Dietary fiber and whole grains contain a unique blend of bioactive components including resistant starches, vitamins, minerals, phytochemicals and antioxidants. As a result, research regarding their potential health benefits has received considerable attention in the last several decades. Epidemiological and clinical studies demonstrate that intake of dietary fiber and whole grain is inversely related to obesity, type two diabetes, cancer and cardiovascular disease (CVD). Defining dietary fiber is a divergent process and is dependent on both nutrition and analytical concepts. The most common and accepted definition is based on nutritional physiology. Generally speaking, dietary fiber is the edible parts of plants, or similar carbohydrates, that are resistant to digestion and absorption in the small intestine. Dietary fiber can be separated into many different fractions. Recent research has begun to isolate these components and determine if increasing their levels in a diet is beneficial to human health. These fractions include arabinoxylan, inulin, pectin, bran, cellulose, β-glucan and resistant starch. The study of these components may give us a better understanding of how and why dietary fiber may decrease the risk for certain diseases. The mechanisms behind the reported effects of dietary fiber on metabolic health are not well established. It is speculated to be a result of changes in intestinal viscosity, nutrient absorption, rate of passage, production of short chain fatty acids and production of gut hormones. Given the inconsistencies reported between studies this review will examine the most up to date data concerning dietary fiber and its effects on metabolic health.

The involvement of the gut microbiota in metabolic disorders, and the ability of whole grains to affect both host metabolism and gut microbial ecology, suggest that some benefits of whole grains are mediated through their effects on the gut microbiome. Nutritional studies that assess the effect of whole grains on both the gut microbiome and human physiology are needed. We conducted a randomized cross-over trial with four-week treatments in which 28 healthy humans consumed a daily dose of 60 g of whole-grain barley (WGB), brown rice (BR), or an equal mixture of the two (BR þ WGB), and characterized their impact on fecal microbial ecology and blood markers of inflammation, glucose and lipid metabolism. All treatments increased microbial diversity, the Firmicutes/Bacteroidetes ratio, and the abundance of the genus Blautia in fecal samples. The inclusion of WGB enriched the genera Roseburia, Bifidobacterium and Dialister, and the species Eubacterium rectale, Roseburia faecis and Roseburia intestinalis. Whole grains, and especially the BR þ WGB treatment, reduced plasma interleukin-6 (IL-6) and peak postprandial glucose. Shifts in the abundance of Eubacterium rectale were associated with changes in the glucose and insulin postprandial response. Interestingly, subjects with greater improvements in IL-6 levels harbored significantly higher proportions of Dialister and lower abundance of Coriobacteriaceae. In conclusion, this study revealed that a short-term intake of whole grains induced compositional alterations of the gut microbiota that coincided with improvements in host physiological measures related to metabolic dysfunctions in humans.

These data suggest that increases in muscle strength and size were not influenced by the predominant source of protein consumed by older men with adequate total protein intake.

Weight control by exercise and dietary calorie restriction (DCR) has been associated with reduced cancer risk, but the underlying mechanisms are not well understood. This study was designed to compare the effects of weight loss by increasing physical activity or decreasing calorie intake on tumor promoter-induced Ras-MAPK and PI3K-Akt pathways. SENCAR mice were randomly assigned to one of the following five groups: ad libitum-fed sedentary control, ad libitum-fed exercise (AL؉Exe), exercise but pair-fed at the amount as controls (PF؉Exe), 20% DCR, and 20% DCR plus exercise (DCR؉Exe). After 10 weeks, body weight and body fat significantly decreased in the groups of DCR, DCR؉Exe, and PF؉Exe when compared with the controls. AL؉Exe did not induce weight loss due to, at least in part, increased food intake. Plasma IGF-1 levels reduced significantly in DCR and DCR؉Exe but not PF؉Exe. The protein H-Ras and activated Ras-GTP significantly decreased in TPA-induced skin tissues of DCR-fed mice but not exercised mice. PI3K protein, phosphoserine Akt, and p42/p44-MAPK were reduced, however, in both DCR and PF؉Exe groups. Immunohistochemistry demonstrated that the significantly reduced H-Ras occurred in subcutaneous fat cells, while the reduced PI3K and PCNA took place only in the epidermis. Plasma leptin decreased in PF؉Exe, DCR, and DCR؉Exe, while the caspase-3 activity increased in DCR؉Exe only. Genomic microarray analysis further indicated that the expression of 34 genes relevant to PI3K and 31 genes to the MAPK pathway were significantly regulated by either DCR or PF؉Exe treatments. The reduced PI3K in PF؉Exe mice was partially reversed by IGF-1 treatment. The overall results of this study demonstrated that DCR abrogated both Ras and PI3K signaling, which might inhibit TPA-induced proliferation and anti-apoptosis. Selective inhibition of PI3K by PF؉Exe but not AL؉Exe seems more attributable to the magnitude of the caloric deficit and/or body fat loss than diet versus exercise comparison.The National Health and Nutrition Examination Survey indicates growing rates of obesity in American adults and overweight children over the past 20 years (1). Numerous prospective and case-control studies associated with weight control and physical activity estimate that excess body weight and sedentary life style account for about 39% endometrial, 25% kidney, 11% colon, 9% postmenopausal breast cancer, and 5% total cancer incidence (2-3). It has been suggested that those 25% over normal weight have a 33% greater cancer risk than those who maintain ideal body weight (4). Therefore, for many individuals, it would be advisable to maintain weight within the normal range to reduce their risk of cancer.Overweight/obesity is recognized as a reflection of a positive energy state that results from either over-consumption of energy or low energy expenditure. There is ample evidence that weight control via decreasing calorie intake and/or increasing physical activity reduces cancer risk in animal models. For almost a century, dietary calorie restr...

