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Almond Snacking For 8 Weeks Differentially Altered the Serum Omics Profiles of Young Adults in Comparison to a Control Snack

ABSTRACT: Abstract Objectives Almond consumption can improve cardiometabolic health. However, the mechanisms underlying those physiological changes are not well characterized. This study explored the effects of consuming a snack of almonds for 8 weeks on changes in omics profiles in young adults. Methods Newly enrolled, college students (n = 73, age: 18–19 years, BMI: 18–41 kg/m2) were randomly assigned to consume a morning snack, i.e., either almonds (2 oz./d, n = 38) or an isocaloric control snack of graham crackers (325 kcal/d, n = 35) daily for 8 weeks (Clinical trials: NCT03084003). Blood samples were collected every 4 weeks over the 8 week intervention. Metabolite abundances in the serum were quantified by hydrophilic Interaction chromatography (HILIC) quadrupole (Q) time-of-flight (TOF) mass spectrometry (MS/MS), gas chromatography time-of-flight (GCTOF) MS, and CSH-ESI (electrospray) QTOF MS/MS. Data were reported as quantitative ion peak heights and were normalized by systematic error removal using random forest (SERRF) normalization. The baseline-adjusted means of the almond and cracker groups at week 8 were analyzed using ChemRICH which is a chemical similarity enrichment analysis software for metabolomics datasets that uses medical subject headings and Tanimoto substructure chemical similarity coefficients to cluster metabolites into non-overlapping chemical groups. Statistically significant p-values for clusters were obtained by self-contained Kolmogorov–Smirnov tests. Results Out of the 5716 features detected, 857 were identified as known compounds. ChemRICH mapped 660 of the identified metabolites to 63 nonoverlapping chemical classes, of which 2 were found to be significantly different between the almond and cracker groups (false discovery rate adjusted P value (FDR) < 0.05). Almond snacking for 8 weeks was associated with altered unsaturated lipid metabolism represented by significantly increased levels of unsaturated triglycerides and unsaturated lysophosphatidylcholines compared with cracker snacking (cluster FDR < 0.05). Conclusions These findings indicate that almond and cracker snacking for 8 weeks differentially altered lipid metabolism. Funding Sources Research supported by Almond Board of California and NIH-NIMHD.

SUBMITTER: Dhillon J

PROVIDER: S-EPMC7258053 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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Project description:Abstract Objectives Almond consumption can improve the cardiometabolic phenotype in young college students that routinely skip breakfast. However, the mechanisms underlying the above physiological changes are not well characterized. The study aimed to explore the effects of consuming a morning snack of almonds (high-fat) vs. crackers (high-carbohydrate) for 8 weeks on primary metabolites such as sugars, amino acids, sterols, hormones, catecholamines, hydroxyl acids, fatty acids, aromatics and other intermediates of primary metabolism in young adults. Methods Newly enrolled, college students (n = 73, age: 18–19 years, BMI: 18–41 kg/m2), primarily breakfast skippers, were randomly assigned to consume a morning snack, i.e., either almonds (2 oz./d, n = 38) or an isocaloric graham cracker snack (325 kcal/d, n = 35) daily for 8 weeks (Clinical trials: NCT03084003). Fasted blood samples were collected at baseline, mid-point and at the end of the 8-week intervention. Metabolite abundances in the serum were quantified by gas chromatography time-of-flight (GCTOF) mass spectrometry (MS). Data were reported as quantitative ion peak heights and were normalized by the sum intensity of all annotated metabolites. Linear mixed model analyses were conducted to assess the effects of the snack groups on the metabolites over the 8-week intervention. The P-values were adjusted for false discovery rate (FDR). Results Out of the 542 features detected, 160 were identified as known compounds. Aspartic acid, phenylalanine and taurine (amino acids), azelaic acid (dicarboxylic acid), octadeconol (fatty alcohol), threonic acid (sugar acid) increased (time effect, P < 0.05) while linoleic acid, myristic acid and palmitoleic acid (fatty acids) decreased (time effect, P < 0.05) over the 8-week snacking intervention. In addition, alpha-tocopherol (biomarker of almond consumption) and aconitic acid (TCA cycle intermediate) increased over 8 weeks in the almond group but not in the cracker group (time x snack effect, P < 0.05, Figure 1). Conclusions Consumption of a morning snack for 8 weeks altered the abundance of specific primary metabolites including those involved in biochemical pathways such as aconitic acid (almond snacking only) in routinely breakfast skipping young adults. The findings on the whole indicate a differential shift in metabolism with almond and cracker snacking which will be further analyzed through associations with glucoregulatory and cardiovascular outcomes. Funding Sources Almond Board of California, NIH-NIMHD. Supporting Tables, Images and/or Graphs

