Abstract
Diet-induced obesity and metabolic syndrome are associated with the onset of gastrointestinal diseases, such as hepatic steatosis and gut inflammation. Prior research shows that a proprietary soil-derived organic mineral complex (OMC) prevents hyperglycemia, endotoxemia, and liver injury in rats fed a high-fat diet (HFD) for 10 weeks. The aim of this study was to further examine the effects of OMC on the liver and gastrointestinal health of these rats. Six-week-old male Sprague-Dawley rats (n = 36) were divided into two dietary groups: Chow or HFD fed for 10 weeks. Animals were further divided (n = 6/group) and administered 0, 0.6, or 3.0 mg/mL OMC in their drinking water. The 10-week HFD resulted in significant liver fat accumulation. Both OMC doses prevented hepatic increases in the glycation end product Nε-(carboxymethyl)lysine (CML) induced by HFD (p < 0.05). Low-dose OMC was associated with higher expression of occludin in the small intestine of rats fed either diet (two-way ANOVA, p < 0.042). Linear discriminant analysis (LDA) effect size (LEfSe) indicated significant differences in fecal microbial composition of untreated HFD-fed rats in comparison to untreated Chow rats at 10 weeks (LDA score > 2.0 : 18). After 10 weeks, untreated HFD-fed rats were also more abundant in bacteria associated with obesity and metabolic disease in comparison to corresponding week 0 samples (LDA score > 2.0 : 31), 10-week untreated Chow (LDA > 2.0 : 18), or 10-week OMC-treated HFD-fed rats (0.6 mg/mL; LDA > 2.0 : 80, 3.0 mg/mL; LDA > 2.0 : 8). Low-dose OMC prevented the HFD-induced increase in the Firmicutes-to-Bacteroidetes (F/B) ratio (p < 0.0416). Study animals treated with OMC exhibited no significant changes in the gut microbiota at week 10, although gut inflammatory biomarkers were not significantly altered by diet or OMC treatment. These results indicate that OMC supplementation ameliorates glycosylation reactions and modifies HFD-induced alterations in the intestinal microbiota.
Highlights
Metabolic syndrome is characterized by a cluster of pathologies consisting of hypertension, insulin resistance, abdominal obesity, and dyslipidemia [1]
In comparison to Chow-fed rats, fecal samples from untreated high-fat diet (HFD)-fed rats were more enriched in Firmicutes, Deferribacteres (Desulfovibrio, Deferribacteraceae, Deferribacterales, Deferribacteres, and Mucispirillum), Bacteroidetes (Rikenellaceae, Streptococcaceae, and acidifaciens), Proteobacteria (Desulfovibrio), and Tenericutes (Anaeroplasmatales, Anaeroplasma, and Anaeroplasmataceae) families and species at 10 weeks; all of which are associated with the development of inflammation, obesity, and type 2 diabetes [55,56,57,58,59,60]
Fecal samples from these HFDfed rats were more abundant in bacteria associated with high-fat diet intake from the phyla Bacteroidetes (Parabacteroides, a commensal microbe) [61], Firmicutes (Oscillospira, Ruminococcus, garvieae, gnvaus, Roseburia, and Peptococcaceae), Actinobacteria (Christensenellaceae, Coriobacteriia, and Coriobacteriales), and Proteobacteria (Enterobacteriales) in comparison to fecal samples collected at week 0
Summary
Metabolic syndrome is characterized by a cluster of pathologies consisting of hypertension, insulin resistance, abdominal obesity, and dyslipidemia [1]. Obesity further contributes to the development of a multitude of hepatic and gastrointestinal (GI) disorders including nonalcoholic fatty liver disease (NAFLD) [2]. Characterized by steatosis (excessive buildup of fat), NAFLD is the most prevalent chronic liver disorder in the world [3], affecting over 65 million Americans with an estimated annual financial burden of $103 billion [4]. Concurrent with the rise of obesity and type 2 diabetes [5], the increase in NAFLD is strongly associated with consumption of a Westernized diet [6]. Erefore, the so-called “gut-liver axis” is increasingly recognized as an important factor in the etiology of metabolic syndrome and NAFLD [11, 15]. Due to the Journal of Nutrition and Metabolism complexity of this interaction, many open research questions have emerged, in relation to overall diet and dietary components
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