In mice, WGOs improved insulin sensitivity and plasma cholesterol profile compared with LBOs, and the effects were associated with the changes in cecal microbiota composition. Increasing WGO consumption may help improve insulin sensitivity and dyslipidemia in chronic diseases.

Dynamic interactions between lipid metabolism, gut permeability, and systemic inflammation remain unclear in the context of obesity. Milk polar lipids, lipids derived from the milk fat globule membrane, could positively affect the aforementioned obesity-related endpoints. This study aimed to test the hypotheses that milk polar lipids will reduce gut permeability, systemic inflammation, and liver lipid levels, and differentially affect the hepatic expression of genes associated with fatty acid synthesis and cholesterol regulation in preexisting obesity. We fed 3 groups of C57BL/6J ob/ob mice (n = 6 per group) for 2 wk: (1) a modified AIN-93G diet (CO) with 34% fat by energy; (2) CO with milk gangliosides (GG) at 0.2 g/kg of diet; and (3) CO with milk phospholipids (PL) at 10 g/kg of diet. The GG and PL were provided as semi-purified concentrates and replaced 2.0% and 7.2% of dietary fat by energy. The GG and PL did not affect total food intake, weight gain, fasting glucose, or gut permeability. The PL decreased liver mass and the mesenteric fat depot compared with the CO. The GG increased tight junction protein occludin in colon mucosa compared with the CO. The GG and PL decreased tight junction protein zonula occludens-1 in jejunum mucosa compared with the CO. Plasma endotoxin increased during the study but was unaffected by the treatments. Compared with the CO and GG, the PL increased plasma sphingomyelin and plasma IL-6. The GG and PL differentially regulated genes associated with lipid metabolism in the liver compared with the CO. Regarding general effects on lipid metabolism, the GG and PL decreased lipid levels in the liver and the mesenteric depot, and increased lipid levels in the plasma. Diet consumption decreased significantly when the ob/ob mice were kept in metabolic cages, which were not big enough and resulted in unwanted animal deaths. Future studies may keep this in mind and use better metabolic equipment for ob/ob mice. In conclusion, dietary milk polar lipids may have limited beneficial effects on gut barrier integrity, systemic inflammation, and lipid metabolism in the context of severe obesity.

The AIN-76A diet causes fatty liver in rodents when fed for long periods of time. The aim of this study was to utilize fatty acid analysis and transcriptomics to investigate the effects of different fat sources in the AIN-76A diet on tissue lipid profiles and gene expression in male, weanling Fischer-344 rats. Animals were fed isocaloric diets that differed only in the fat source: (1) corn oil (CO) (2) anhydrous milk fat (AMF), and (3) AMF supplemented with 10% phospholipids from the milk fat globule membrane (AMF-MFGM). There were no differences in food intake, body weight, growth rate, or body fat composition among the groups, and the fatty acid compositions of red blood cells (RBC), plasma, muscle, and visceral adipose tissues reflected the dietary fat sources. Modifying the fat source resulted in 293 genes differentially regulated in skeletal muscle, 1,124 in adipose, and 831 in liver as determined by analysis of variance (ANOVA). Although tissue fatty acid profiles mostly reflected the diet, there were several quantitative differences in lipid classes in the liver and plasma. The AMF diet resulted in the highest level of hepatic triacylglycerols, but the lowest level in plasma. The CO diet resulted in significant accumulation of hepatic unesterified fatty acids and decreased DGAT expression and activity, a potential trigger for steatohepatitis. These results indicate that the fatty acid composition and presence of polar lipids in the AIN-76A diets have significant effects on lipid partitioning, gene expression, and potentially the development of liver pathology.

Background Milk fat globule membrane (MFGM), natural to breast milk, is essential for neonatal development, but lacking from standard infant formulas. Objectives To evaluate the safety and tolerability of MFGM supplementation in formula for infants 0 to 12 months. Methods In a prospective, multicentre, double-blind, randomized trial, healthy term infants were randomized to a standard formula (SF, n = 104) or an MFGM-enriched formula (MF, n = 108) for 6 months and a corresponding follow-on formula until 12 months. Exclusively breast-fed infants (n = 206) were recruited as the reference group (BFR). Tolerance and safety events were recorded continuously. Anthropometric measurements were assessed at enrolment, 42 days and 4, 6, 8 and 12 months. Results Infants (n = 375) completed the study with average dropout of < 20%. Stool frequency, color, and consistency between SF and MF were not significantly different throughout, except the incidence of loose stools in MF at 6 months being lower than for SF (odds ratio 0.216, P < 0.05) and the frequency of green-colored stools at 12 months being higher in MF (CI 95%, odds ratio 8.92, P < 0.05). The BFR had a higher frequency of golden stools and lower rate of green stools (4–6 months) than the two formula-fed groups (P < 0.05). SF displayed more diarrhoea (4.8%) than MF (1%) and BFR (1%) at the 8-month visit (P < 0.05). BFR (0–1%) had significantly less (P < 0.05) lower respiratory infections than MF (4.6–6.5%) and SF (2.9–5.8%) at 6- and 8-months, respectively. Formula intake, frequency of spit-up/vomiting or poor sleep were similar between SF and MF. Growth rate (g/day) was similar at 4, 6, 8 and 12 months between the 3 groups, but growth rate for BFR was significantly higher than for SF and MF at 42 days (95% CI, P = 0.001). Conclusions MFGM-enriched formula was safe and well-tolerated in healthy term infants between 0 and 12 months, and total incidences of adverse events were similar to that for the SF group. A few differences in formula tolerance were observed, however these differences were not in any way related to poor growth.

Background Diet plays an important role in the pathogenesis of Alzheimer’s disease (AD). Dietary fatty acids that are not synthesized in humans may serve as tissue markers for intakes of those source foods. A growing body of evidence supports that erythrocyte pentadecanoic acid (15:0) is a potential biomarker for dairy intake. Objective To investigate the associations between dairy intakes, erythrocyte 15:0, and cognitive function among elderly participants in the Cache County Study on Memory, Health and Aging. Design Erythrocyte fatty acids were profiled as a percentage of total fatty acids for 1987 nondemented subjects. Cognitive function was assessed with an adapted Modified Mini‐Mental State examination (3MS). Food intakes were surveyed with a 142‐item food frequency questionnaire and were adjusted by total energy using the residual method. Spearman partial correlations adjusted for age, gender and BMI were examined for erythrocyte 15:0, intake of individual dairy product, and 3MS score. Multivariable linear regression models were fit on dairy intakes with erythrocyte 15:0 as the outcome controlling for potential confounding factors. Results Erythrocyte 15:0 was positively associated with dietary intakes of 1‐2% milk (r = 0.12, p < 0.001), whole milk (r = 0.28, p = 0.001), butter (r = 0.16, p < 0.001), and cheese besides Cottage/Ricotta or cream cheese (r = 0.12, p < 0.001) but was not associated with the intakes of skim/chocolate milk, (frozen) yogurt, ice cream, and Cottage/Ricotta/cream cheese. In multivariable regression models each increase in servings of whole milk, butter, 1‐2% milk, and cheese besides Cottage/Ricotta or cream cheese was associated with a 0.30, 0.16, 0.13, and 0.12 points increase on the erythrocyte 15:0 (p < 0.001 for all). Erythrocyte 15:0 was not correlated with 3MS score. Conclusion Erythrocyte pentadecanoic acid is a biomarker for the consumption of less modified dairy products and is not correlated with 3MS score in elderly adults living in Northern Utah. Grant Funding Source: Supported by Dairy Research Institute