Co-administration of a konjac-based fibre blend and American ginseng (Panax quinquefolius L.) on glycaemic control and serum lipids in type 2 diabetes: a randomized controlled, cross-over clinical trial.

PURPOSE: Use of polypharmacy in the treatment of diabetes is the norm; nonetheless, optimal control is often not achieved. Konjac-glucomannan-based fibre blend (KGB) and American ginseng (AG) have individually been shown to improve glycaemia and CVD risk factors in type 2 diabetes. The aim of this study was to determine whether co-administration of KGB and AG could improve diabetes control beyond conventional treatment. METHOD: Thirty-nine participants with type 2 diabetes (6.5 > A1c < 8.4%) were enrolled between January 2002 and May 2003 at the Risk Factor Modification Centre at St Michaels Hospital in a randomized, placebo-controlled, crossover trial with each intervention lasting 12-weeks. Medications, diet and lifestyle were kept constant. Interventions consisted of 6 g of fibre from KGB together with 3 g of AG (KGB and AG) or wheat bran-based, fibre-matched control. Primary endpoint was the difference in HbA1c levels at week 12. RESULTS: Thirty participants (18M:12F; age: 64 ± 7 years; BMI: 28 ± 5 kg/m2; HbA1c: 7.0 ± 1.0%) completed the study, and consumed 5.5 and 4.9 g/day of fibre from KGB and wheat bran control, respectively, and 2.7 g/day of AG. At week 12, HbA1c levels were 0.31% lower on the KGB and AG compared to control (p = 0.011). Mean (±SEM) plasma lipids decreased on the KGB and AG vs control by 8.3 ± 3.1% in LDL-C (p = 0.002), 7.5 ± 2.4% in non-HDL-C (p = 0.013), 5.7 ± 1.9% in total-C (p = 0.012), 4.1 ± 2.1% in total-C:HDL-C ratio (p = 0.042), 9.0 ± 2.3% in ApoB (p = 0.0005) and 14.6 ± 4.2% in ApoB:ApoA1 ratio (p = 0.049). CONCLUSIONS: Co-administration of KGB and AG increases the effectiveness of conventional therapy through a moderate but clinically meaningful reduction in HbA1c and lipid concentrations over 12 weeks in patients with type 2 diabetes. CLINICAL TRIALS REGISTRATION: NCT02806349 ( https://clinicaltrials.gov/ ).

Randomized clinical trial in healthy individuals on the effect of viscous fiber blend on glucose tolerance when incorporated in capsules or into the carbohydrate or fat component of the meal.

BACKGROUND/OBJECTIVE: Addition of viscous fiber to foods has been shown to significantly reduce postprandial glucose excursions. However, palatability issues and the variability in effectiveness due to different methods of administration in food limits it use. This study explores the effectiveness of a viscous fiber blend (VFB) in lowering postprandial glycemia using different methods of incorporation. METHODS: Two acute, randomized, controlled studies were undertaken: Study 1: Twelve healthy individuals (mean ± SD, age: 36 ± 13 years, body mass index [BMI]: 27 ± 4 kg/m(2)) consumed 8 different breakfasts. All meals consisted of 50 g of available carbohydrate from white bread (WB) and 10 g margarine. Zero, 1, 2, or 4 g of the VFB was baked into WB or mixed with the margarine. Study 2: Thirteen healthy individuals (mean ± SD, age: 39 ± 17 years, BMI: 25 ± 5 kg/m(2)) consumed 6 test meals, consisting of 50 g of available carbohydrate from WB. Six capsules containing either cornstarch or VFB were taken at 4 different time points during the glucose tolerance test. After obtaining a fasting finger-prick blood sample, volunteers consumed the test meal over a 10-minute period. Additional blood samples were taken at 15, 30, 45, 60, 90, and 120 minutes from the start of the meal. For study 2, an additional fasting sample was obtained at -30 minutes. RESULTS: Study 1: Irrespective of VFB dose, glucose levels were lower at 30 and 45 minutes when VFB was mixed into the margarine compared to the control (p < 0.05). Incremental areas under the curve were significantly lower compared to control when 4 g of VFB was mixed into the margarine. Study 2: There was no effect of the VFB on postprandial glucose levels when administered in capsules. CONCLUSION: Incorporation of VFB into margarine was more effective in lowering postprandial glycemia than when the VFB was baked into bread and no effect when given in capsules.

