Nutritional Support in Malnourished Outpatients with Chronic Obstructive Pulmonary Disease (COPD): A Randomized Controlled Pilot Study.

(1) Background: The evidence for nutritional support in COPD is almost entirely based on ready-to-drink oral nutritional supplements (ONSs). This study aimed to explore the effectiveness of powdered ONSs alongside individualized dietary counseling in the management of malnutrition. (2) Methods: Malnourished outpatients with COPD were randomized to receive either routine care (Group A: counseling + recommended to purchase powdered ONSs) or an enhanced intervention (Group B: counseling + provision of powdered ONSs at no cost to the patient) for 12 weeks. Outcomes of interest were nutritional intake, weight status, and quality of life. (3) Results: A total of 33 outpatients were included, categorized as follows: Group A (n = 21); Group B (n = 12); severely malnourished (n = 9), moderately malnourished (n = 24), mean BMI 18.0 SD 2.5 kg/m2. No differences were observed between groups at baseline or at week 12; however, analysis of the whole cohort (Group A + B) revealed nutrition intervention resulted in significant improvements in protein intake (+25.4 SD 53.4 g/d; p = 0.040), weight (+1.1 SD 2.6 kg; p = 0.032) and quality of life (-4.4 SD 10.0; p = 0.040). Only 41.2% of Group A and 58.3% of Group B reported consuming ONSs at week 12. Adherence to ONSs was associated with weight gain (+1.9 SD 2.5 kg vs. +0.4 SD 2.5 kg; p = 0.098). (4) Conclusions: Nutritional support results in significant improvements in nutrition status and quality of life in malnourished outpatients with COPD. However, improvements are associated with adherence to ONSs, suggesting the type of ONSs and how they are provided are important considerations in clinical practice and future studies.

Interaction between BMI and APOE genotype is associated with changes in the plasma long-chain-PUFA response to a fish-oil supplement in healthy participants.

BACKGROUND: Carriers of the apolipoprotein E ɛ4 (APOE4) allele are lower responders to a docosahexaenoic acid (DHA) supplement than are noncarriers. This effect could be exacerbated in overweight individuals because DHA metabolism changes according to body mass index (BMI; in kg/m²). OBJECTIVES: We evaluated the plasma fatty acid (FA) response to a DHA-rich supplement in APOE4 carriers and noncarriers consuming a high-saturated fat diet (HSF diet) and, in addition, evaluated whether being overweight changed this response. DESIGN: This study was part of the SATgenɛ trial. Forty-one APOE4 carriers and 41 noncarriers were prospectively recruited and consumed an HSF diet for 8-wk followed by 8 wk of consumption of an HSF diet with the addition of DHA and eicosapentaenoic acid (EPA) (HSF + DHA diet; 3.45 g DHA/d and 0.5 g EPA/d). Fasting plasma samples were collected at the end of each intervention diet. Plasma total lipids (TLs) were separated into free FAs, neutral lipids (NLs), and phospholipids by using solid-phase extraction, and FA profiles in each lipid class were quantified by using gas chromatography. RESULTS: Because the plasma FA response to the HSF + DHA diet was correlated with BMI in APOE4 carriers but not in noncarriers, the following 2 groups were formed according to the BMI median: low BMI (<25.5) and high BMI (≥25.5). In response to the HSF + DHA diet, there were significant BMI × genotype interactions for changes in plasma concentrations of arachidonic acid and DHA in phospholipids and TLs and of EPA in NLs and TLs (P ≤ 0.05). APOE4 carriers were lower plasma responders to the DHA supplement than were noncarriers but only in the high-BMI group. CONCLUSIONS: Our findings indicate that apolipoprotein E genotype and BMI may be important variables that determine the plasma long-chain PUFA response to dietary fat manipulation. APOE4 carriers with BMI ≥25.5 may need higher intakes of DHA for cardiovascular or other health benefits than do noncarriers.

