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The current review examines the totality of the evidence to determine if there exists a relationship between β-glucan and body weight and adiposity and whether such a relationship is a consistent, causal and plausible one. Observational studies suggest an association between oat (i.e., β-glucan) intake and reduced body weight, waist circumference and adiposity. High and moderate quality randomized controlled trials that were specifically designed to evaluate the efficacy of β-glucan on anthropometric outcomes were given the highest weight. Several of these studies indicated a causal relationship between β-glucan consumption and reduction in body weight, BMi, and at least one measure of body fat within diets that were not calorie-restricted. A review of additional animal and human evidence suggests multiple plausible mechanisms by which β-glucan may impact satiety perception, gastric emptying, gut hormones, gut microbiota and short chain fatty acids in the complex interplay of appetite and energy regulation. [ABSTRACT FROM AUTHOR]

The APOE4 allele of apolipoprotein E (apoE) is the greatest genetic risk factor for Alzheimer's disease (AD) compared to APOE2 and APOE3. Amyloid-β (Aβ), particularly in a soluble oligomeric form (oAβ), is considered a proximal cause of neurodegeneration in AD. Emerging data indicate that levels of soluble oAβ are increased with APOE4, providing a potential mechanism of APOE4-induced AD risk. However, the pathway(s) by which apoE4 may increase oAβ levels are unclear and the subject of continued inquiry. In this editorial review, we present the hypothesis that apoE isoform-specific interactions with Aβ, namely apoE/Aβ complex, modulate Aβ levels. Specifically, we propose that compared to apoE3, apoE4-containing lipoproteins are less lipidated, leading to less stable apoE4/Aβ complexes, resulting in reduced apoE4/Aβ levels and increased accumulation, particularly of oAβ. Evidence that support or counter this argument, as well as the therapeutic significance of this pathway to neurodegeneration, are discussed. [ABSTRACT FROM AUTHOR]

The human diet contains &bgr;-carotene as the most abundant precursor of vitamin A, an essential nutrient for embryogenesis. Our laboratory previously showed the importance of&bgr;-carotene metabolism via &bgr;-carotene-15,15'-oxygenase (CMOI) to support mouse embryonic development. However, the mechanisms regulating embryonic acquisition and utilization of &bgr;-carotene from the maternal circulation via placenta remain unknown. We used wild-type (WT) and Lrat-/- Rbp-/- (L-/-R-/-) mice, the latter being a model of marginal vitamin A deficiency. Pregnant dams, fed a nonpurlfled diet sufficient In vitamin A throughout life, were i.p. supplemented with &bgr;-carotene or vehicle at 13.5 d postcoitum (dpc). Effects of this acute maternal supplementation on retinoid and &bgr;-carotene metabolism in maternal (serum, liver) and developing tissues (placenta, yolk sac, embryo) were investigated at 14.5 dpc. We showed that, upon supplementation, placental &bgr;-carotene concentrations were greater in L-/-R-/- than in WT mice. However, the retinoid (retlnol and retinyl ester) concentrations remained unchanged in placenta (and in all other tissues analyzed) of both genotypes upon &bgr;-carotene administration. We also showed that upon a single i.p. &bgr;-carotene supplementation, placental LDL receptor-related protein (Lrp1) mRNA expression was lower in WT mice, and embryonic CmolmRNA expression was greater In L-/-R-/- mice. Together, these data suggest a potential role of LRP1 in mediating the uptake of&bgr;-carotene across the placenta and that even a marginally impaired maternal vitamin A status may influence uptake and utilization of &bgr;-carotene by the placenta and the embryo. [ABSTRACT FROM AUTHOR]