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Background: Foods that enhance satiety can help consumers to resist environmental cues to eat and help adherence to calorie restriction. The objective of this study was to compare the effect of 2 oat-based breakfast cereals on appetite, satiety, and food intake.Methods: Forty-eight healthy individuals, 18 years of age or older, were enrolled in a randomized, crossover trial. Subjects consumed isocaloric servings of either oatmeal or an oat-based ready-to-eat breakfast cereal (RTEC) in random order at least a week apart. Visual analogue scales measuring appetite and satiety were completed before breakfast and throughout the morning. Lunch was served 4 hours after breakfast. The physicochemical properties of oat soluble fiber (β-glucan) were determined. Appetite and satiety responses were analyzed by area under the curve. Food intake and β-glucan properties were analyzed using t tests.Results: Oatmeal increased fullness (p = 0.001) and reduced hunger (p = 0.005), desire to eat (p = 0.001), and prospective intake (p = 0.006) more than the RTEC. Energy intake at lunch was lower after eating oatmeal compared to the RTEC (p = 0.012). Oatmeal had higher viscosity (p = 0.03), β-glucan content, molecular weight (p < 0.001), and radius of gyration (p < 0.001) than the RTEC.Conclusions: Oatmeal suppresses appetite, increases satiety, and reduces energy intake compared to the RTEC. The physicochemical properties of β-glucan and sufficient hydration of oats are important factors affecting satiety and subsequent energy intake. [ABSTRACT FROM AUTHOR]

Abstract: Alzheimer’s disease (AD), a chronic neurodegenerative disorder associated with the abnormal accumulations of amyloid β (Aβ) peptide and oxidative stress in the brain, is the most common form of dementia among the elderly. Crude caffeine (CC), a major by-product of the decaffeination of coffee, has potent hydrophilic antioxidant activity and may reduce inflammatory processes. Here, we showed that CC and pure caffeine intake had beneficial effects in a mouse model of AD. Administration of CC or pure caffeine for 2months partially prevented memory impairment in AD mice, with CC having greater effects than pure caffeine. Furthermore, consumption of CC, but not pure caffeine, reduced the Aβ1–42 levels and the number of amyloid plaques in the hippocampus. Moreover, CC and caffeine protected primary neurons from Aβ-induced cell death and suppressed Aβ-induced caspase-3 activity. Our data indicate that CC may contain prophylactic agents against the cell death and the memory impairment in AD. [Copyright &y& Elsevier]

The supercritical CO2-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, Kmix 405 nm, of 0.02. Membrane dialysis (molecular weight cut-off, 12 to 14 kDa) increased the Kmix 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 IC50= 499 μg/mL, more potent than that of regular-roast coffee (IC50= 766 μg/mL). Our results indicate that melanoidins form during the supercritical CO2-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. [ABSTRACT FROM AUTHOR]

Research on the health impacts of coffee has escalated. However, few studies were devoted to understanding the potential impact of mechanical processing on coffee's chemistry and subsequent health implications. Coffee flaking is a commonly used process to improve extractability and aroma characteristics. In this study, we studied the biochemical activity, chemical composition, and microstructure of coffee before and after flaking. We found that flaked coffee extract had 3.3-fold higher activity in inhibiting nuclear factor-kappa B (NF-κB) activation than regular coffee extract. Interestingly, flaking did not significantly alter the amount of coffee phenolics. It increased coffee melanoidin, by 2.1-fold, which likely contributed to the observed higher activity in inhibiting NF-κB activation. Flaking crushed cell walls revealed by microscopy might possibly result in disruption of polysaccharide entanglement and release of high-molecular-weight compounds, such as melanoidins. Consequently, the increased melanoidin content in the brew resulted in the increased inhibition of NF-κB activation. Small molecules, like coffee phenolics, are readily soluble in water during coffee brewing even without flaking, suggesting that flaking has no effect on its extractability. In summary, our investigation revealed that flaking enhanced NF-κB inhibition activity, possibly through the release of melanoidins from crushed cell microstructures.