Milk protein digestion and the gut microbiome influence gastrointestinal discomfort after cow milk consumption in healthy subjects.

Many healthy people suffer from milk-related gastrointestinal discomfort (GID) despite not being lactose intolerant; the mechanisms underpinning such condition are unknown. This study aimed to explore milk protein digestion and related physiological responses (primary outcome), gut microbiome and gut permeability in 19 lactose-tolerant healthy nonhabitual milk consumers [NHMCs] reporting GID after consuming cow milk compared to 20 habitual milk consumers [HMCs] without GID. NHMCs and HMCs participated in a milk-load (250 mL) test, underwent blood sample collection at 6 time points over 6 h after milk consumption and collected urine samples and GID self-reports over 24 h. We measured the concentrations of 31 milk-derived bioactive peptides (BAPs), 20 amino acids, 4 hormones, 5 endocannabinoid system mediators, glucose and the dipeptidyl peptidase-IV (DPPIV) activity in blood and indoxyl sulfate in urine samples. Subjects also participated in a gut permeability test and delivered feces sample for gut microbiome analysis. Results showed that, compared to HMCs, milk consumption in NHMCs, along with GID, elicited a slower and lower increase in circulating BAPs, lower responses of ghrelin, insulin, and anandamide, a higher glucose response and serum DPPIV activity. The gut permeability of the two groups was similar, while the habitual diet, which was lower in dairy products and higher in the dietary-fibre-to-protein ratio in NHMCs, possibly shaped the gut microbiome; NHMCs exhibited lower abundance of Bifidobacteria, higher abundance of Prevotella and lower abundance of protease-coding genes, which may have reduced protein digestion, as evidenced by lower urinary excretion of indoxyl sulfate. In conclusion, the findings showed that a less efficient digestion of milk proteins, supported by a lower proteolytic capability of the gut microbiome, may explain GID in healthy people after milk consumption.

Human bioavailability of flavanols and phenolic acids from cocoa-nut creams enriched with free or microencapsulated cocoa polyphenols.

Human bioavailability of cocoa flavanols and phenolic acids from a cocoa-nut cream (CC) and from CC enriched with a 1·5 % (w/w) cocoa polyphenol extract in free form (FPC) or encapsulated with a gastric-resistant high-amylose maize starch (EPC), was studied. In a randomised cross-over protocol, with 1-week wash-out in between, twelve healthy volunteers had three portions/d of each cream, providing approximately 190 µmol/d of total flavanols and 12 µmol/d of total phenolic acids with CC and 385 and 28 µmol/d with both FPC and EPC, respectively. Blood, urine and faecal samples were analysed by HPLC/MS/MS. Serum (epi)catechin was absent at baseline and after CC consumption, while 22·1 (SEM 2·62) and 1·59 (SEM 0·22) nmol (P <0·05) were found after FPC and EPC, respectively. The EPC increased faecal excretion of total flavanols compared to FPC (151·0 (SEM 54·6) v. 28·0 (SEM 14·0) nmol; P <0·05). Within 6 h after consumption, serum phenolic acid content was 50-fold higher than (epi)catechin; no difference between CC and FPC was observed, but a significant reduction after EPC (1954 (SEM 236·3) and 1459 (SEM 137·6) v. 726·8 (SEM 73·4) nmol, P <0·05) was recorded. Short-term phenolic acid urinary excretions were significantly higher after FPC than CC and EPC, the values being 11·4 (SEM 5·1) v. 3·1 (SEM 1·7) and 0·9 (SEM 0·5) µmol, respectively. Faecal phenolic acids were approximately 60-fold reduced after FPC (8·1 (SEM 0·13) nmol) and EPC (14·7 (SEM 2·7) nmol) consumption compared to CC (641·4 (SEM 99·1) nmol) consumption. The data demonstrated that: (i) (epi)catechin was absorbed from CC; (ii) cocoa polyphenols' consumption increased circulating phenolic acids; and (iii) encapsulated ingredient increased flavanol delivering into the gut. Further studies should evaluate whether encapsulated cocoa polyphenols may be a functional prebiotic ingredient.

Curcumin bioavailability from enriched bread: the effect of microencapsulated ingredients.

Human bioavailability of curcumin from breads enriched with 1 g/portion of free curcumin (FCB), encapsulated curcumin (ECB), or encapsulated curcumin plus other polyphenols (ECBB) was evaluated. Parental and metabolized curcuminoids and phenolic acids were quantified by HPLC/MS/MS in blood, urine, and feces collected over 24 h. The concentrations of serum curcuminoids were always below 4 nmol/L and those of glucuronides 10-fold less. Encapsulation delayed and increased curcuminoid absorption as compared to the free ingredient. Serum and urinary concentrations of ferulic and vanillic acid were between 2- and 1000-fold higher than those of curcuminoids, with ECBB eliciting the highest amounts. Fecal curcuminoids were 6-fold more abundant after ECB than FCB, while phenolic acids after ECBB quadruplicated those after ECB. Curcuminoid encapsulation increased their bioavailability from enriched bread, probably preventing their biotransformation, with combined compounds slightly reducing this effect. Phenolic acids are the major metabolites of curcuminoids and may contribute to their biological properties.

Sugar and dietary fibre composition influence, by different hormonal response, the satiating capacity of a fruit-based and a ß-glucan-enriched beverage.

In this study the satiating capacity of three beverages containing 3 g barley ß-glucan, or 2.5 g dietary fibre (DF) from fruit, or without DF (control) was evaluated. Fourteen healthy volunteers were randomized to have isocaloric breakfasts including one of the beverages in different occasions. Appetite ratings over 3 h post-breakfast and energy intakes at ad libitum lunch, blood glucose, insulin, ghrelin, PYY, GLP-1, GIP, and PP concentrations, and 24 h food intake, were assessed. The bevaerages containing DF increased fullness and satiety over 3 h post-breakfast, but only the ß-glucan-enriched vs. the control significantly reduced energy intakes by 18% at lunch and 40% over the rest of the day. Blood ghrelin and PP responses were differently modulated by beverages. The fruit-based and the ß-glucan-enriched beverage suppressed by 8.9% and 8.1% ghrelin response over the 3 h and the first hour post-breakfast, respectively, while only the latter increased PP response by 34.6%, compared to the control. A sucrose-sweetened beverage providing 3 g barley ß-glucans can control food intake by modulating PP response and it can even reduce 24 h energy intake. Ghrelin suppression by fruit dietary fibre and mixed sugars was not sufficient to significantly reduce food intake compared to the control.