Mechanism of action of pre-meal consumption of whey protein on glycemic control in young adults.

Whey protein (WP), when consumed in small amounts prior to a meal, improves post-meal glycemic control more than can be explained by insulin-dependent mechanisms alone. The objective of the study was to identify the mechanism of action of WP beyond insulin on the reduction of post-meal glycemia. In a randomized crossover study, healthy young men received preloads (300 ml) of WP (10 and 20 g), glucose (10 and 20 g) or water (control). Paracetamol (1.5 g) was added to the preloads to measure gastric emptying. Plasma concentrations of paracetamol, glucose, and ß-cell and gastrointestinal hormones were measured before preloads (baseline) and at intervals before (0-30 min) and after (50-230 min) a preset pizza meal (12 kcal/kg). Whey protein slowed pre-meal gastric emptying rate compared to the control and 10 g glucose (P<.0001), and induced lower pre-meal insulin and C-peptide than the glucose preloads (P<.0001). Glucose, but not WP, increased pre-meal plasma glucose concentrations (P<.0001). Both WP and glucose reduced post-meal glycemia (P=.0006) and resulted in similar CCK, amylin, ghrelin and GIP responses (P<.05). However, compared with glucose, WP resulted in higher post-meal GLP-1 and peptide tyrosine-tyrosine (PYY) and lower insulin concentrations, without altering insulin secretion and extraction rates. For the total duration of this study (0-230 min), WP resulted in lower mean plasma glucose, insulin and C-peptide, but higher GLP-1 and PYY concentrations than the glucose preloads. In conclusion, pre-meal consumption of WP lowers post-meal glycemia by both insulin-dependent and insulin-independent mechanisms.

Supercritical CO2 decaffeination of unroasted coffee beans produces melanoidins with distinct NF-κB inhibitory activity.

UNLABELLED: The supercritical CO(2)-decaffeination process causes unroasted coffee beans to turn brown. Therefore, we suspected that the decaffeinated beans contained melanoidins. Decaffeinated unroasted coffee extract absorbed light at 405 nm with a specific extinction coefficient, K(mix 405 nm), of 0.02. Membrane dialysis (molecular weight cut-off, 12 to 14 kDa) increased the K(mix 405 nm) value 15 fold. Gel filtration chromatography showed that the high-MW fraction (MW > 12 kDa) had an elution profile closer to that of melanoidins of medium-roast coffee than to the corresponding fraction of unroasted coffee, indicating the presence of melanoidins in decaffeinated unroasted beans. Using murine myoblast C2C12 cells with a stably transfected nuclear factor-κB (NF-κB) luciferase reporter gene, we found that the high-MW fraction of decaffeinated unroasted beans had an NF-κB inhibitory activity of IC(50) = 499 µg/mL, more potent than that of regular-roast coffee (IC(50) = 766 µg/mL). Our results indicate that melanoidins form during the supercritical CO(2)-decaffeination process and possess biological properties distinct from those formed during the regular roasting process. PRACTICAL APPLICATION: We discovered the roasting effect of decaffeination process, reporting the discovery of melanoidins in green (unroasted) decaf coffee beans. Our results indicated that melanoidins form during the supercritical CO2-decaffeination process and possess biological properties distinct from those formed during the regular roasting process. Our results offer new insights into the formation of bioactive coffee components during coffee decaffeination process.

Effect of premeal consumption of whey protein and its hydrolysate on food intake and postmeal glycemia and insulin responses in young adults.

BACKGROUND: Dairy protein ingestion before a meal reduces food intake and, when consumed with carbohydrate, reduces blood glucose. OBJECTIVE: The objective was to describe the effect of whey protein (WP) or its hydrolysate (WPH) when consumed before a meal on food intake, pre- and postmeal satiety, and concentrations of blood glucose and insulin in healthy young adults. DESIGN: Two randomized crossover studies were conducted. WP (10-40 g) in 300 mL water was provided in experiment 1, and WP (5-40 g) and WPH (10 g) in 300 mL water were provided in experiment 2. At 30 min after consumption, the subjects were fed an ad libitum pizza meal (experiment 1) or a preset pizza meal (12 kcal/kg, experiment 2). Satiety, blood glucose, and insulin were measured at baseline and at intervals both before and after the meals. RESULTS: In experiment 1, 20-40 g WP suppressed food intake (P < 0.0001) and 10-40 g WP reduced postmeal blood glucose concentrations and the area under the curve (AUC) (P < 0.05). In experiment 2, 10-40 g WP, but not WPH, reduced postmeal blood glucose AUC and insulin AUC in a dose-dependent manner (P < 0.05). The ratio of cumulative blood glucose to insulin AUCs (0-170 min) was reduced by > or =10 g WP but not by 10 g WPH. CONCLUSIONS: WP consumed before a meal reduces food intake, postmeal blood glucose and insulin, and the ratio of cumulative blood glucose to insulin AUCs in a dose-dependent manner. Intact WP, but not WPH, contributes to blood glucose control by both insulin-dependent and insulin-independent mechanisms. This trial was registered at clinicaltrials.gov as NCT00988377 and NCT00988182.

Roasted coffees high in lipophilic antioxidants and chlorogenic acid lactones are more neuroprotective than green coffees.

Oxidative stress is involved in many neurodegenerative processes leading to age-related cognitive decline. Coffee, a widely consumed beverage, is rich in many bioactive components, including polyphenols with antioxidant potential. In this study, regular and decaffeinated samples of both roasted and green coffee all showed high hydrophilic antioxidant activity in vitro, whereas lipophilic antioxidant activities were on average 30-fold higher in roasted than in green coffee samples. In primary neuronal cell culture, pretreatment with green and roasted coffees (regular and decaffeinated) protected against subsequent H(2)O(2)-induced oxidative stress and improved neuronal cell survival (green coffees increased neuron survival by 78%, compared to 203% by roasted coffees). All coffee extracts inhibited ERK1/2 activation, indicating a potential attenuating effect in stress-induced neuronal cell death. Interestingly, only roasted coffee extracts inhibited JNK activation, evidencing a distinctive neuroprotective benefit. Analysis of coffee phenolic compounds revealed that roasted coffees contained high levels of chlorogenic acid lactones (CGLs); a significant correlation between CGLs and neuroprotective efficacy was observed (R(2) = 0.98). In conclusion, this study showed that roasted coffees are high in lipophilic antioxidants and CGLs, can protect neuronal cells against oxidative stress, and may do so by modulation of the ERK1/2 and JNK signaling pathways.