Research findings over the past several decades have shown that inflammation is a prominent feature of many chronic diseases, with poor diet being one likely inflammatory stimulus. Specifically, a single high-fat meal (HFM) has been suggested to increase inflammation, although there is currently no consensus with regard to the specific changes in many of the proinflammatory markers that are frequently assessed after an HFM. The aim of this systematic review was to objectively describe the postprandial timing and magnitude of changes in 5 common inflammatory markers: interleukin (IL) 6, C-reactive protein (CRP), tumor necrosis factor (TNF) a, IL-1b, and IL-8. Ten relevant databases were searched, yielding 494 results, of which 47 articles met the pre-established inclusion criteria: 1) healthy men and women aged 18-60 y, 2) consuming a single HFM ($30% fat, $500 kcal), and 3) assessing relevant inflammatory markers postmeal for $2 h. The only marker found to consistently change in the postprandial period was IL-6: on average, from a baseline of ;1.4 pg/mL, it peaked at ;2.9 pg/mL ;6 h post-HFM (an average relative change of ;100%). CRP, TNF-a, IL-1b, and IL-8 did not change significantly in 79% (23 of 29), 68% (19 of 28), 67% (2 of 3), and 75% (3 of 4) of included studies, respectively. We conclude that there is strong evidence that CRP and TNF-a are not responsive at the usual time scale observed in postprandial studies in healthy humans younger than age 60 y. However, future research should further investigate the role of IL-6 in the postprandial period, because it routinely increases even in healthy participants. We assert that the findings of this systematic review on markers of inflammation in the postprandial period will considerably aid in informing future research and advancing clinical knowledge. Adv Nutr 2017;8:213-25.

Objective. The objective was to compare the postprandial glycemic and insulinemic responses to nutrition bars containing either cross-linked RS type 4 (RS4XL) or standard wheat starch in normoglycemic adults (n = 13; age = 27 ± 5 years; BMI = 25 ± 3 kg/m2). Methods. Volunteers completed three trials during which they consumed a glucose beverage (GLU), a puffed wheat control bar (PWB), and a bar containing cross-linked RS4 (RS4XL) matched for available carbohydrate content. Serial blood samples were collected over two hours and glucose and insulin concentrations were determined and the incremental area under the curve (iAUC) was calculated. Results. The RS4XL peak glucose and insulin concentrations were lower than the GLU and PWB (P < .05). The iAUC for glucose and insulin were lower following ingestion of RS4 compared with the GLU and PWB trials. Conclusions. These data illustrate, for the first time, that directly substituting standard starch with RS4XL, while matched for available carbohydrates, attenuated postprandial glucose and insulin levels in humans. It remains to be determined whether this response was due to the dietary fiber and/or resistant starch aspects of the RS4XL bar.

No abstract

The purpose of this study was to determine whether different types of resistant starch (RS) elicited different glycemic responses. Eleven healthy subjects consumed solutions containing 30 g of either dextrose (DEX), resistant starch type 2 (RS2), or cross-linked resistant wheat starch type 4 (RS4XL) on three separate occasions, which were assigned randomly. Finger stick blood samples were collected before and over the following two hours and measured for glucose. The incremental area under the curve (iAUC) for the glucose response was calculated for all trials. The two types of resistant starch significantly (P < .05) decreased iAUC compared with DEX. The response with RS4XL was significantly decreased compared with the RS2 trial. These data demonstrate that different types of resistant starch elicit significantly different glycemic responses.