Adolescent girls often skip breakfast due to time constraints and reduced morning appetite. This study examined the acute impact of breakfast consumption timing versus breakfast omission (BO) on glycaemic and insulinaemic responses to lunch in infrequent breakfast-consuming girls. Fifteen girls (13.1±0.8 years) completed three conditions in a randomised crossover design: early-morning breakfast consumption (EM-BC; 8:30), mid-morning breakfast consumption (MM-BC; 10:30), and BO. A standardised lunch was provided at 12:30, followed by a 2-h post-lunch observation period. Blood and expired gas samples were collected periodically. Linear mixed models with Cohen’s d effect sizes compared outcomes between conditions. Pre-lunch glucose and insulin incremental area under the curve (iAUC) were higher in the breakfast conditions versus BO (P≤0.009), with no differences between breakfast conditions. MM-BC reduced post-lunch glucose iAUC by 36% and 25% compared with BO and EM-BC, respectively (P<0.001, d=0.92–1.44). A moderate, non-significant 15% reduction in post-lunch glucose iAUC was seen with EM-BC versus BO (P=0.077, d=0.52). These reductions occurred without changes in post-lunch insulinemia (P≥0.323) and were accompanied by increased post-lunch carbohydrate oxidation compared with BO (P≤0.018, d=0.58–0.75); with no differences between EM-BC and MM-BC. MM-BC lowered glycaemic response over the experimental period compared with BO (P=0.033, d=0.98) and EM-BC (P=0.123, d=0.93), with no difference between EM-BC and BO. Compared with BO, both breakfast conditions lowered post-lunch glycaemic responses with mid-morning breakfast eliciting a greater second-meal effect than early-morning breakfast. These findings indicate the breakfast-to-lunch meal interval may be a crucial factor affecting postprandial glycaemia in infrequent breakfast-consuming girls.

Poor post-prandial glucose control is a risk factor for multiple health conditions. The second-meal effect refers to the progressively improved glycaemic control with repeated feedings, an effect which is achievable with protein ingestion at the initial eating occasion. The most pronounced glycaemic response each day therefore typically occurs following breakfast, so the present study investigated whether ingesting protein during the night could improve glucose control at the first meal of the day. In a randomised crossover design, fifteen adults (seven males, eight females; age, 22 (sd 3) years; BMI, 24·0 (sd 2·8) kg/m2; fasting blood glucose, 4·9 (sd 0·5) mmol/l) woke at 04.00 (sd 1) hours to ingest 300 ml water with or without 63 g whey protein. Participants then completed a mixed-macronutrient meal tolerance test (1 g carbohydrate/kg body mass, 2356 (sd 435) kJ), 5 h 39 min following the nocturnal feeding. Nocturnal protein ingestion increased the glycaemic response (incremental AUC) to breakfast by 43·5 (sd 55·5) mmol × 120 min/l (P = 0·009, d = 0·94). Consistent with this effect, individual peak blood glucose concentrations were 0·6 (sd 1·0) mmol/l higher following breakfast when protein had been ingested (P = 0·049, d = 0·50). Immediately prior to breakfast, rates of lipid oxidation were 0·02 (sd 0·03) g/min higher (P = 0·045) in the protein condition, followed by an elevated post-prandial energy expenditure (0·38 (sd 0·50) kJ/min, P = 0·018). Post-prandial appetite and energy intake were similar between conditions. The present study reveals a paradoxical second-meal phenomenon whereby nocturnal whey protein feeding impaired subsequent glucose tolerance, whilst increasing post-prandial energy expenditure.

Because obesity is associated with many co-morbidities, including diabetes mellitus, this study evaluated the second-meal effect of a commercial prebiotic, inulin-type fructans, and the effects of the prebiotic on faecal microbiota, metabolites and bile acids (BA). Nine overweight beagles were used in a replicated 3×3 Latin square design to test a non-prebiotic control (cellulose) against a low (equivalent to 0·5 % diet) and high dose (equivalent to 1·0 % diet) of prebiotic over 14-d treatments. All dogs were fed the same diet twice daily, with treatments provided orally via gelatin capsules before meals. On days 13 or 14 of each period, fresh faecal samples were collected, dogs were fed at 08.00 hours and then challenged with 1 g/kg body weight of maltodextrin in place of the 16.00 hours meal. Repeated blood samples were analysed for glucose and hormone concentrations to determine postprandial incremental AUC (IAUC) data. Baseline glucose, insulin and active glucagon-like peptide-1 levels were similar between all groups (P>0·10). Glucose and insulin IAUC after glucose challenge appeared lower following the high dose, but did not reach statistical relevance. Prebiotic intervention resulted in an increase in relative abundance of some Firmicutes and a decrease in the relative abundance of some Proteobacteria. Individual and total faecal SCFA were significantly increased (P<0·05) following prebiotic supplementation. Total concentration of excreted faecal BA tended to increase in dogs fed the prebiotic (P=0·06). Our results indicate that higher doses of inulin-type prebiotics may serve as modulators of gut microbiota, metabolites and BA pool in overweight dogs.