Project description:BackgroundChanges in gut microbiota are associated with cardiometabolic disorders and are influenced by diet. Almonds are a rich source of fiber, unsaturated fats, and polyphenols, all nutrients that can favorably alter the gut microbiome.ObjectivesThe aim of this study was to examine the effects of 8 wk of almond snacking on the gut (fecal) microbiome diversity and abundance compared with an isocaloric snack of graham crackers in college freshmen.MethodsA randomized, controlled, parallel-arm, 8-wk intervention in 73 college freshmen (age: 18-19 y; 41 women and 32 men; BMI: 18-41 kg/m2) with no cardiometabolic disorders was conducted. Participants were randomly allocated to either an almond snack group (56.7 g/d; 364 kcal; n = 38) or graham cracker control group (77.5 g/d; 338 kcal/d; n = 35). Stool samples were collected at baseline and 8 wk after the intervention to assess primary microbiome outcomes, that is, gut microbiome diversity and abundance.ResultsAlmond snacking resulted in 3% greater quantitative alpha-diversity (Shannon index) and 8% greater qualitative alpha-diversity (Chao1 index) than the cracker group after the intervention (P < 0.05). Moreover, almond snacking for 8 wk decreased the abundance of the pathogenic bacterium Bacteroides fragilis by 48% (overall relative abundance, P < 0.05). Permutational multivariate ANOVA showed significant time effects for the unweighted UniFrac distance and Bray-Curtis beta-diversity methods (P < 0.05; R 2 ≤ 3.1%). The dietary and clinical variables that best correlated with the underlying bacterial community structure at week 8 of the intervention included dietary carbohydrate (percentage energy), dietary fiber (g), and fasting total and HDL cholesterol (model Spearman rho = 0.16; P = 0.01).ConclusionsAlmond snacking for 8 wk improved alpha-diversity compared with cracker snacking. Incorporating a morning snack in the dietary regimen of predominantly breakfast-skipping college freshmen improved the diversity and composition of the gut microbiome. This trial was registered at clinicaltrials.gov as NCT03084003.

Project description:BackgroundIn addition to inborn metabolic disorders, altered metabolic profiles were reported to be associated with the risk and prognosis of some non-metabolic diseases, while as a rare metabolic disease, the overall secondary metabolic spectrum in congenital hyperinsulinemic hypoglycemia (HH) is largely undetermined. Therefore, we investigated metabolic profiles in HH patients and used ketotic hypoglycemia (KH) patients as a control cohort to unveil their distinct metabolic features.MethodsA total of 97 hypoglycemia children, including 74 with hyperinsulinemic hypoglycemia and 23 with ketotic hypoglycemia, and 170 euglycemia control subjects were studied retrospectively. Clinical and biochemical data were collected. The normoglycemic spectra of amino acids and acylcarnitines were determined by liquid chromatography tandem mass spectrometry. The serum insulin and fatty acid concentrations during standardized fasting tests in hypoglycemia patients were also collected. Receiver operating characteristic curve analysis was performed to screen potential biomarkers.ResultsAmong the normoglycemic spectra of amino acids, blood valine (p < 0.001), arginine (p < 0.001), threonine (p = 0.001), glutamate (p = 0.002), methionine (p = 0.005), ornithine (p = 0.008), leucine (p = 0.014), alanine (p = 0.017), proline (p = 0.031), citrulline (p = 0.042), aspartate (p = 0.046), and glycine (p = 0.048) levels differed significantly among the three groups. Significantly decreased levels of long- (C14:1, p < 0.001; C18, p < 0.001), medium- (C8, p < 0.001; C10, p < 0.001; C10:1, p < 0.001), and short-chain (C4-OH, p < 0.001; C5OH, p < 0.001) acylcarnitines were found in the hyperinsulinemic hypoglycemia group. Hyperinsulinemic hypoglycemia children with focal lesions and diffuse lesions had similar amino acid and acylcarnitine spectra. C10:1 < 0.09 μmol/L, threonine > 35 μmol/L, and threonine/C10:1 > 440 showed sensitivities of 81.1, 66.2, and 81.1% and specificities of 72.7, 78.3, and 81.8%, respectively, in distinguishing HH from KH.ConclusionsWe found significantly different altered serum amino acid and acylcarnitine profiles at normoglycemia, especially decreased C10:1 and increased threonine levels, between HH and KH children, which may reflect the insulin ketogenesis inhibition effect in HH patients; however, the detailed mechanisms and physiological roles remain to be studied in the future.

