The hypocholesterolemic effect of soy is well-documented and this has led to the regulatory approval of a health claim relating soy protein to a reduced risk of cardiovascular disease (CVD). However, soybeans contain additional components, such as isoflavones, lecithins, saponins and fiber that may improve cardiovascular health through independent mechanisms. This review summarizes the evidence on the cardiovascular benefits of non-protein soy components in relation to known CVD risk factors such as hypertension, hyperglycemia, inflammation, and obesity beyond cholesterol lowering. Overall, the available evidence suggests non-protein soy constituents improve markers of cardiovascular health; however, additional carefully designed studies are required to independently elucidate these effects. Further, work is also needed to clarify the role of isoflavone-metabolizing phenotype and gut microbiota composition on biological effect.

Pulse consumption has been shown to confer beneficial effects on blood glucose and insulin levels. Lentil consumption, in particular, consistently lowers acute blood glucose and insulin response when compared to starchy control foods. The mechanism by which lentils lower postprandial blood glucose response (PBGR) and insulin levels is unclear; however, evidence suggests that this effect may be linked to macronutrients and/or the amount of lentils consumed. This review attempts to consolidate existing studies that examined lentil consumption and glycemic and/or insulinemic responses and declared information on macronutrient composition and dietary fibre content of the foods tested. Collectively, these studies suggest that consumption of lentils reduces PBGR, with the minimum effective serving being ~110g cooked to reduce PBGR by 20%. Reductions in PBGR show modest-to-strong correlations with protein (45–57 g) and dietary fibre (22–30 g) content, but has weaker correlations with available carbohydrates. Increased lentil serving sizes were found to moderately influence relative reductions in peak blood glucose concentrations and lower the area under the blood glucose curve (BG AUC). However, no clear relationship was identified between serving and relative reductions in the BG AUC, making it challenging to characterize consistent serving–response effects.

The mechanism by which high fat-diet induced obesity affects cardiac protein expression is unclear, and the extent to which this is modulated by prebiotic treatment is not known. These outcomes were assessed in rats initially fed a high-fat diet, then the top 40% weight gain group were randomly allocated to control (CON), high-fat (HF) and HF supplemented with fructooligosaccharide (32 g; HF-FOS) treatments for 12 weeks (n = 10/group). At sacrifice, left ventricles were either frozen or preserved in formalin. Serum was stored for glucose and insulin measurements. Protein spectra was obtained using an Orbitrap analyzer, processed with Sequest and fold changes assessed with Scaffold Q +. Treatment effects for body weights, glucose and insulin were assessed using one-way ANOVA, and the differential protein expression was assessed by a Mann–Whitney U test. The Database for Annotation, Visualization and Integrated Discovery and the Kyoto Encyclopedia of Genes and Genomes identified pathways containing overrepresented proteins. Hematoxylin and eosin sections were graded for hypertrophy and also quantified; differences were identified using Chi-square analyses and Mann-Whitney U tests. HF diet fed rats were significantly (p < 0.05) heavier than CON, and 23 proteins involved in mitochondrial function and lipid metabolism were differentially expressed between HF and CON. Between HF-FOS and HF, 117 proteins involved in contractility, lipid and carbohydrate metabolism were differentially expressed. HF cardiomyocytes were significantly (p < 0.05) more hypertrophic than CON. We conclude that high-fat feeding and FOS are associated with subcellular deviations in cardiac metabolism and contractility, which may influence myocardial function and alter the risk of cardiovascular disease.