Disrupted fatty acid distribution in HDL and LDL according to apolipoprotein E allele.

OBJECTIVES: Omega-3 polyunsaturated fatty acid (ω-3 PUFA) metabolism seems to be disrupted in carriers of the epsilon 4 allele of apolipoprotein E (E4+). The objective of this study was to investigate whether the ω-3 PUFA distribution in the high and low density lipoproteins is APOE-genotype dependant before and after supplementation with ω-3 PUFAs. METHODS: Eighty participants, aged between 20 and 35 y old were recruited and supplemented with 900 mg of eicosapentaenoic acid plus 680 mg of docosahexaenoic acid for 4 wk. Over the 4-wk intervention, blood samples were collected and HDL and LDL particles were obtained using sucrose gradient ultracentifugation. Fatty acid profiles of the HDL and LDL fractions were performed by gas chromatography. RESULTS: Baseline anthropometric characteristics of participants were not significantly different between the two APOE-groups (E4+, N = 10; E4-, N = 70). At baseline, in the LDL of E4+ subjects, the ω-6/ω-3 PUFA ratio was 17% higher than E4- subjects. At week 4, the ω-6/ω-3 PUFA ratio was significantly higher in the LDL of E4+ than E4- subjects. There was a significant genotype × time interaction for 16:0 in HDL and LDL and for 18:2 ω-6 in HDL. DHA in the HDL was positively correlated to HDL-C levels pre- and postsupplementation in E4- only. CONCLUSIONS: Contrary to what we anticipated, ω-3 PUFAs content? in HDL and LDL were not APOE isoform-dependant in young participants. However, young E4+ participants already had a tendency toward lower baseline-DHA levels in LDL particles as well as a more atherogenic ω-6/ω-3 PUFA ratio in LDL pre- and post-supplementation.

Apolipoprotein E isoforms disrupt long-chain fatty acid distribution in the plasma, the liver and the adipose tissue of mice.

Evidences suggest that omega-3 fatty acid (n-3 PUFA) metabolism is imbalanced in apolipoprotein E epsilon 4 isoform carriers (APOE4). This study aimed to investigate APOE genotype-dependant modulation of FA profiles, protein and enzyme important to fatty acid (FA) metabolism in the adipose tissue, the liver and the plasma using human APOE-targeted replacement mouse-model (N=37). FA transport (FATP) and binding (FABP) protein levels in tissues and concentrations of liver carnitine palmitoyltransferase 1 (CPT1) were performed. N-3 PUFA concentration was >45% lower in the adipose tissue and liver of APOE4 mice compared to APOE3 mice. In APOE4 mice, there were higher levels of FATP and FABP in the liver and higher FATP in the adipose tissue compared to APOE2 mice. There was a trend towards higher CPT1 concentrations in APOE4 mice compared to APOE3 mice. Therefore, since APOE-isoform differences were not always in line with the unbalanced n-3 PUFA profiles in organs, other proteins may be involved in maintaining n-3 PUFA homeostasis in mice with different APOE-isoforms.

Postprandial enrichment of triacylglycerol-rich lipoproteins with omega-3 fatty acids: lack of an interaction with apolipoprotein E genotype?

