Abstract

Cooked common beans (Phaseolus vulgaris) improve intestinal health in lean mice and attenuate intestinal dysbiosis and inflammation when consumed concurrent with obesity development. We determined the effects of a high-fat (HF) bean supplemented diet in mice with established obesity (induced by 12 weeks of HF diet (60% fat as kcal)) compared to obese mice consuming a HF or low-fat (LF) weight loss control diet. Obese C57BL/6 male mice remained consuming HF for eight weeks or were randomly switched from HF to an isocaloric HF with 15.7% cooked navy bean powder diet (HF→HFB) or LF (11% fat as kcal; HF→LF) (n = 12/group). HF→HFB improved the obese phenotype, including (i) fecal microbiome (increased Prevotella, Akkermansia muciniphila, and short-chain fatty acid levels), (ii) intestinal health (increased ZO-1, claudin-2, Muc2, Relmβ, and Reg3γ expression), and (iii) reduced adipose tissue (AT) inflammatory proteins (NFκBp65, STAT3, IL-6, MCP-1, and MIP-1α), versus HF (p < 0.05). Conversely, HF→LF reduced body weight and circulating hormones (leptin, resistin, and PAI-1) versus HF and HF→HFB (p < 0.05); however, AT inflammation and intestinal health markers were not improved to the same degree as HF→HFB (p < 0.05). Despite remaining on a HF obesogenic diet, introducing beans in established obesity improved the obese phenotype (intestinal health and adipose inflammation) more substantially than weight loss alone.

Highlights

  • Obesity is a chronic disease [1] characterized by low-grade systemic and adipose tissue (AT) inflammation (e.g., resistin, leptin, tumor necrosis factor alpha (TNFα), interleukin (IL)-6), metabolic disorders, and a dysbiotic and dysfunctional intestinal microenvironment [2], which collectively drive comorbidities, including type 2 diabetes, cardiovascular diseases (CVD), and cancer [3,4]

  • Epididymal adipose tissue (EAT) depot weights were significantly reduced in HF→LF mice compared to HF and HF→high-fat bean (HFB), which did not differ from each other (Figure 1B)

  • We demonstrated a reproducible effect of navy bean supplementation to an obesogenic diet on intestinal health parameters, which is apparent in two distinct obesity models, namely navy bean supplementation during the development of obesity [32] and the introduction of navy beans within established obesity

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Summary

Introduction

Obesity is a chronic disease [1] characterized by low-grade systemic and adipose tissue (AT) inflammation (e.g., resistin, leptin, tumor necrosis factor alpha (TNFα), interleukin (IL)-6), metabolic disorders (e.g., hyperglycemia, insulin resistance, and dyslipidemia), and a dysbiotic and dysfunctional intestinal microenvironment [2], which collectively drive comorbidities, including type 2 diabetes, cardiovascular diseases (CVD), and cancer [3,4]. We have shown that dietary pulses (e.g., beans, chickpeas, and lentils) can improve intestinal health by modulating the cecal and/or fecal microbial composition and activity and by improving the mucus and epithelial barrier integrity and function in lean mice [15,16,17,18,19] Many of these beneficial effects of beans on intestinal health may be driven by microbial-derived metabolites, including fermentation of NDCs enriched in beans (including soluble fiber, resistant starch, and galacto-oligosaccharides) as well as phenolic compounds, which are the dietary precursors for intestinal health-promoting metabolites (short-chain fatty acids (SCFAs), acetic acid, propionic acid and butyric acid [20,21], and secondary phenolic metabolites [22,23,24])

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