An 8-week feeding experiment was conducted to investigate the effects of dl-methionine (Met) supplementation in a low-fishmeal diet on growth, key gene expressions of amino acid transporters and target of rapamycin (TOR) pathway in juvenile cobia, Rachycentron canadum. Seven isonitrogenous and isolipidic diets were formulated, containing 0·72, 0·90, 1·00, 1·24, 1·41, 1·63 and 1·86 % Met. Weight gain and specific growth rates increased gradually with Met levels of up to 1·24 % and then decreased gradually. In dorsal muscle, mRNA levels of ASCT2 in the 1·00 % Met group were significantly up-regulated compared with 0·72, 1·63, and 1·86 %. The insulin-like growth factor-I (IGF-I) mRNA levels in the dorsal muscle of fish fed 1·00 and 1·24 % Met were higher than those in fish fed other Met levels. In addition, fish fed 1·24 % Met showed the highest mRNA levels of TOR and phosphorylation of TOR on Ser2448. The phosphorylation of ribosomal p70-S6 kinase (S6K) on Ser371 in the dorsal muscle of fish fed 1·86 % Met was higher than those in the 0·72 % group. In conclusion, straight broken-line analysis of weight gain rate against dietary Met level indicates that the optimal Met requirement for juvenile cobia is 1·24 % (of DM, or 2·71 % dietary protein). Met supplementation in a low-fishmeal diet increased cobia growth via a mechanism that can partly be attributed to Met’s ability to affect the TOR/S6K signalling pathway by enhancing ASCT2 and IGF-I transcription in cobia dorsal muscle.

The early-life origins of disease hypothesis has been applied to obesity research and modeled through overnutrition, usually with a high-fat diet (HFD). Since the obesity epidemic coincided with societal change in dietary fat consumption, rather than amount, manipulation of fatty acid (FA) profile is an under-investigated area of study. Additionally, the binding of FAs to nuclear receptors may have persistent intergenerational, extranutritive endocrinological effects that interact with the actions of reproductive steroids causing sex-dependent effects. To determine the role of FA type in the effects underlying maternal HFD, we fed wild-type C57BL6/J mating pairs, from preconception through lactation, a HFD with high saturated fat levels from coconut oil or high linoleic acid (LA) levels from vegetable oil. Male and female offspring body weight and food intake were measured weekly for 25 weeks. Assays for glucose metabolism, body composition, and calorimetry were performed at 25 weeks. Plasma metabolic peptides and liver mRNA were measured terminally. Obesity was primarily affected by adult rather than maternal diet in males, yet in females, maternal HFD potentiated the effects of adult HFD. Maternal HFD high in LA impaired glucose disposal in males weaned onto HFD and insulin sensitivity of females. Plasma leptin correlated with adiposity, but insulin and insulin receptor expression in the liver were altered by maternal LA in males. Our results suggest that maternal FA profile is most influential on offspring glucose metabolism and that adult diet is more important than maternal diet for obesity and other parameters of metabolic syndrome.

A high protein content combined with its enormous growth capacity make duckweed an interesting alternative protein source, but information about postprandial responses in humans is lacking. The present study aimed to assess the postprandial serum amino acid profile of Lemna minor in healthy adults in comparison with green peas. A secondary objective was to obtain insights regarding human safety. A total of twelve healthy volunteers participated in a randomised, cross-over trial. Subjects received two protein sources in randomised order with a 1-week washout period. After an overnight fast, subjects consumed L. minor or peas (equivalent to 20 g of protein). After a baseline sample, blood samples were taken 15, 30, 45, 60, 75, 90, 120, 150 and 180 min after consumption to assess amino acid, glucose and insulin levels. Heart rate, blood pressure and aural temperature were measured before and after consumption, and subjects reported on gastrointestinal discomfort for four subsequent days. Compared with green peas, significantly lower blood concentrations of amino acids from L. minor were observed, indicating lower digestibility. L. minor consumption resulted in lower plasma glucose and insulin levels compared with peas, probably due to different glucose content. There were no significant differences concerning the assessed health parameters or the number of gastrointestinal complaints, indicating that a single bolus of L. minor – grown under controlled conditions – did not induce acute adverse effects in humans. Further studies need to investigate effects of repeated L. minor intake and whether proteins purified from L. minor can be digested more easily.