Gut hormone release and appetite regulation in healthy non-obese participants following oligofructose intake. A dose-escalation study.

Prevention of weight gain in adults is a major public health target. Animal experiments have consistently demonstrated a relationship between fermentable carbohydrate intake, such as oligofructose, anorectic gut hormones, and appetite suppression and body weight control. This study was designed to determine the dose of oligofructose which would augment the release of anorectic gut hormones and reduce appetite consistently in non-obese humans. Twelve non-obese participants were recruited for a 5-week dose-escalation study. Following a 9-14-day run-in, participants increased their daily oligofructose intake every week from 15, 25, 35, 45, to 55 g daily. Subjective appetite and side effects were monitored daily. Three-day food diaries were completed every week. Appetite study sessions explored the acute effects of 0, 15, 35, and 55 g oligofructose on appetite-related hormones, glycaemia, subjective appetite, and energy intake. In the home environment, oligofructose suppressed hunger, but did not affect energy intake. Oligofructose dose-dependently increased peptide YY, decreased pancreatic polypeptide and tended to decrease ghrelin, but did not significantly affect appetite profile, energy intake, glucose, insulin, or glucagon-like peptide 1 concentrations during appetite study sessions. In conclusion, oligofructose supplementation at ≥ 35 g/day increased peptide YY and suppressed pancreatic polypeptide and hunger; however, energy intake did not change significantly.

Variation in the effects of three different breakfast meals on subjective satiety and subsequent intake of energy at lunch and evening meal.

PURPOSE: To determine the relative impact of three iso-caloric breakfast meals, of variable composition, on satiety, hunger and subsequent intake of energy. METHODS: In a three-way, crossover design, 30 healthy men (age of 21.7 ± 1.2 years; BMI, 23.1 ± 2.7 kg/m²) were randomised to one of three test breakfasts, on three separate occasions, separated by 1 week. The breakfasts consisted of eggs on toast, cereal (cornflakes) with milk and toast, or a croissant and orange juice. Subjective ratings of satiety, hunger, fullness and desire to eat were recorded at 30-min intervals by electronic visual analogue scales (VAS). Energy intake was assessed by weighed food intake at an ad libitum lunch and evening meal. RESULTS: Participants showed increased satiety, less hunger and a lower desire to eat after the breakfast containing eggs relative to the cereal (p < 0.02), and croissant-based meals (p < 0.0001). The egg breakfast was also accompanied by a significantly lower intake of energy relative to the croissant- and cereal-based breakfasts at the buffet lunch and evening meal, respectively, 1,284 ± 464 (egg) versus 1,442 ± 426 kcal (croissant), p = 0.03, 1,407 ± 379 (cereal) at lunch and 1,899 ± 729 (egg) versus 2,214 ± 620 kcal (cereal), p = 0.02, 2,047 ± 712 (croissant) at evening meal. The breakfast meal with the greatest effect on satiety and subsequent intake of energy was distinct in having the highest protein and lowest carbohydrate content relative to the other two breakfasts. CONCLUSION: These findings provide evidence to support the importance of food choice at breakfast as a means of increasing satiety in the morning and reducing energy intake at lunch.

Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers.