Breakfast omission is associated with obesity and CVD/diabetes, but the acute effects of extended morning fasting upon subsequent energy intake and metabolic/hormonal responses have received less attention. In a randomised cross-over design, thirty-five lean men (n 14) and women (n 21) extended their overnight fast or ingested a typical carbohydrate-rich breakfast in quantities relative to RMR (i.e. 1963 (sd 238) kJ), before an ad libitum lunch 3 h later. Blood samples were obtained hourly throughout the day until 3 h post-lunch, with subjective appetite measures assessed. Lunch intake was greater following extended fasting (640 (sd 1042) kJ, P< 0·01) but incompletely compensated for the omitted breakfast, with total intake lower than the breakfast trial (3887 (sd 1326) v. 5213 (sd 1590) kJ, P< 0·001). Systemic concentrations of peptide tyrosine–tyrosine and leptin were greater during the afternoon following breakfast (both P< 0·05) but neither acylated/total ghrelin concentrations were suppressed by the ad libitum lunch in the breakfast trial, remaining greater than the morning fasting trial throughout the afternoon (all P< 0·05). Insulin concentrations were greater during the afternoon in the morning fasting trial (all P< 0·01). There were no differences between trials in subjective appetite during the afternoon. In conclusion, morning fasting caused incomplete energy compensation at an ad libitum lunch. Breakfast increased some anorectic hormones during the afternoon but paradoxically abolished ghrelin suppression by the second meal. Extending morning fasting until lunch altered subsequent metabolic and hormonal responses but without greater appetite during the afternoon. The present study clarifies the impact of acute breakfast omission and adds novel insights into second-meal metabolism.

The present study evaluated the effects of fibre fermentability and viscosity in a morning meal on glucose, insulin and glucagon-like peptide-1 (GLP-1) responses to a glucose challenge later in the day in six healthy female dogs. For this purpose, two Latin square design experiments were performed. In Expt 1, dogs were fed a low-fibre (LF; 1 % Solka-Floc (International Fiber Corporation) and 1 % soya hulls) diet, a low-fermentable fibre (LFF; 5 % Solka-Floc (International Fiber Corporation) and 3 % soya hulls) diet or a high-fermentable fibre (HFF; 5 % pectin and 3 % short-chain fructo-oligosaccharides) diet. In Expt 2, dogs were fed a low-viscosity fibre (5 % Solka-Floc (International Fiber Corporation) and 3 % soya hulls) diet, a moderate-viscosity fibre (MVF; 2 % Solka-Floc (International Fiber Corporation), 2 % soya hulls, 2 % psyllium and 2 % pectin) diet or a high-viscosity fibre (HVF; 4 % psyllium and 4 % pectin) diet. Dogs were fed at 08.00, 12.00 and 16.00 hours on days 1–6 of each period. On day 7, dogs were fed at 08.00 hours and then dosed with maltodextrin at 12.00 hours. Data were analysed to identify baseline and incremental AUC (IAUC) changes among the treatments. In Expt 1, glucose IAUC0–180min was lower (P< 0·05) in dogs fed the HFF v. LF and LFF diets. Insulin and GLP-1 IAUC0–180min were not affected. In Expt 2, baseline GLP-1 was greater (P< 0·005) and baseline insulin was lower (P< 0·05) in dogs fed the HVF v. MVF diet, but glucose, insulin and GLP-1 IAUC0–180min were not affected. In summary, HFF in a morning meal has the potential to decrease blood glucose response in a consequent meal.

Low glycaemic index (LGI) foods have been proposed as potential means to decrease postprandial glucose excursions and thus to improve diabetes management. We modulated glucose availability of cereal products and thus their glycaemic index to study the metabolic effect of LGI foods on daylong glucose control acutely and in the long term following a 5-week GI intervention diet in free-living subjects. In this randomised, parallel trial, two groups of nineteen overweight subjects followed an ad libitum 5-week intervention diet in which usual starch was replaced by either LGI or high GI (HGI) starch. During the exploration days (days 1 and 36), subjects ate their assigned 13C-labelled test breakfast (LGI or HGI), and total and exogenous glucose kinetics (using stable isotopes), postprandial concentrations of glucose, insulin, lipid profile and nutrient oxidation were assessed after the test breakfast and a standardised lunch. At day 1, LGI breakfast significantly decreased post-breakfast glycaemic response with a parallel decrease in exogenous and total glucose appearance (P < 0·05). Post-lunch and post-breakfast glycaemic responses were positively correlated (r 0·79, P < 0·0001). Following the 5-week diet, difference between the groups in terms of glucose kinetics and response was maintained (no significant interaction group × time) but tended to decrease over time for the post-breakfast glycaemic response. Post-lunch and post-breakfast glycaemic responses remained positively correlated (r 0·47, P = 0·004). Modulation of postprandial glucose availability at breakfast decreased plasma exogenous glucose appearance and improved glucose control at the subsequent lunch. After 5 weeks, these effects were maintained in healthy subjects but remained to be confirmed in the longer term.

Accumulating data indicate that a diet characterized by low glycaemic-index (GI) foods not only improves certain metabolic ramifications of insulin resistance, but also reduces insulin resistance per se. Epidemiological data also suggest a protective role against development of non-insulin-dependent diabetes mellitus and cardiovascular disease. A major disadvantage in this connection is the shortage of low-GI foods, and many common starchy staple foods, such as bread products, breakfast cereals and potato products, have a high GI. Studies in our laboratory show that it is possible to significantly lower the GI of starchy foods, for example by choice of raw material and/or by optimizing the processing conditions. Such low-GI foods may or may not influence glucose tolerance at a subsequent meal. Consequently, certain low-GI breakfasts capable of maintaining a net increment in blood glucose and insulin at the time of the next meal significantly reduced post-prandial glycaemia and insulinaemia following a standardized lunch meal, whereas others had no ‘second-meal’ impact. These results imply that certain low-GI foods may be more efficient in modulating metabolism in the long term. Although the literature supports a linear correlation between the GI and insulinaemic index (II) of foods, this is not always the case. Consequently, milk products elicited elevated IIs, indistinguishable from a white bread reference meal, despite GIs in the lower range. This inconsistent behaviour of milk products has not been acknowledged, and potential metabolic consequences remain to be elucidated.