Despite the lack of international agreement regarding the definition and classification of fiber, there is established evidence on the role of dietary fibers in obesity and metabolic syndrome. Beta glucan (β-glucan) is a soluble fiber readily available from oat and barley grains that has been gaining interest due to its multiple functional and bioactive properties. Its beneficial role in insulin resistance, dyslipidemia, hypertension, and obesity is being continuously documented. The fermentability of β-glucans and their ability to form highly viscous solutions in the human gut may constitute the basis of their health benefits. Consequently, the applicability of β-glucan as a food ingredient is being widely considered with the dual purposes of increasing the fiber content of food products and enhancing their health properties. Therefore, this paper explores the role of β-glucans in the prevention and treatment of characteristics of the metabolic syndrome, their underlying mechanisms of action, and their potential in food applications.

The innate immune receptor toll-like receptor 4 (TLR4) has been implicated in mediating some of the effects of dietary lipids on inflammation and type 2 diabetes (T2D). Similar to TLR4, the nucleotide-binding oligomerization domains (Nods) 1 and 2 are also proteins of innate immunity, which can respond to lipids and initiate pro-inflammatory signalling that plays a role in the aetiology of T2D. The objective was to determine the effect of Nod1 (Glu266Lys) and Nod2 (Ser268Pro) genotypes on factors associated with the metabolic syndrome (MetS), and whether they modify the association between dietary lipids and biomarkers of the MetS. Men and women (n = 998) between the ages of 20-29 years were genotyped for both polymorphisms, completed a one-month, semiquantitative food frequency questionnaire and provided a fasting blood sample. The Glu266Lys polymorphism in Nod1 was not associated with any of the biomarkers of the MetS, but modified the association between dietary saturated fat (SFA) and insulin sensitivity, as measured by HOMA-IR (p for interaction = 0.04). Individuals with the Glu/Glu or Glu/Lys genotype showed no significant relationship between dietary SFA and HOMA-IR (b = -0.002 ± 0.006, p = 0.77; and b = -0.003 ± 0.006, p = 0.61), while those with the Lys/Lys genotype showed a positive association (b = 0.033 ± 0.02, p = 0.03). The Nod2 Ser268Pro polymorphism was not associated with components of the MetS and did not modify the relationship between dietary lipid intake and the biomarkers of MetS. In summary, the Nod1 Glu266Lys polymorphism modifies the relationship between dietary SFA intake and HOMA-IR, suggesting that Nod1 may act as an intracellular lipid sensor affecting insulin sensitivity.

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The metabolic consequences of obesity have made this highly prevalent condition one of the most common risk factors for type 2 diabetes, hypertension and atherosclerosis. Simultaneous occurrence of these conditions can be explained through the manifestations of metabolic syndrome [MetS]. Clinical indication of MetS is characterized by a clustering of risk factors for complex chronic diseases which all feature metabolic deterioration as a common component. Diagnosis of MetS can be made if a patient exhibits three of the identified risk factors, some of which include: elevated waist circumference, elevated triglycerides, low high density lipoprotein levels, hypertension and elevated blood glucose. The progression from obesity to MetS involves an alteration in body metabolism mediated by cytokines- signalling molecules that coordinate the inflammatory response. Increased visceral adipose tissue contributes to augmented secretion of pro-inflammatory cytokines which can activate several transcription factors, including NF-κB, which promote these inflammatory conditions and lead to increased oxidative stress. Exacerbation of the condition then ensues as oxidative stress results in oxidized low density lipoprotein, dyslipidemia, insulin resistance, hypertension and atherogenesis. This review will not only focus on the role of inflammation in the manifestations of MetS, but also outlines some lifestyle and nutritional treatments that can be used to treat the condition and reduce the risk of chronic disease.

BackgroundIncreasing evidence suggests a role for inflammation in the development of type 2 diabetes. Elevated levels of inflammatory cytokines, including interleukin-6, have been associated with insulin resistance, and dietary lipids can increase cytokine production. The objective of this study was to determine whether a single nucleotide polymorphism near the IL6 gene (rs7801406) modifies the relationship between dietary fat and markers of insulin sensitivity.MethodsSubjects were healthy men and women aged 20–29 years from the Toronto Nutrigenomics and Health Study. Dietary intake was estimated using a one-month semiquantitative food frequency questionnaire. Fasting blood samples were taken for genotyping and biomarker measurement.ResultsThe single nucleotide polymorphism was not associated with any of the measures of insulin sensitivity. However, it modified the relationship between total dietary fat and the homeostasis model assessment of insulin resistance (P = 0.053 for interaction). Total fat intake was positively related to HOMA-IR in individuals homozygous for the G allele (β = 0.005 ± 0.002, P = 0.03), but not among heterozygotes. There was an inverse relationship between total fat intake and HOMA-IR in individuals who were homozygous for the A allele (β = −0.012 ± 0.006, P = 0.047).ConclusionThese findings suggest that dietary fat influences insulin sensitivity differently depending on genotype.