Nutrition, the gut microbiome and the metabolic syndrome

Sahlgrenska Center for Cardiovascular and Metabolic Research, Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Bruna Straket 16, 413 45 Gothenburg, Sweden. Electronic address: .
Best practice & research. Clinical gastroenterology (Impact Factor: 3.48). 02/2013; 27(1):59-72. DOI: 10.1016/j.bpg.2013.03.017
Source: PubMed


Metabolic syndrome is a lifestyle disease, determined by the interplay of genetic and environmental factors. Obesity is a significant risk factor for development of the metabolic syndrome, and the prevalence of obesity is increasing due to changes in lifestyle and diet. Recently, the gut microbiota has emerged as an important contributor to the development of obesity and metabolic disorders, through its interactions with environmental (e.g. diet) and genetic factors. Human and animal studies have shown that alterations in intestinal microbiota composition and shifts in the gut microbiome towards increased energy harvest are associated with an obese phenotype. However, the underlying mechanisms by which gut microbiota affects host metabolism still need to be defined. In this review we discuss the complexity surrounding the interactions between diet and the gut microbiota, and their connection to obesity. Furthermore, we review the literature on the effects of probiotics and prebiotics on the gut microbiota and host metabolism, focussing primarily on their anti-obesity potential.

Download full-text


Available from: Petia Kovatcheva-Datchary, Feb 25, 2014
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The incidence of metabolic disease, including type 2 diabetes and obesity, has increased to epidemic levels in recent years. A growing body of evidence suggests that the intrauterine environment plays a key role in the development of metabolic disease in offspring. Among other perturbations in early life, alteration in the provision of nutrients has profound and lasting effects on the long term health and well being of offspring. Rodent and non-human primate models provide a means to understand the underlying mechanisms of this programming effect. These different models demonstrate converging effects of a maternal high fat diet on insulin and glucose metabolism, energy balance, cardiovascular function and adiposity in offspring. Furthermore, evidence suggests that the early life environment can result in epigenetic changes that set the stage for alterations in key pathways of metabolism that lead to type 2 diabetes or obesity. Identifying and understanding the causal factors responsible for this metabolic dysregulation is vital to curtailing these epidemics. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease.
    Full-text · Article · Jul 2013 · Biochimica et Biophysica Acta
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In the face of the global epidemic of metabolic syndrome (MetS) and its strong association with the increasing rate of cardiovascular morbidity and mortality, it is critical to detect MetS at an early stage in the clinical setting to implement preventive intervention long before the complications arise. Lipopolysaccharide (LPS), the cell wall component of Gram-negative bacteria produced from diet-disrupted gut microbiota, has been shown to induce metabolic endotoxemia, chronic low-grade inflammation, and ultimately insulin resistance. Therefore, ameliorating the inflammation and insulin resistance underlying MetS by gut microbiota-targeted, dietary intervention has gained increasing attention. In this review, we propose using dynamic monitoring of a set of translational biomarkers related with the etiological role of gut microbiota, including LPS binding protein (LBP), C-reactive protein (CRP), fasting insulin, and homeostasis model assessment of insulin resistance (HOMA-IR), for early detection and prevention of MetS via nutritional modulation. LBP initiates the recognition and monomerization of LPS and amplifies host immune responses, linking the gut-derived antigen load and inflammation indicated by the plasma levels of CRP. Fasting plasma insulin and HOMA-IR are measured to evaluate insulin sensitivity that is damaged by pro-inflammatory cytokines. The dynamic monitoring of these biomarkers in high risk populations may provide translational methods for the quantitative and dynamic evaluation of dysbiosis-induced insulin resistance and the effectiveness of dietary treatment for MetS. This article is protected by copyright. All rights reserved.
    Full-text · Article · Nov 2013 · FEMS Microbiology Ecology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Evaluation of: Ng KM, Ferreyra JA, Higginbottom SK et al. Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens. Nature 502(7469), 96-99 (2013). The human gut microbiota is a complex system of commensal microorganisms required for normal host physiology. Disruption of this protective barrier by antibiotics creates opportunities for enteric pathogens to establish infections. Although the correlation between the use of antibiotics and enteric infections have been known for some time, the specific signals that allow enteric pathogens to recognize a susceptible host have not been determined. In a recent article, Ng et al. demonstrated that the expansion of both Salmonella typhimurium and Clostridium difficile infections is enhanced by the availability of host-specific sugars liberated from the intestinal mucus by commensal bacteria. These results show how antibiotic removal of specific species from the gut microbiome allows symbiotic functions to be hijacked by pathogenic species.
    No preview · Article · Jan 2014 · Future Microbiology
Show more