Project description:BackgroundPolymyositis (PM) and dermatomyositis (DM) are severe chronic autoimmune diseases, characterized by muscle fatigue and low muscle endurance. Conventional treatment includes high doses of glucocorticoids and immunosuppressive drugs; however, few patients recover full muscle function. One explanation of the persistent muscle weakness could be altered lipid metabolism in PM/DM muscle tissue as we previously reported. Using a targeted lipidomic approach we aimed to characterize serum lipid profiles in patients with PM/DM compared to healthy individuals (HI) in a cross-sectional study. Also, in the longitudinal study we compared serum lipid profiles in patients newly diagnosed with PM/DM before and after immunosuppressive treatment.MethodsLipidomic profiles were analyzed in serum samples from 13 patients with PM/DM, 12 HI and 8 patients newly diagnosed with PM/DM before and after conventional immunosuppressive treatment using liquid chromatography tandem mass spectrometry (LC-MS/MS) and a gas-chromatography flame ionization detector (GC-FID). Functional Index (FI), as a test of muscle performance and serum levels of creatine kinase (s-CK) as a proxy for disease activity were analyzed.ResultsThe fatty acid (FA) composition of total serum lipids was altered in patients with PM/DM compared to HI; the levels of palmitic (16:0) acid were significantly higher while the levels of arachidonic (20:4, n-6) acid were significantly lower in patients with PM/DM. The profiles of serum phosphatidylcholine and triacylglycerol species were changed in patients with PM/DM compared to HI, suggesting disproportionate levels of saturated and polyunsaturated FAs that might have negative effects on muscle performance. After immunosuppressive treatment the total serum lipid levels of eicosadienoic (20:2, n-6) and eicosapentaenoic (20:5, n-3) acids were increased and serum phospholipid profiles were altered in patients with PM/DM. The correlation between FI or s-CK and levels of several lipid species indicate the important role of lipid changes in muscle performance and inflammation.ConclusionsSerum lipids profiles are significantly altered in patients with PM/DM compared to HI. Moreover, immunosuppressive treatment in patients newly diagnosed with PM/DM significantly affected serum lipid profiles. These findings provide new evidence of the dysregulated lipid metabolism in patients with PM/DM that could possibly contribute to low muscle performance.

Project description:ObjectivesThis study aimed to compare the expressed microRNA (miRNA) profiles of serum-derived exosomes of patients with sudden sensorineural hearing loss (SSNHL) and normal hearing controls to identify exosomal miRNAs that may be associated with SSNHL or serve as biomarkers for SSNHL.MethodsPeripheral venous blood of patients with SSNHL and healthy controls was collected to isolate exosomes. Nanoparticle tracking analysis, transmission electron microscopy, and Western blotting were used to identify the isolated exosomes, after which total RNA was extracted and used for miRNA transcriptome sequencing. Differentially expressed miRNAs (DE-miRNAs) were identified based on the thresholds of P < 0.05 and |log2fold change| > 1 and subjected to functional analyses. Finally, four exosomal DE-miRNAs, including PC-5p-38556_39, PC-5p-29163_54, PC-5p-31742_49, and hsa-miR-93-3p_R+1, were chosen for validation using quantitative real-time polymerase chain reaction (RT-qPCR).ResultsExosomes were isolated from serum and identified based on particle size, morphological examination, and expression of exosome-marker proteins. A total of 18 exosomal DE-miRNAs, including three upregulated and 15 downregulated miRNAs, were found in SSNHL cases. Gene ontology (GO) functional annotation analysis revealed that target genes in the top 20 terms were mainly related to "protein binding," "metal ion binding," "ATP binding," and "intracellular signal transduction." Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that these target genes were functionally enriched in the "Ras," "Hippo," "cGMP-PKG," and "AMPK signaling pathways." The expression levels of PC-5p-38556_39 and PC-5p-29163_54 were significantly downregulated and that of miR-93-3p_R+1 was highly upregulated in SSNHL. Consequently, the consistency rate between sequencing and RT-qPCR was 75% and sequencing results were highly reliable.ConclusionThis study identified 18 exosomal DE-miRNAs, including PC-5p-38556_39, PC-5p-29163_54, and miR-93-3p, which may be closely related to SSNHL pathogenesis or serve as biomarkers for SSNHL.

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Almond Snacking For 8 Weeks Differentially Altered the Serum Omics Profiles of Young Adults in Comparison to a Control Snack

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