A novel flexible radio frequency (RF) sensor is designed to facilitate the accurate testing of various samples used in the biomedical industry at the industrial, scientific and medical (ISM) frequency band. The proposed RF biosensor comprises a liquid channel-loaded interdigitated capacitor, which is integrated on a coplanar waveguide structure. The prototype of the sensor is fabricated on a 0.13 mm thin biodegradable polyethylene terephthalate polyester film to perform the testing of various bio-graded samples by recording the corresponding resonant frequency. It is observed that there is a noticeable change between the measured resonant frequencies of these samples, which primarily occurs due to the difference in their dielectric properties. The designed sensor was used to monitor and investigate the quality of glycerol, which is the most commonly used raw ingredient in the biomedical and food industry. The determination of glucose concentration in base fluids is considered to ease the challenges faced by doctors and biochemists regarding the monitoring of glucose concentration. It is found that the proposed sensor can quantify the glycerol purity up to the minimum specified adulteration level of 2 and 1% corresponding to toxic contaminants diethylene glycol and ethylene glycol, respectively, and the glucose concentration of 0.5 mg/ml.

Abnormal Ca homeostasis has been associated with impaired glucose metabolism. However, the epidemiological evidence is controversial. We aimed to assess the association between circulating Ca levels and the risk of type 2 diabetes mellitus (T2DM) or abnormal glucose homeostasis through conducting a systematic review and meta-analysis. Eligible studies were identified by searching electronic database (PubMed, Embase and Google Scholar) and related references with de novo results from primary studies up to December 2018. A random-effects meta-analysis was performed to estimate the weighted relative risks (RR) and 95 % CI for the associations. The search yielded twenty eligible publications with eight cohort studies identified for the meta-analysis, which included a total of 89 165 participants. Comparing the highest with the lowest category of albumin-adjusted serum Ca, the pooled RR was 1·14 (95 % CI 1·05, 1·24) for T2DM (n 51 489). Similarly, serum total Ca was associated with incident T2DM (RR 1·25; 95 % CI 1·10, 1·42) (n 64 502). Additionally, the adjusted RR for 1 mg/dl increments in albumin-adjusted serum Ca or serum total Ca levels was 1·16 (95 % CI 1·07, 1·27) and 1·19 (95 % CI 1·11, 1·28), respectively. The observed associations remained with the inclusion of a cohort study with ionised Ca as the exposure. However, data pooled from neither case–control (n 4) nor cross-sectional (n 8) studies manifested a significant correlation between circulating Ca and glucose homeostasis. In conclusion, accumulated data from the cohort studies suggest that higher circulating Ca levels are associated with an augmented risk of T2DM.

Chronic low-grade inflammation has been observed in major depression and other major psychiatric disorders and has been implicated in metabolic changes that are commonly associated with these disorders. This raises the possibility that the effects of dysfunctional metabolism may facilitate changes in neuronal structure and function which contribute to neuroprogression. Such changes may have implications for the progress from major depression to dementia in the elderly patient. The purpose of this review is to examine the contribution of inflammation and hypercortisolaemia, which are frequently associated with major depression, to neurodegeneration and how they detrimentally impact on brain energy metabolism. A key factor in these adverse events is insulin insensitivity caused by pro-inflammatory cytokines in association with desensitised glucocorticoid receptors. Identifying the possible metabolic changes initiated by inflammation opens new targets to ameliorate the adverse metabolic changes. This has resulted in the identification of dietary and drug targets which are of interest in the development of a new generation of psychotropic drugs.

Consuming whey protein before a meal may reduce postprandial glucose excursions, however, optimising timing of supplementation is important to improve its clinical utility. A total of thirteen centrally obese, insulin-resistant males (waist circumference: 121 (sem 3) cm; homeostasis model assessment for insulin resistance (HOMA-IR): 6·4 (sem 1·2)) completed four experimental conditions in a single-blind, crossover design. Participants consumed mixed-macronutrient breakfast and lunch meals on all occasions, with 20 g whey protein consumed 15 min before (PRE), alongside (DUR) or 15 min post-breakfast (POST) or omitted (CON). Capillary glucose and plasma concentrations of insulin, TAG and NEFA, in addition to subjective appetite ratings, were collected for 180 min after each meal. PRE and DUR reduced post-breakfast glucose peak by 17·0 (sem 1·9) % (P<0·001) and 9·2 (sem 2·9) % (P=0·046), respectively, compared with CON. Post-breakfast glucose AUC was lower following PRE compared with POST and CON (PRE: 982 (sem 30) v. POST: 1031 (sem 36) and CON: 1065 (sem 37) mmol/l×180 min; P≤0·042) but similar to DUR (1013 (sem 32) mmol/l×180 min; P=0·77). Insulin was lower during PRE, when compared with POST and DUR (both P≤0·042) but similar to CON. There were no between-condition differences in measures of postprandial lipaemia or appetite, and no effect of condition post-lunch. Consumption of whey protein as a preload or alongside a mixed-macronutrient breakfast reduces postprandial glucose excursions in centrally obese, insulin-resistant males. Whey consumed as a preload has superior glycaemic-lowering effects. Supplementation at breakfast does not alter glycaemic responses to subsequent meals.