Shiftworkers have a higher risk of CHD and type 2 diabetes. They consume a large proportion of their daily energy and carbohydrate intake in the late evening or night-time, a factor which could be linked to their increase in disease risk. We compared the metabolic effects of varying both dietary glycaemic index (GI) and the time at which most daily energy intake was consumed. We hypothesised that glucose control would be optimal with a low-GI diet, consumed predominantly early in the day. A total of six healthy lean volunteers consumed isoenergetic meals on four occasions, comprising either high- or low-GI foods, with 60 % energy consumed predominantly early (breakfast) or late (supper). Interstitial glucose was measured continuously for 20 h. Insulin, TAG and non-esterified fatty acids were measured for 2 h following every meal. Highest glucose values were observed when large 5021 kJ (1200 kcal) high-GI suppers were consumed. Glucose levels were also significantly higher in predominantly late high- v. low-GI meals (P<0·01). Using an estimate of postprandial insulin sensitivity throughout the day, we demonstrate that this follows the same trend, with insulin sensitivity being significantly worse in high energy consumed in the evening meal pattern. Both meal timing and GI affected glucose tolerance and insulin secretion. Avoidance of large, high-GI meals in the evening may be particularly beneficial in improving postprandial glucose profiles and may play a role in reducing the risk of type 2 diabetes; however, longer-term studies are needed to confirm this.

Age and experience predict accurate short-term energy compensation in adults.

Many factors thought to influence the control of food intake have been investigated independently, but the relative importance of each of these factors remains unknown. This study investigated the concurrent role of 21 factors in accurate compensation for energy consumed 60min previously. Energy compensation was assessed by measuring the difference in energy intake at an ad libitum test meal following two preloads of differing energy content, in 105 participants. Using regression, energy compensation was associated only with age (B=-2.39, ß=-0.345, p<0.01), and accuracy of energy compensation was associated only with age (B=1.81, ß=0.376, p<0.01) and order of preload presentation (B=-21.80, ß=-0.233, p=0.01). These findings suggest that our ability to detect and/or adjust for energy intake deteriorates with age, and that individuals adjust more easily for missing, as opposed to additional, energy. Notably however, only these predictors were associated with energy compensation and they account for only 11-18% of total variance.

Multivitamin use among non-pregnant females of childbearing age in the Western North Carolina multivitamin distribution program.

BACKGROUND: Daily consumption of 400 mcg of folic acid prior to conception and throughout the first trimester of pregnancy reduces the risk of neural tube defects (NTDs) by 50%-80%. A daily multivitamin with folic acid can ensure that females receive the recommended amount of folic acid during childbearing years. OBJECTIVE: The purpose of this study was to determine if vitamin consumption is influenced by providing a free bottle of multivitamins to non-pregnant women of childbearing age during a face-to-face interaction with a health care provider in health departments. METHODS: An eight-question survey was given to a sample of women who had received a free bottle of multivitamins. Vitamin consumption behavior prior to the intervention was compared to current usage at the time of the survey. RESULTS: Twenty-five percent of all survey respondents reported taking a daily multivitamin or folic acid tablet before the intervention. Fifty-three percent reported taking a daily multivitamin 8-10 months later, a greater than two-fold increase (PR=2.1). Latino women reported the greatest increase in daily multivitamin intake, from 21% to 70% (PR=3.3). LIMITATIONS: The results may be difficult to extrapolate to the general population as the survey population differs from the general population. Prior vitamin use was determined by patient recall. The intervention occurred simultaneously with a multifaceted, public folic acid campaign. CONCLUSIONS: Eight to ten months after receiving a free three-month supply of multivitamins during a face-to-face interaction with a health care provider, the number of participants reporting daily use increased significantly.

Effects of exercise and restrained eating behaviour on appetite control.

Obesity is a global epidemic; increased consumption of energy-dense food and reduced physical activity levels are likely to be the main drivers. Previous cross-sectional research has shown that sedentary males, unlike their active counterparts, are unable to compensate for previous energy intake (EI). Using a longitudinal design a 6-week exercise intervention was found to improve short-term appetite control, leading to a more 'sensitive' eating behaviour in response to previous EI, both acutely at a test meal and for the next 24 h. Although the mechanisms whereby acute and chronic exercise improves short-term appetite remain unknown, post-ingestive satiety peptides are likely to be involved. Acute exercise was found to increase postprandial levels of polypeptide YY, glucagon-like peptide-1 and pancreatic polypeptide but to have no impact on ghrelin, suggesting that exercise can trigger physiological changes in satiety hormone secretion that could help in appetite control and weight maintenance. In the context of an increased availability of highly-palatable food, dietary restraint may be increasingly important. Although restraint has been associated with abnormal eating behaviour, in the laboratory no counter-regulation was found in restrained eaters when presented with a buffet meal 60 min after a high-energy preload or when a pasta-meal was presented 3 h after preloading. Although restraint was not found to impact on polypeptide YY or TAG, lower postprandial glucose and insulin plasma levels were observed in restrained eaters, together with increased feelings of fullness. In conclusion, short-term appetite control seems to be favourably modified by exercise, while the impact of restraint on appetite seems to be more complex.

