive intestinal peptide in the dumping syndrome.

To determine the effect of gastric surgery on the plasma vasoactive intestinal peptide (VIP) concentration, 13 patients with gastrectomy and seven controls were given an oral hypertonic load (200 ml 50% glucose solution). Blood was taken at intervals during the test for measurement of VIP and blood glucose concentrations and packed cell volume. At the same time observations were made on the occurrence of dumping symptoms and a record kept of the pulse rate. VIP values in the patients with gastrectomy were significantly increased by glucose ingestion, while these did not alter in controls (p less than 0.001). There was a highly significant correlation between the rate of rise in plasma VIP concentration and the rates of rise in packed cell volume (r = 0.85; p less than 0.001) and blood glucose concentration (r = 0.76; p less than 0.01) in patients with gastrectomy. Changes in packed cell volume and blood glucose values and the occurrence of dumping symptoms during the test were significantly different when postoperative patients were compared with controls (p less than 0.001, p less than 0.005, and p less than 0.001 respectively). Furthermore, when the patients with gastrectomy were divided into those without symptoms and those with dumping after meals the latter group showed a significantly greater rise of VIP (p less than 0.05). Despite the increased plasma VIP concentrations observed during dumping, VIP cannot be taken as the sole factor in the pathogenesis of the dumping syndrome.