The present paper reviews the physiological responses of human liver carbohydrate metabolism to physical activity and ingestion of dietary sugars. The liver represents a central link in human carbohydrate metabolism and a mechanistic crux point for the effects of dietary sugars on athletic performance and metabolic health. As a corollary, knowledge regarding physiological responses to sugar ingestion has potential application to either improve endurance performance in athletes, or target metabolic diseases in people who are overweight, obese and/or sedentary. For example, exercise increases whole-body glycogen utilisation, and the breakdown of liver glycogen to maintain blood glucose concentrations becomes increasingly important as exercise intensity increases. Accordingly, prolonged exercise at moderate-to-high exercise intensity results in depletion of liver glycogen stores unless carbohydrate is ingested during exercise. The exercise-induced glycogen deficit can increase insulin sensitivity and blood glucose control, and may result in less hepatic lipid synthesis. Therefore, the induction and maintenance of a glycogen deficit with exercise could be a specific target to improve metabolic health and could be achieved by carbohydrate (sugar) restriction before, during and/or after exercise. Conversely, for athletes, maintaining and restoring these glycogen stores is a priority when competing in events requiring repeated exertion with limited recovery. With this in mind, evidence consistently demonstrates that fructose-containing sugars accelerate post-exercise liver glycogen repletion and could reduce recovery time by as much as half that seen with ingestion of glucose (polymers)-only. Therefore, athletes aiming for rapid recovery in multi-stage events should consider ingesting fructose-containing sugars to accelerate recovery.

The hypothesis of the study was that inhibition of PPARβ/δ increases glucose uptake and lactose synthesis in bovine mammary epithelial cells by reducing the expression of the glucose transporter mRNA destabiliser calreticulin. Three experiments were conducted to test the hypothesis using immortalised bovine mammary alveolar (MACT) and primary bovine mammary (PBMC) cells. In Experiment 1, the most effective dose to inhibit PPARβ/δ activity among two synthetic antagonists (GSK-3787 and PT-s58) was assessed using a gene reporter assay. In Experiment 2, the effect on glucose uptake and lactose synthesis was evaluated by measuring glucose and lactose in the media and expression of related key genes upon modulation of PPARβ/δ using GSK-3787, the synthetic PPARβ/δ agonist GW-501516, or a combination of the two in cells cultivated in plastic. In Experiment 3, the same treatments were applied to cells cultivated in Matrigel and glucose and lactose in media were measured. In Experiment 1 it was determined that a significant inhibition of PPARβ/δ in the presence or absence of fetal bovine serum was achieved with ≥ 1000 nm GSK-3787 but no significant inhibition was observed with PT-s58. In Experiment 2, inhibition of PPARβ/δ had no effect on glucose uptake and lactose synthesis but they were both increased by GW-501516 in PBMC. The mRNA abundance of PPARβ/δ target gene pyruvate dehydrogenase kinase 4 was increased but transcription of calreticulin was decreased (only in MACT cells) by GW-501516. Treatment with GSK-3787 did not affect the transcription of measured genes. No effects on glucose uptake or lactose synthesis were detected by modulation of PPARβ/δ activity on cells cultivated in Matrigel. The above data do not provide support for the original hypothesis and suggest that PPARβ/δ does not play a major role in glucose uptake and lactose synthesis in bovine mammary epithelial cells.