Short-term appetite control in response to a 6-week exercise programme in sedentary volunteers.

Previous cross-sectional studies have shown that sedentary males, unlike their active counterparts, are unable to compensate for previous energy intake (EI). The present study therefore investigated the effects of a 6-week moderate exercise programme (4 times per week, 65-75 % maximal heart rate) on appetite regulation in healthy sedentary volunteers using a longitudinal design. EI at a buffet meal 60 min after high-energy (HEP; 607 kcal) and low-energy (LEP; 246 kcal) preloads, together with 24 h cumulative EI, were measured in twenty-five healthy volunteers (eleven men; mean age 30 (SD 12) years, mean BMI 22.7 (SD 2.3) kg/m2), at baseline and after the exercise intervention. Subjective hunger and fullness were assessed throughout using visual analogue scales. ANOVA showed a significant preload x exercise interaction on 24 h cumulative EI, supporting an improvement in appetite control over this time period with the exercise programme. There was a trend towards improvement in energy compensation over the same period (8.9 (SD 118.5) % v. 79.5 (SD 146..4) %; P = 0.056). No preload x exercise interaction was observed for buffet EI. Secondary analysis, however, showed that although buffet EI after the two preloads was not significantly different at baseline, buffet EI after the HEP was significantly lower than after the LEP following the exercise intervention. The improvement in short-term appetite control with exercise was not explained by changes in subjective hunger or satiety. This longitudinal study supports the original cross-sectional findings and suggests that exercise may have a significant impact on short-term appetite control by leading to a more sensitive eating behaviour in response to previous EI. Further studies are needed to clarify the mechanisms involved.

Effects of exercise on gut peptides, energy intake and appetite.

This study investigated the acute effects of exercise on the postprandial levels of appetite-related hormones and metabolites, energy intake (EI) and subjective measures of appetite. Ghrelin, polypeptide YY (PYY), glucagon-like peptide-1 (GLP-1) and pancreatic polypeptide (PP) were measured in the fasting state and postprandially in 12 healthy, normal-weight volunteers (six males and six females) using a randomised crossover design. One hour after a standardised breakfast, subjects either cycled for 60 min at 65% of their maximal heart rate or rested. Subjective appetite was assessed throughout the study using visual analogue scales and subsequent EI at a buffet meal was measured at the end (3-h post-breakfast and 1-h post-exercise). Exercise significantly increased mean PYY, GLP-1 and PP levels, and this effect was maintained during the post-exercise period for GLP-1 and PP. No significant effect of exercise was observed on postprandial levels of ghrelin. During the exercise period, hunger scores were significantly decreased; however, this effect disappeared in the post-exercise period. Exercise significantly increased subsequent absolute EI, but produced a significant decrease in relative EI after accounting for the energy expended during exercise. Hunger scores and PYY, GLP-1 and PP levels showed an inverse temporal pattern during the 1-h exercise/control intervention. In conclusion, acute exercise, of moderate intensity, temporarily decreased hunger sensations and was able to produce a short-term negative energy balance. This impact on appetite and subsequent energy homeostasis was not explained by changes in postprandial levels of ghrelin; however, 'exercise-induced anorexia' may potentially be linked to increased PYY, GLP-1 and PP levels.

Effects of altering the ratio of dietary n-6 to n-3 fatty acids on insulin sensitivity, lipoprotein size, and postprandial lipemia in men and postmenopausal women aged 45-70 y: the OPTILIP Study.

