Prior exercise does not affect chylomicron particle number following a mixed meal of moderate fat content

BACKGROUND: A single session of exercise has been reported to reduce fasting and postprandial triacylglycerol concentrations on the subsequent day. It is possible that exercise also reduces chylomicron particle number, which may underlie the observed reduction in postprandial triacylglycerol concentration. In the present study we aimed to determine whether a single session of exercise reduces fasting and postprandial chylomicron particle number on the subsequent day. In a randomised crossover design eight lean and healthy male and female subjects attended two postprandial testing days. On the previous day the subjects either performed 90 minutes of moderate intensity exercise or did not perform any exercise. Fasting blood samples were then collected prior to ingestion of a moderate fat mixed meal (0.44 g fat, 0.94 g carbohydrate, 0.27 g protein/kg body weight), blood was then collected after 1 h, 2 h, 4 h, 6 h, and 8 h. RESULTS: The fasting and postprandial apolipoprotein B48 concentration (marker of chylomicron particle number) was not affected by prior exercise. However exercise reduced fasting triacylglycerol concentration by 16% (P < 0.05) and there was a trend towards a reduction in the total area under the postprandial triacylglycerol curve (23%; P = 0.053). However when corrected for baseline concentration postprandial triacylglycerol concentration was not affected by prior exercise. CONCLUSION: A single session of exercise of moderate intensity and 90 minutes duration reduces fasting triacylglycerol levels, however fasting and postprandial chylomicron particle number was unaffected. Furthermore it appears that previously observed reductions in postprandial triacylglycerol levels following exercise are only mediated following consumption of high, non-physiologically relevant doses of fat

Tailored, iterative, printed dietary feedback is as effective as group education in improving dietary behaviours: results from a randomised control trial in middle-aged adults with cardiovascular risk factors

<p>Abstract</p> <p>Background</p> <p>Tailored nutrition interventions have been shown to be more effective than non-tailored materials in changing dietary behaviours, particularly fat intake and fruit and vegetable intake. But further research examining efficacy of tailored nutrition education in comparison to other nutrition education methods and across a wider range of dietary behaviours is needed. The Stages to Healthy Eating Patterns Study (STEPs) was an intervention study, in middle-aged adults with cardiovascular risk factors, to examine the effectiveness of printed, tailored, iterative dietary feedback delivered by mail in improving short-term dietary behaviour in the areas of saturated fat, fruit, vegetable and grain and cereal intake.</p> <p>Methods</p> <p>STEPs was a 3-month randomised controlled trial with a pre and post-test design. There were three experimental conditions: 1) tailored, iterative, printed dietary feedback (TF) with three instalments mail-delivered over a 3-month period that were re-tailored to most recent assessment of dietary intake, intention to change and assessment of self-adequacy of dietary intake. Tailoring for dietary intake was performed on data from a validated 63-item combination FFQ designed for the purpose 2) small group nutrition education sessions (GE): consisting of two 90-minute dietitian-led small group nutrition education sessions and 3) and a wait-listed control (C) group who completed the dietary measures and socio-demographic questionnaires at baseline and 3-months later. Dietary outcome measures in the areas of saturated fat intake (g), and the intake of fruit (serves), vegetables (serves), grain and cereals as total and wholegrain (serves) were collected using 7-day estimated dietary records. Descriptive statistics, paired t-tests and general linear models adjusted for baseline dietary intake, age and gender were used to examine the effectiveness of different nutrition interventions.</p> <p>Results</p> <p>The TF group reported a significantly greater increase in fruit intake (0.3 serves/d P = 0.031) in comparison to GE and the C group. All three intervention groups showed a reduction in total saturated fat intake. GE also had a within-group increase in mean vegetable intake after 3 months, but this increase was not different from changes in the other groups.</p> <p>Conclusions</p> <p>In this study, printed, tailored, iterative dietary feedback was more effective than small group nutrition education in improving the short-term fruit intake behaviour, and as effective in improving saturated fat intake of middle-aged adults with cardiovascular risk factors. This showed that a low-level dietary intervention could achieve modest dietary behaviour changes that are of public health significance.</p

Amyloid-β colocalizes with apolipoprotein B in absorptive cells of the small intestine