Ubiquinone is a lipid antioxidant, and a novel liquid ubiquinol (a hydro-soluble, reduced form of coenzyme Q10) supplement was recently developed. The purpose of this study was to examine the levels of glucose, lipids and antioxidant capacity of type 2 diabetes patients after liquid ubiquinol supplementation. This study was designed as a randomised, double-blind, placebo-controlled trial. In all, fifty participants were randomly assigned to a placebo (n 25) or liquid ubiquinol (100 mg/d, n 25) group, and the intervention lasted for 12 weeks. Plasma coenzyme Q10, glucose homoeostasis parameters, lipid profiles, oxidative stress and antioxidative enzyme activities were measured during the study. After 12 weeks of supplementation, glyco Hb (HbA1c) value was significantly decreased in the liquid ubiquinol group (P=0·03), and subjects in the liquid ubiquinol group had significantly lower anti-glycaemic medication effect scores (MES) compared with those in the placebo group (P=0·03). The catalase (P<0·01) and glutathione peroxidase (P=0·03) activities were increased significantly after supplementation. Plasma coenzyme Q10 was correlated with the insulin level (P=0·05), homoeostatic model assessment-insulin resistance (P=0·07), quantitative insulin sensitivity check index (P=0·03) and the anti-hyperglycaemic agents’ MES (P=0·03) after supplementation. Lipid profiles did not change after supplementation; however, the subjects in the placebo group had a significantly lower level of HDL-cholesterol after 12 weeks of intervention. In conclusion, oral intake of 100 mg/d liquid ubiquinol might benefit type 2 diabetes patients by increasing antioxidant enzyme activity levels, reducing HbA1c levels and maintaining HDL-cholesterol levels.

A low-glycaemic-index (GI) breakfast has been shown to lower blood glucose levels throughout the day. A wide variety of breakfast foods are consumed, but their GI values are largely unknown, hence limiting consumers’ ability to select healthier options. This study investigated the GI values of ten common breakfast (five Asian and five Western) foods in this region using a randomised, cross-over study design. Participants arrived after an overnight fast, and fasting blood sample was taken before participants consumed test foods. Next, blood samples were taken at fixed intervals for 180 min. Glycaemic and insulinaemic responses to test foods were calculated as incremental AUC over 120 min, which were subsequently reported as glycaemic and insulinaemic indices. In all, nineteen healthy men (nine Chinese and ten Indians) aged 24·7 (sem 0·4) years with a BMI of 21·7 (sem 0·4) kg/m2 completed the study. Asian breakfast foods were of medium (white bun filled with red bean paste=58 (sem 4); Chinese steamed white bun=58 (sem 3)) to high GI (rice idli=85 (sem 4); rice dosa=76 (sem 5); upma=71 (sem 6)), whereas Western breakfast foods were all of low GI (whole-grain biscuit=54 (sem 5); whole-grain biscuit filled with peanut butter=44 (sem 3); whole-grain oat muesli=55 (sem 4); whole-grain oat protein granola=51 (sem 4); whole-grain protein cereal=49 (sem 3)). The GI of test foods negatively correlated with protein (r s −0·366), fat (r s −0·268) and dietary fibre (r s −0·422) (all P<0·001). GI values from this study contribute to the worldwide GI database, and may assist healthcare professionals in recommending low-GI breakfast to assist in lower daily glycaemia among Asians who are susceptible to type 2 diabetes mellitus.

There is much epidemiological evidence suggesting a reduced risk of development of type 2 diabetes (T2D) in habitual coffee drinkers, however to date there have been few longer-term interventions, directly examining the effects of coffee intake on glucose and lipid metabolism. Previous studies may be confounded by inter-individual variation in caffeine metabolism. Specifically, the rs762551 SNP in the CYP1A2 gene has been demonstrated to influence caffeine metabolism, with carriers of the C allele considered to be of a ‘slow’ metaboliser phenotype. This study investigated the effects of regular coffee intake on markers of glucose and lipid metabolism in coffee-naïve individuals, with novel analysis by rs762551 genotype. Participants were randomised to either a coffee group (n 19) who consumed four cups/d instant coffee for 12 weeks or a control group (n 8) who remained coffee/caffeine free. Venous blood samples were taken pre- and post-intervention. Primary analysis revealed no significant differences between groups. Analysis of the coffee group by genotype revealed several differences. Before coffee intake, the AC genotype (‘slow’ caffeine metabolisers, n 9) displayed higher baseline glucose and NEFA than the AA genotype (‘fast’ caffeine metabolisers, n 10, P<0·05). Post-intervention, reduced postprandial glycaemia and reduced NEFA suppression were observed in the AC genotype, with the opposite result observed in the AA genotype (P<0·05). These observed differences between genotypes warrant further investigation and indicate there may be no one-size-fits-all recommendation with regard to coffee drinking and T2D risk.