BACKGROUND: Insulin resistance is associated with elevated plasma triacylglycerol, low HDL concentrations, elevated postprandial lipemia, and a predominance of small, dense LDLs (sdLDLs). It has been hypothesized that the dietary ratio of n-6 to n-3 (n-6:n-3) polyunsaturated fatty acids (PUFAs) may have favorable effects on these risk factors by increasing insulin sensitivity. OBJECTIVE: The objective was to measure changes in insulin sensitivity, lipoprotein size, and postprandial lipemia after a 6-mo alteration in n-6:n-3. DESIGN: In a randomized, parallel design in 258 subjects aged 45-70 y, we compared 4 diets providing 6% of energy as PUFAs with an n-6:n-3 between 5:1 and 3:1 with a control diet that had an n-6:n-3 of 10:1. The diets were enriched in alpha-linolenic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), or both. Insulin sensitivity was assessed with the homeostatic model assessment of insulin resistance and the revised quantitative insulin sensitivity test. RESULTS: Dietary intervention did not influence insulin sensitivity or postprandial lipase activities. Fasting and postprandial triacylglycerol concentrations were lower, and the proportion of sdLDLs decreased (by 12.7%; 95% CI: -22.9%, 2.4%), with an n-6:n-3 of approximately 3:1, which was achieved by the addition of long-chain n-3 PUFAs (EPA and DHA). CONCLUSIONS: Decreasing the n-6:n-3 does not influence insulin sensitivity or lipase activities in older subjects. The reduction in plasma triacylglycerol after an increased intake of n-3 long-chain PUFAs results in favorable changes in LDL size.

Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from the BBC "diet trials".

OBJECTIVE: To compare the effectiveness of four commercial weight loss diets available to adults in the United Kingdom. DESIGN: Six month multicentre randomised unblinded controlled trial. SETTING: Community based sample of otherwise healthy overweight and obese adults. INTERVENTIONS: Dr Atkins' new diet revolution, Slim-Fast plan, Weight Watchers pure points programme, and Rosemary Conley's eat yourself slim diet and fitness plan. MAIN OUTCOME MEASURES: Weight and body fat changes over six months. RESULTS: All diets resulted in significant loss of body fat and weight over six months. Groups did not differ significantly but loss of body fat and weight was greater in all groups compared with the control group. In an intention to treat analysis, average weight loss was 5.9 kg and average fat loss was 4.4 kg over six months. The Atkins diet resulted in significantly higher weight loss during the first four weeks, but by the end was no more or less effective than the other diets. CONCLUSIONS: Clinically useful weight loss and fat loss can be achieved in adults who are motivated to follow commercial diets for a substantial period. Given the limited resources for weight management in the NHS, healthcare practitioners should discuss with their patients programmes known to be effective. TRIAL REGISTRATION: Clinical trials NCT00327821.

Quercetin metabolites downregulate cyclooxygenase-2 transcription in human lymphocytes ex vivo but not in vivo.

Flavonoids have the potential to modulate inflammation by inhibition of cyclooxygenase-2 (COX-2) transcription. In this study, we compared the effect of the human flavonoid plasma metabolites (quercetin 3'-sulfate, quercetin 3-glucuronide and 3'-methylquercetin 3-glucuronide) on expression of COX-2 mRNA in human lymphocytes ex vivo using TaqMan real-time RT-PCR. We show that the flavonoid quercetin metabolites as detected in human plasma at physiologically significant concentrations inhibit COX-2 expression in human lymphocytes ex vivo. To examine the effect in vivo, we measured COX-2 mRNA levels in 8 subjects (5 men and 3 women) participating in a 3-way, single-blind, randomized crossover study after consumption of a single meal of white, low-quercetin onions, compared with yellow, high-quercetin onions. After consumption of high-quercetin onions, quercetin conjugates were detected in plasma (up to a maximum concentration of 4 micro mol/L at approximately 1 h). However, the expression of COX-2 mRNA in lymphocytes was unchanged by the consumption of high-quercetin onions compared with the low-quercetin group. The results show that a single high dose of the flavonoid quercetin from onions does not change COX-2 mRNA expression in human lymphocytes in vivo even though this change occurred in vitro and ex vivo.

