Abstract

Administration of freeze-dried powder of Saskatoon berry (SB), a popular fruit enriched with antioxidants, reduced glucose level, inflammatory markers and gut microbiota disorder in high fat-high sucrose (HFHS) diet-induced insulin resistant mice. The present study examined the dose-response relationship in metabolic, inflammatory and gut microbiotic variables to SB power (SBp) supplementation in HFHS diet-fed mice. Male C57 BL/6J mice were fed with HFHS diet supplemented with 0, 1%, 2.5% or 5% SBp for 11 weeks. HFHS diet significantly increased the levels of fast plasma glucose (FPG), cholesterol, triglycerides, insulin, homeostatic model assessment of insulin resistance (HOMA-IR), tumor necrosis factor-α, monocyte chemotactic protein-1 and plasminogen activator inhibitor-1, but decreased fecal Bacteroidetes phylum bacteria and Muribaculaceae family bacteria compared to low fat diet. SBp dose-dependently reduced metabolic and inflammatory variables and gut dysbiosis in mice compared with mice receiving HFHS diet alone. Significant attenuation of HFHS diet-induced biochemical disorders were detected in mice receiving ≥1% SBp. The abundances of Muribaculaceae family bacteria negatively correlated with body weights, FPG, lipids, insulin, HOMA-IR and inflammatory markers in the mice. The results suggest that SBp supplementation dose-dependently attenuated HFHS diet-induced metabolic and inflammatory disorders, which was associated with the amelioration of gut dysbiosis in the mice.

Highlights

  • The prevalence of diabetes has rapidly increased worldwide

  • high fat-high sucrose (HFHS) diet significantly increased body weights, fast plasma glucose (FPG), cholesterol, triglycerides, insulin, homeostatic model assessment of insulin resistance (HOMA-IR) and inflammatory markers (PAI-1, tumor necrosis factor-α (TNFα) and monocyte chemotactic protein-1 (MCP-1)) in mice compared with low fat diet after 11 weeks of dietary intervention (p < 0.01, Table 1)

  • No significant difference in FPG or lipids between mice treated with HFHS + 5% SB power (SBp) and mice receiving HFHS + 1% or those fed with HFHS + 2.5% SBp diet (Figure 1A–C) were found

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Summary

Introduction

The prevalence of diabetes has rapidly increased worldwide. The primary type of diabetes contributing to this increase is type 2 diabetes (T2D) [1]. T2D is characterized by insulin resistance and is often associated with obesity [2]. Lack of physical activity and genetic factors contribute to the epidemic of T2D [4]; diets containing high level of fat and/or sugar play an important role in the development of obesity, insulin resistance and T2D [5]. T2D is associated with low-grade chronic inflammation [6]. Gut microbiota is regulated by daily diet and implicated in both metabolism and inflammation [7]; accumulating lines of evidence suggest that gut dysbiosis contributes to the development of T2D and obesity [8]

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