Marine n-3 (omega-3) fatty acids alter gene expression by regulating the activity of transcription factors. Krill oil is a source of marine n-3 fatty acids that has been shown to modulate gene expression in animal studies; however, the effect in humans is not known. Hence, we aimed to compare the effect of intake of krill oil, lean and fatty fish with a similar content of n-3 fatty acids, and high-oleic sunflower oil (HOSO) with added astaxanthin on the expression of genes involved in glucose and lipid metabolism and inflammation in peripheral blood mononuclear cells (PBMC) as well as circulating inflammatory markers. In an 8-week trial, healthy men and women aged 18–70 years with fasting TAG of 1·3–4·0 mmol/l were randomised to receive krill oil capsules (n 12), HOSO capsules (n 12) or lean and fatty fish (n 12). The weekly intakes of marine n-3 fatty acids from the interventions were 4654, 0 and 4103 mg, respectively. The mRNA expression of four genes, PPAR γ coactivator 1A (PPARGC1A), steaoryl-CoA desaturase (SCD), ATP binding cassette A1 (ABCA1) and cluster of differentiation 40 (CD40), were differently altered by the interventions. Furthermore, within-group analyses revealed that krill oil down-regulated the mRNA expression of thirteen genes, including genes involved in glucose and cholesterol metabolism and β-oxidation. Fish altered the mRNA expression of four genes and HOSO down-regulated sixteen genes, including several inflammation-related genes. There were no differences between the groups in circulating inflammatory markers after the intervention. In conclusion, the intake of krill oil and HOSO with added astaxanthin alter the PBMC mRNA expression of more genes than the intake of fish.

Epidemiological studies have found coffee consumption is associated with a lower risk for type 2 diabetes mellitus, but the underlying mechanisms remain unclear. Thus, the aim of this randomised, cross-over single-blind study was to investigate the effects of regular coffee, regular coffee with sugar and decaffeinated coffee consumption on glucose metabolism and incretin hormones. Seventeen healthy men participated in five trials each, during which they consumed coffee (decaffeinated, regular (containing caffeine) or regular with sugar) or water (with or without sugar). After 1 h of each intervention, they received an oral glucose tolerance test with one intravenous dose of [1-13C]glucose. The Oral Dose Intravenous Label Experiment was applied and glucose and insulin levels were interpreted using a stable isotope two-compartment minimal model. A mixed-model procedure (PROC MIXED), with subject as random effect and time as repeated measure, was used to compare the effects of the beverages on glucose metabolism and incretin parameters (glucose-dependent insulinotropic peptide (GIP)) and glucagon-like peptide-1 (GLP-1)). Insulin sensitivity was higher with decaffeinated coffee than with water (P<0·05). Regular coffee with sugar did not significantly affect glucose, insulin, C-peptide and incretin hormones, compared with water with sugar. Glucose, insulin, C-peptide, GLP-1 and GIP levels were not statistically different after regular and decaffeinated coffee compared with water. Our findings demonstrated that the consumption of decaffeinated coffee improves insulin sensitivity without changing incretin hormones levels. There was no short-term adverse effect on glucose homoeostasis, after an oral glucose challenge, attributable to the consumption of regular coffee with sugar.

The intermittent energy restriction (IER) approach to weight loss involves short periods of substantial (>70 %) energy restriction (ER) interspersed with normal eating. Studies to date comparing IER to continuous energy restriction (CER) have predominantly measured fasting indices of cardiometabolic risk. This study aimed to compare the effects of IER and CER on postprandial glucose and lipid metabolism following matched weight loss. In all, twenty-seven (thirteen male) overweight/obese participants (46 (sem 3) years, 30·1 (sem 1·0) kg/m2) who were randomised to either an IER intervention (2638 kJ for 2 d/week with an overall ER of 22 (sem 0·3) %, n 15) or a CER intervention (2510 kJ below requirements with overall ER of 23 (sem 0·8) %) completed the study. Postprandial responses to a test meal (over 360 min) and changes in anthropometry (fat mass, fat-free mass, circumferences) were assessed at baseline and upon attainment of 5 % weight loss, following a 7-d period of weight stabilisation. The study found no statistically significant difference in the time to attain a 5 % weight loss between groups (median 59 d (interquartile range (IQR) 41–80) and 73 d (IQR 48–128), respectively, P=0·246), or in body composition (P≥0·437). For postprandial measures, neither diet significantly altered glycaemia (P=0·266), whereas insulinaemia was reduced comparatively (P=0·903). The reduction in C-peptide tended (P=0·057) to be greater following IER (309 128 (sem23 268) to 247781 (sem20 709) pmol×360 min/l) v. CER (297 204 (sem25 112) to 301 655 (sem32 714) pmol×360 min/l). The relative reduction in TAG responses was greater (P=0·045) following IER (106 (sem30) to 68 (sem 15) mmol×360 min/l) compared with CER (117 (sem 43) to 130 (sem 31) mmol×360 min/l). In conclusion, these preliminary findings highlight underlying differences between IER and CER, including a superiority of IER in reducing postprandial lipaemia, which now warrant targeted mechanistic evaluation within larger study cohorts.