Background: Amyloid-β is recognized as the major constituent of senile plaque found in subjects with Alzheimer's disease. However, there is increasing evidence that in a physiological context amyloid-β may serve as regulating apolipoprotein, primarily of the triglyceride enriched lipoproteins. To consider this hypothesis further, this study utilized an in vivo immunological approach to explore in lipogenic tissue whether amyloid-β colocalizes with nascent triglyceride-rich lipoproteins. Results: In murine absorptive epithelial cells of the small intestine, amyloid-β had remarkable colocalization with chylomicrons (Manders overlap coefficient = 0.73 ± 0.03 (SEM)), the latter identified as immunoreactive apolipoprotein B. A diet enriched in saturated fats doubled the abundance of both amyloid-β and apo B and increased the overlap coefficient of the two proteins (0.87 ± 0.02). However, there was no evidence that abundance of the two proteins was interdependent within the enterocytes (Pearson's Coefficient < 0.02 ± 0.03), or in plasma (Pearson's Coefficient < 0.01). Conclusion: The findings of this study are consistent with the possibility that amyloid-β is secreted by enterocytes as an apolipoprotein component of chylomicrons. However, secretion of amyloid-β appears to be independent of chylomicron biogenesis

Synergistic effects of high fat feeding and apolipoprotein E deletion on enterocytic amyloid-beta abundance

Background: Amyloid-β (Aβ), a key protein found in amyloid plaques of subjects with Alzheimer's disease is expressed in the absorptive epithelial cells of the small intestine. Ingestion of saturated fat significantly enhances enterocytic Aβ abundance whereas fasting abolishes expression. Apolipoprotein (apo) E has been shown to directly modulate Aβ biogenesis in liver and neuronal cells but it's effect in enterocytes is not known. In addition, apo E modulates villi length, which may indirectly modulate Aβ as a consequence of differences in lipid absorption. This study compared Aβ abundance and villi length in wild-type (WT) and apo E knockout (KO) mice maintained on either a low-fat or high-fat diet. Wild-type C57BL/6J and apo E KO mice were randomised for six-months to a diet containing either 4% (w/w) unsaturated fats, or chow comprising 16% saturated fats and 1% cholesterol. Quantitative immunohistochemistry was used to assess Aβ abundance in small intestinal enterocytes. Apo E KO mice given the low-fat diet had similar enterocytic Aβ abundance compared to WT controls. Results: The saturated fat diet substantially increased enterocytic Aβ in WT and in apo E KO mice, however the effect was greater in the latter. Villi height was significantly greater in apo E KO mice than for WT controls when given the low-fat diet. However, WT mice had comparable villi length to apo E KO when fed the saturated fat and cholesterol enriched diet. There was no effect of the high-fat diet on villi length in apo E KO mice. Conclusion: The findings of this study are consistent with the notion that lipid substrate availability modulates enterocytic Aβ. Apo E may influence enterocytic lipid availability by modulating absorptive capacity

Amyloid-β colocalizes with apolipoprotein B in absorptive cells of the small intestine

Abstract Background Amyloid-β is recognized as the major constituent of senile plaque found in subjects with Alzheimer's disease. However, there is increasing evidence that in a physiological context amyloid-β may serve as regulating apolipoprotein, primarily of the triglyceride enriched lipoproteins. To consider this hypothesis further, this study utilized an in vivo immunological approach to explore in lipogenic tissue whether amyloid-β colocalizes with nascent triglyceride-rich lipoproteins. Results In murine absorptive epithelial cells of the small intestine, amyloid-β had remarkable colocalization with chylomicrons (Manders overlap coefficient = 0.73 ± 0.03 (SEM)), the latter identified as immunoreactive apolipoprotein B. A diet enriched in saturated fats doubled the abundance of both amyloid-β and apo B and increased the overlap coefficient of the two proteins (0.87 ± 0.02). However, there was no evidence that abundance of the two proteins was interdependent within the enterocytes (Pearson's Coefficient Conclusion The findings of this study are consistent with the possibility that amyloid-β is secreted by enterocytes as an apolipoprotein component of chylomicrons. However, secretion of amyloid-β appears to be independent of chylomicron biogenesis.</p

Synergistic effects of high fat feeding and apolipoprotein E deletion on enterocytic amyloid-beta abundance

