Daily Intake of a Phaseolus vulgaris L. Snack Bar Attenuates Hypertriglyceridemia and Improves Lipid Metabolism-Associated Plasma Proteins in Mexican Women: A Randomized Clinical Trial

Abstract

Current efforts to prevent dyslipidemia are focused on the development of functional products as an alternative for hypertriglyceridemia management. This study assessed the metabolic effect of the daily consumption of a bean and oats snack bar (BOSB) on hypertriglyceridemia biomarkers among Mexican women. An 8-weeks randomized parallel clinical trial (ID: NCT0496694, https://ichgcp.net/clinical-trials-registry/NCT04966494) was conducted with 26 hypertriglyceridemic women allocated to BOSB group (TG = 208.18 ± 56.97 mg/dL) and control group (TG = 182.28 ± 51.39 mg/dL). Only the BOSB group consumed 50 g of the product per day. Fasting blood samples were taken from women with an adherence ≥ 90%. A targeted proteomic analysis with plasma samples of control and BOSB groups were conducted using a human obesity antibody array kit and bioinformatic tools provided by the Ingenuity Pathways Analysis (IPA) software. Serum TG levels in the BOSB group decreased by 37.80% (132.04 ± 27.83 mg/dL) compared with the control group (178.87 ± 32.01 mg/dL); glucose levels decreased by 5.69% in the BOSB group (87.55 ± 3.36 mg/dL). A modest body weight (5%) reduction was also found. Forty proteins were differentially modulated by the BOSB consumption (fold change > 1.2). The proteomic analysis revealed the involvement of BOSB bioactives in prevention of monocytes recruitment and localized inflammatory response, inhibition of pre-adipocyte maturation and adipogenesis, inhibition of hepatic b-oxidation, and potential satiety regulation. These results are promising since the mere intervention with the BOSB reduced serum TG without diet restriction, giving insights for further research in prevention of hypertriglyceridemia.

Keywords: common bean (Phaseolus vulgaris L.); dyslipidemia; microarrays; oat (Avena sativa); targeted plasma proteomics; triglycerides.

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Copyright © 2022 Ramírez-Jiménez, Luzardo-Ocampo, Cuellar-Nuñez, Anaya-Loyola, León-Galván and Loarca-Piña.

Figures

FIGURE 1

Study design. Flow chart for overall screening procedure.

FIGURE 2

Individual triglyceride differences in (A) Control group and (B) BOSB group after 8-weeks consumption.

FIGURE 3

Differential expression of plasma proteins and downstream analysis showing the main regulated pathways after BOSB consumption. (A) Fold-changes of the modulated plasmatic proteins after the BOSB consumption; (B) Top morphological functions; (C) Top regulated canonical pathways; (D) IPA protein network associating cytokine/growth factors, enzymes, transmembrane receptors, and complexes; (E) Main regulated pathways linked to the synthesis of lipids.

FIGURE 4

(A) Predicted effects of BOSB consumption on atherosclerosis-related metabolic pathways; (B) Integration of the main BOSB-regulated systemic pathways associated to neuropeptide regulation, lipid metabolism and atherosclerosis signaling. This figure was generated with BioRender.com. (1) The atherosclerosis pathway initiates with LDL deposition and monocyte recruitment to the endothelial barrier mediated by MCP-1 and CCR2. (2) After monocyte rolling mediated by E-selectin and receptor ESL-1, (3) the lower levels of VCAM-1 found in the microarray analysis, and predicted reductions in plasma LDL levels, reduce endothelial cell adhesion. (4) Lower predicted LDL also inhibits CCR-2 expression and MCP-1 mediated trans endothelial migration of monocytes into the intima. It is known that ROS and oxidized-LDL uptake via scavenger receptors leads to lipid accumulation and foam cell formation that secrete a number of inflammatory cytokines. (5) Reduced M-CSF levels inhibit monocyte-to-macrophage differentiation, (6) as well as a decreased LDL migration into the intima and inhibition of CD36/IL-8RA. (7) This has a predicted effect on TNFRSF14 which may inhibit the NF-kB pathway and the downstream production of inflammatory cytokines (IL-3, MCP-1, TNF, IL-1, IL6), as well as TNF and matrix metalloproteases, involved also in inflammation processes and in atherosclerosis onset. (8) Finally, reduction observed for PDGF and TGF-β inhibits exacerbated collagen production via the CD40 receptor found in the surface of foam cells and T-lymphocytes, that may act via IFN-γ. Collagens constitute a component of the extracellular matrix in the atherosclerotic plaque.