Coffee acutely modifies gastrointestinal hormone secretion and glucose tolerance in humans: glycemic effects of chlorogenic acid and caffeine.

BACKGROUND: Accumulating evidence suggests that certain dietary polyphenols have biological effects in the small intestine that alter the pattern of glucose uptake. Their effects, however, on glucose tolerance in humans are unknown. OBJECTIVE: The objective was to investigate whether chlorogenic acids in coffee modulate glucose uptake and gastrointestinal hormone and insulin secretion in humans. DESIGN: In a 3-way, randomized, crossover study, 9 healthy fasted volunteers consumed 25 g glucose in either 400 mL water (control) or 400 mL caffeinated or decaffeinated coffee (equivalent to 2.5 mmol chlorogenic acid/L). Blood samples were taken frequently over the following 3 h. RESULTS: Glucose and insulin concentrations tended to be higher in the first 30 min after caffeinated coffee consumption than after consumption of decaffeinated coffee or the control (P < 0.05 for total and incremental area under the curve for glucose and insulin). Glucose-dependent insulinotropic polypeptide secretion decreased throughout the experimental period (P < 0.005), and glucagon-like peptide 1 secretion increased 0-120 min postprandially (P < 0.01) after decaffeinated coffee consumption compared with the control. Glucose and insulin profiles were consistent with the known metabolic effects of caffeine. However, the gastrointestinal hormone profiles were consistent with delayed intestinal glucose absorption. CONCLUSIONS: Differences in plasma glucose, insulin, and gastrointestinal hormone profiles further confirm the potent biological action of caffeine and suggest that chlorogenic acid might have an antagonistic effect on glucose transport. Therefore, a novel function of some dietary phenols in humans may be to attenuate intestinal glucose absorption rates and shift the site of glucose absorption to more distal parts of the intestine.

Exaggerated postprandial lipaemia and lower post-heparin lipoprotein lipase activity in middle-aged men.

An exaggerated postprandial lipaemic response is thought to play a central role in the development of an atherogenic lipoprotein phenotype, a recognized lipid risk factor for coronary heart disease. A small number of limited studies have compared postprandial lipaemia in subjects of varying age, but have not investigated mechanisms underlying age-associated changes in postprandial lipaemia. In order to test the hypothesis that impaired lipaemia in older subjects is associated with loss of insulin sensitivity, the present study compared the postprandial lipaemic and hormone responses for 9 h following a standard mixed meal in normolipidaemic healthy young and middle-aged men. Lipoprotein lipase (LPL) and hepatic lipase (HL) activities were determined in post-heparin plasma 9 h postprandially and on another occasion under fasting conditions. Postprandial plasma glucose (P<0.02), retinyl ester (indirect marker for chylomicron particles; P<0.005) and triacylglycerol (TAG)-rich lipoprotein (density<1.006 g/ml fraction of plasma) TAG (P<0.05) and retinyl ester (P<0.005) responses were higher in middle-aged men, whereas plasma insulin responses were lower in this group (P<0.001). Fasting and 9 h postprandial LPL and HL activities were also significantly lower in the middle-aged men compared with the young men (P<0.006). In conclusion, the higher incremental postprandial TAG response in middle-aged men than young men was attributed to the accumulation of dietary-derived TAG-rich lipoproteins (density<1.006 g/ml fraction of plasma) and occurred in the absence of marked differences in fasting TAG levels between the two groups. Fasting and postprandial LPL and HL activities were markedly lower in middle-aged men, but lack of statistical associations between measures of insulin response and post-heparin lipase activities, as well as between insulin and measures of postprandial lipaemia, suggest that this lower activity cannot be attributed to lack of sensitivity of lipases to activation by insulin. Alternatively, post-heparin lipase activities may not be good markers for the insulin-sensitive component of lipase that is activated postprandially.