BACKGROUND: We have previously demonstrated that carrying the apolipoprotein (apo) E epsilon 4 (E4+) genotype disrupts omega-3 fatty acids (n - 3 PUFA) metabolism. Here we hypothesise that the postprandial clearance of n - 3 PUFA from the circulation is faster in E4+ compared to non-carriers (E4-). The objective of the study was to investigate the fasted and postprandial fatty acid (FA) profile of triacylglycerol-rich lipoprotein (TRL) fractions: Sf >400 (predominately chylomicron CM), Sf 60 - 400 (VLDL1), and Sf 20 - 60 (VLDL2) according to APOE genotype. METHODS: Postprandial TRL fractions were obtained in 11 E4+ (ϵ3/ϵ4) and 12 E4- (ϵ3/ϵ3) male from the SATgenϵ study following high saturated fat diet + 3.45 g/d of docosahexaenoic acid (DHA) for 8-wk. Blood samples were taken at fasting and 5-h after consuming a test-meal representative of the dietary intervention. FA were characterized by gas chromatography. RESULTS: At fasting, there was a 2-fold higher ratio of eicosapentaenoic acid (EPA) to arachidonic acid (P = 0.046) as well as a trend towards higher relative% of EPA (P = 0.063) in the Sf >400 fraction of E4+. Total n - 3 PUFA in the Sf 60 - 400 and Sf 20 - 60 fractions were not APOE genotype dependant. At 5 h, there was a trend towards a time × genotype interaction (P = 0.081) for EPA in the Sf >400 fraction. When sub-groups were form based on the level of EPA at baseline within the Sf >400 fraction, postprandial EPA (%) was significantly reduced only in the high-EPA group. EPA at baseline significantly predicted the postprandial response in EPA only in E4+ subjects (R2 = 0.816). CONCLUSION: Despite the DHA supplement contain very low levels of EPA, E4+ subjects with high EPA at fasting potentially have disrupted postprandial n - 3 PUFA metabolism after receiving a high-dose of DHA. TRIAL REGISTRATION: Registered at clinicaltrials.gov/show/NCT01544855.

Effect of buttermilk consumption on blood pressure in moderately hypercholesterolemic men and women.

OBJECTIVES: Milk fat globule membrane (MFGM) found in buttermilk is rich in unique bioactive proteins. Several studies suggest that MFGM proteins possess biological activities such as cholesterol-lowering, antiviral, antibacterial, and anticancer properties, but data in humans are lacking. Furthermore, to our knowledge, no study has yet investigated the antihypertensive potential of MFGM proteins from buttermilk. The aim of this study was to investigate the effects of buttermilk consumption on blood pressure and on markers of the renin-angiotensin-aldosterone (RAS) system in humans. METHODS: Men and women (N = 34) with plasma low-density lipoprotein cholesterol < 5 mmol/L and normal blood pressure (< 140 mm Hg) were recruited in this randomized, double-blind, placebo-controlled, crossover study. Their diets were supplemented with 45 g/d of buttermilk and with 45 g/d of a macro-/micronutrient-matched placebo in random order (4 wk for each diet). RESULTS: Buttermilk consumption significantly reduced systolic blood pressure (-2.6 mm Hg; P = 0.009), mean arterial blood pressure (-1.7 mm Hg; P = 0.015), and plasma levels of the angiotensin I-converting enzyme (-10.9%; P = 0.003) compared with the placebo, but had no effect on plasma concentrations of angiotensin II and aldosterone. CONCLUSION: Short-term buttermilk consumption reduces blood pressure in normotensive individuals.

Antioxidant activities of buttermilk proteins, whey proteins, and their enzymatic hydrolysates.

The oxygen radical absorbance capacities (ORAC) and metal chelating capacities (MCC) of protein concentrates prepared from buttermilk and cheese whey by ultrafiltration were compared with those of skim milk protein. Samples were also heat-denatured and hydrolyzed by pepsin for 2 h followed by trypsin for 3 h. The highest MCC was obtained for hydrolyzed skim milk protein. ORAC values ranged from 554.4 to 1319.6 µmol Trolox equivalents/g protein, with the highest value obtained for hydrolyzed buttermilk protein. Liquid-phase isoelectric focusing (IEF) of this hydrolysate yielded peptide fractions with lower ORAC values. LC-MS analysis of the hydrolyzed skim milk and buttermilk proteins and IEF fractions of the latter showed that peptides derived from milk fat globule membrane proteins, primarily butyrophilin, could be responsible for the superior antioxidant activity of buttermilk. These results suggest overall that hydrolyzed buttermilk protein could be used as a source of natural antioxidants.