Abstract Background Amyloid-β (Aβ), a key protein found in amyloid plaques of subjects with Alzheimer's disease is expressed in the absorptive epithelial cells of the small intestine. Ingestion of saturated fat significantly enhances enterocytic Aβ abundance whereas fasting abolishes expression. Apolipoprotein (apo) E has been shown to directly modulate Aβ biogenesis in liver and neuronal cells but it's effect in enterocytes is not known. In addition, apo E modulates villi length, which may indirectly modulate Aβ as a consequence of differences in lipid absorption. This study compared Aβ abundance and villi length in wild-type (WT) and apo E knockout (KO) mice maintained on either a low-fat or high-fat diet. Wild-type C57BL/6J and apo E KO mice were randomised for six-months to a diet containing either 4% (w/w) unsaturated fats, or chow comprising 16% saturated fats and 1% cholesterol. Quantitative immunohistochemistry was used to assess Aβ abundance in small intestinal enterocytes. Apo E KO mice given the low-fat diet had similar enterocytic Aβ abundance compared to WT controls. Results The saturated fat diet substantially increased enterocytic Aβ in WT and in apo E KO mice, however the effect was greater in the latter. Villi height was significantly greater in apo E KO mice than for WT controls when given the low-fat diet. However, WT mice had comparable villi length to apo E KO when fed the saturated fat and cholesterol enriched diet. There was no effect of the high-fat diet on villi length in apo E KO mice. Conclusion The findings of this study are consistent with the notion that lipid substrate availability modulates enterocytic Aβ. Apo E may influence enterocytic lipid availability by modulating absorptive capacity.</p

Probucol prevents blood–brain barrier dysfunction and cognitive decline in mice maintained on pro-diabetic diet

© The Author(s) 2018. An emerging body of evidence consistently suggests that compromised blood–brain barrier integrity may be causally associated with cognitive decline induced by type-2 diabetes. Our previous studies demonstrated that selected anti-inflammatory/anti-oxidative agents can preserve the integrity of blood–brain barrier and prevent neuroinflammation in mouse models of dysfunctional blood–brain barrier. Therefore, we have tested whether the previously proven blood–brain barrier protective agent, probucol, can prevent blood–brain barrier breakdown and cognitive decline in a dietary-induced murine model of diabetic insulin resistance. After 6-month chronic ingestion of a diet high in fat and fructose, the mice became insulin resistant. The high-fat and high-fructose-fed mice showed significant cognitive decline assessed by Morris water maze, concomitant with significant elevations in cortical and hippocampal glial acidic fibrillary protein and Fluoro Jade-C staining, indicating heightened neuroinflammation and neurodegeneration, respectively. The integrity of blood–brain barrier in high-fat and high-fructose-fed mice was substantially compromised, and this showed a significant association with heightened neurodegeneration. Co-provision of probucol with high-fat and high-fructose diet completely prevented the cognitive decline and blood–brain barrier dysfunction. Similarly, metformin was able to restore the cognitive function in high-fat and high-fructose-fed mice, while its blood–brain barrier protective effects were modest. These data suggest that probucol may prevent cognitive decline induced by insulin resistance by preserving the integrity of blood–brain barrier, whereas metformin’s neuroprotective effects may be mediated through a separate pathway

Synergistic effects of high fat feeding and apolipoprotein E deletion on enterocytic amyloid-beta abundance-0

E as follows: (-) no granular coloration, (+) modest with 1–2 granules, (2+) moderate with 3–4 granules or (3+) high, containing larger intense granules. Data was collected for six mice per group, with a minimum of four tissue sections per mouse studied. A minimum of 200 cells per section were scored and statistical significance was determined by one-way ANOVA with post-hoc Bonferroni test. LF-WT and LF-APOE KO mice have significantly (p < 0.05) fewer cells which stained positive for Aβ compared to mice fed high fats (HF-WT and HF-APOE KO *a and *b respectively). Under high-fat feeding, apo E KO mice had significantly greater proportion of cells which expressed Aβ at higher intensity compared to high-fat fed WT mice (*c, p < 0.05). The inset micrograph shows high-magnification of enterocytes from groups corresponding to graphs below. Beta-amyloid colocalized within the perinuclear regions of the cell containing Golgi and ER within enterocytes from all groups. (Scale bar = 20 μm).<p><b>Copyright information:</b></p><p>Taken from "Synergistic effects of high fat feeding and apolipoprotein E deletion on enterocytic amyloid-beta abundance"</p><p>http://www.lipidworld.com/content/7/1/15</p><p>Lipids in Health and Disease 2008;7():15-15.</p><p>Published online 22 Apr 2008</p><p>PMCID:PMC2359747.</p><p></p