Previous studies show associations between dairy product consumption and type 2 diabetes, but only a few studies conducted detailed analyses for a variety of dairy subgroups. Therefore, we examined cross-sectional associations of a broad variety of dairy subgroups with pre-diabetes and newly diagnosed type 2 diabetes (ND-T2DM) among Dutch adults. In total, 112 086 adults without diabetes completed a semi-quantitative FFQ and donated blood. Pre-diabetes was defined as fasting plasma glucose (FPG) between 5·6 and 6·9 mmol/l or HbA1c% of 5·7–6·4 %. ND-T2DM was defined as FPG ≥7·0 mmol/l or HbA1c ≥6·5 %. Logistic regression analyses were conducted by 100 g or serving increase and dairy tertiles (T1ref), while adjusting for demographic, lifestyle and dietary covariates. Median dairy product intake was 324 (interquartile range 227) g/d; 25 549 (23 %) participants had pre-diabetes; and 1305 (1 %) had ND-T2DM. After full adjustment, inverse associations were observed of skimmed dairy (OR100 g 0·98; 95 % CI 0·97, 1·00), fermented dairy (OR100 g 0·98; 95 % CI 0·97, 0·99) and buttermilk (OR150 g 0·97; 95 % CI 0·94, 1·00) with pre-diabetes. Positive associations were observed for full-fat dairy (OR100 g 1·003; 95 % CI 1·01, 1·06), non-fermented dairy products (OR100 g 1·01; 95 % CI 1·00, 1·02) and custard (ORserving/150 g 1·13; 95 % CI 1·03, 1·24) with pre-diabetes. Moreover, full-fat dairy products (ORT3 1·16; 95 % CI 0·99, 1·35), non-fermented dairy products (OR100 g 1·05; 95 % CI 1·01, 1·09) and milk (ORserving/150 g 1·08; 95 % CI 1·02, 1·15) were positively associated with ND-T2DM. In conclusion, our data showed inverse associations of skimmed and fermented dairy products with pre-diabetes. Positive associations were observed for full-fat and non-fermented dairy products with pre-diabetes and ND-T2DM.

Eggs attenuate postprandial hyperglycaemia (PPH), which transiently impairs vascular endothelial function (VEF). We hypothesised that co-ingestion of a glucose challenge with egg-based meals would protect against glucose-induced impairments in VEF by attenuating PPH and oxidative stress. A randomised, cross-over study was conducted in prediabetic men (n 20) who ingested isoenegertic meals (1674 kJ (400 kcal)) containing 100 g glucose (GLU), or 75 g glucose with 1·5 whole eggs (EGG), seven egg whites (WHITE) or two egg yolks (YOLK). At 30 min intervals for 3 h, brachial artery flow-mediated dilation (FMD), plasma glucose, insulin, cholecystokinin (CCK), lipids (total, LDL- and HDL-cholesterol; TAG), F2-isoprostanes normalised to arachidonic acid (F2-IsoPs/AA), and methylglyoxal were assessed. In GLU, FMD decreased at 30–60 min and returned to baseline levels by 90 min. GLU-mediated decreases in FMD were attenuated at 30–60 min in EGG and WHITE. Compared with GLU, FMDAUC was higher in EGG and WHITE only. Relative to baseline, glucose increased at 30–120 min in GLU and YOLK but only at 30–90 min in EGG and WHITE. GlucoseAUC and insulinAUC were also lower in EGG and WHITE only. However, CCKAUC was higher in EGG and WHITE compared with GLU. Compared with GLU, F2-IsoPs/AAAUC was lower in EGG and WHITE but unaffected by YOLK. Postprandial lipids and methylglyoxal did not differ between treatments. Thus, replacing a portion of a glucose challenge with whole eggs or egg whites, but not yolks, limits postprandial impairments in VEF by attenuating increases in glycaemia and lipid peroxidation.

Hypoglycaemia is a well-known side effect of Propranolol. We described the case of a child presenting severe and recurrent Propranolol-induced hypoglycaemia. Those episodes were not related to prolonged fasting and were associated with only mild ketosis. Thus, therapy with β blockers may not only aggravate classical ketotic hypoglycaemia but also interfere with glucose metabolism.