A randomised four-intervention crossover study investigating the effect of carbohydrates on daytime profiles of insulin, glucose, non-esterified fatty acids and triacylglycerols in middle-aged men.

Postprandial concentrations of glucose, insulin and triacylglycerols (TG) correlate to risk for CHD. Carbohydrates affect many metabolites that could have a potential effect on cardiovascular risk factors. The objective of the present study was to examine, using a randomised prospective study, the acute (day 1) and ad libitum medium-term (day 24) effects of four diets: a high-fat diet (HIGH-FAT; 50 % fat, >34 % monounsaturated fatty acids); a low-glycaemic index (GI) diet (LOW-GI; high-carbohydrate, low-GI); a high-sucrose diet (SUCROSE; high carbohydrate increase of 90 g sucrose/d); a high-GI diet (HIGH-GI; high-carbohydrate, high-GI). Daytime profiles (8 h) (breakfast, lunch and tea) of lipid and carbohydrate metabolism were completed during day 1 and day 24. Seventeen middle-aged men with one or more cardiac risk factors completed the study. There was no change from day 1 or between diets in fasting glucose, lipids or homeostatic assessment model (HOMA) on day 24. The HIGH-FAT compared with the three high-carbohydrate diets was associated with lower postprandial insulin and glucose but higher postprandial TG and non-esterified fatty acids (NEFA). There was a significant increase in the 6 h (15.00 hours) TG concentration (day 1, 2.6 (sem 0.3) mmol/l v. day 24, 3.3 (sem 0.3) mmol/l; P<0.01) on the SUCROSE diet. Postprandial HOMA (i.e. incremental area under the curve (IAUC) glucose (mmol/l per min)xIAUC insulin/22.5 (mU/l per min)) median changes from day 1 to day 24 were -61, -43, -20 and +31 % for the HIGH-FAT, LOW-GI, SUCROSE and HIGH-GI diets respectively. The HIGH-GI percentage change was significantly different from the other three diets (P<0.001). Despite being advised to maintain an identical energy intake there was a significant weight change (-0.27 (sem 0.3) kg; P<0.02) on the LOW-GI diet compared with the SUCROSE diet (+0.84 (sem 0.3) kg). In conclusion the HIGH-FAT diet had a beneficial effect on postprandial glucose and insulin over time but it was associated with higher postprandial concentrations of TG and NEFA. Conversely the HIGH-GI diet appeared to increase postprandial insulin resistance over the study period.

Acute ingestion of a meal rich in n-3 polyunsaturated fatty acids results in rapid gastric emptying in humans.

BACKGROUND: n-3 Polyunsaturated fatty acids (PUFAs) have proven benefits for both the development of atherosclerosis and inflammatory conditions. The effects on atherosclerosis may be partly mediated by the observed reduction in fasting and postprandial triacylglycerol concentrations after both acute and chronic n-3 PUFA ingestion. OBJECTIVE: The aim of this study was to assess gastric emptying and gastrointestinal hormone release after the consumption of mixed meals rich in n-3 PUFAs or other classes of fatty acids. DESIGN: Ten healthy women (aged 50-62 y) completed 4 separate study visits in a single-blind, randomized design. On each occasion, subjects consumed 40 g oil rich in either saturated fatty acids, monounsaturated fatty acids, n-6 PUFAs, or n-3 PUFAs as part of a mixed meal. [1-(13)C]Octanoic acid (100 mg) was added to each oil. Gastric emptying was assessed by a labeled octanoic acid breath test, and concentrations of gastrointestinal hormones and plasma lipids were measured. RESULTS: Recovery of (13)C in breath was enhanced after n-3 PUFA ingestion (P < 0.005). The cholecystokinin response after the n-3 PUFA meal was significantly delayed (P < 0.001), and the glucagon-like peptide 1 response was significantly reduced (P < 0.05). CONCLUSION: The inclusion of n-3 PUFAs in a meal alters the gastric emptying rate, potentially as the result of changes in the pattern of cholecystokinin and glucagon-like peptide 1 release.