Background: Consumption of 3 g oat β-glucan/d is considered sufficient to lower serum LDL cholesterol, but some studies have shown no effect. LDL cholesterol lowering by oat β-glucan may depend on viscosity, which is controlled by the molecular weight (MW) and amount of oat β-glucan solubilized in the intestine (C).

Background: Short-chain fatty acids (SCFA) are produced by colonic microbiota from dietary carbohydrates and proteins that reach the colon. It has been suggested that SCFA may promote obesity via increased colonic energy availability. Recent studies suggest obese humans have higher faecal SCFA than lean, but it is unclear whether this difference is due to increased SCFA production or reduced absorption. Objectives: To compare rectal SCFA absorption, dietary intake and faecal microbial profile in lean (LN) versus overweight and obese (OWO) individuals. Design: Eleven LN and eleven OWO individuals completed a 3-day diet record, provided a fresh faecal sample and had SCFA absorption measured using the rectal dialysis bag method. The procedures were repeated after 2 weeks. Results: Age-adjusted faecal SCFA concentration was significantly higher in OWO than LN individuals (81.3±7.4 vs 64.1±10.4 mmol kg⁻¹, P=0.023). SCFA absorption (24.4±0.8% vs 24.7±1.2%, respectively, P=0.787) and dietary intakes were similar between the groups, except for a higher fat intake in OWO individuals. However, fat intake did not correlate with SCFAs or bacterial abundance. OWO individuals had higher relative Firmicutes abundance (83.1±4.1 vs 69.5±5.8%, respectively, P=0.008) and a higher Firmicutes:Bacteriodetes ratio (P=0.023) than LN individuals. There was a positive correlation between Firmicutes and faecal SCFA within the whole group (r=0.507, P=0.044), with a stronger correlation after adjusting for available carbohydrate (r=0.615, P=0.005). Conclusions: The higher faecal SCFA in OWO individuals is not because of differences in SCFA absorption or diet. Our results are consistent with the hypothesis that OWO individuals produce more colonic SCFA than LN individuals because of differences in colonic microbiota. However, further studies are needed to prove this.

Read the full review for this F1000Prime recommended article: The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein.

In animals, colonic infusion of SCFA does not affect glucagon-like peptide-1 (GLP-1) release whereas intravenous infusion does and SCFA may directly stimulate peptide YY (PYY) release. It is unknown whether SCFA and their route of administration affect human blood concentrations of GLP-1 and PYY. Our aim was to conduct a pilot study to determine the effects of intravenous and rectal acetate on blood concentrations of GLP-1, PYY, ghrelin, adiponectin and TNF-α in hyperinsulinaemic human subjects. Six hyperinsulinaemic female subjects were given 20 mmol sodium acetate intravenously, 60 mmol acetate rectally, or normal saline rectally or intravenously on four separate occasions in randomised order, with blood samples collected at 0, 10, 15, 30, 45 and 60 min. Change in plasma PYY was significantly higher after acetate and rectal infusions (9·69 and 13·78 pg/ml) compared with saline and intravenous (0·60 and − 3·1 pg/ml; P < 0·01), respectively. Change in plasma GLP-1 was increased by rectal and acetate infusions (0·25 and 0·23 mmol/l) v. intravenous and saline ( − 0·26 and − 0·19 mmol/l; P < 0·01). Acetate decreased TNF-α v. saline ( − 0·8 and 0·15 pg/ml; P < 0·05). Rectal infusions increased TNF-α and ghrelin (0·2 and 98·27 pg/ml) v. intravenous ( − 0·9 and − 40 pg/ml; P < 0·01). There was no effect of treatment on plasma adiponectin. These preliminary results suggest that acetate raises plasma PYY and GLP-1, and suppresses TNF-α. Also, distending the rectum increases PYY, GLP-1, TNF-α and ghrelin in hyperinsulinaemic females. Increasing colonic fermentation products, particularly acetate, could yield a new mechanism for modifying weight gain.

Objective: Practical use of the glycaemic index (GI), as recommended by the FAO/WHO, requires an evaluation of the recommended method. Our purpose was to determine the magnitude and sources of variation of the GI values obtained by experienced investigators in different international centres. Design: GI values of four centrally provided foods (instant potato, rice, spaghetti and barley) and locally obtained white bread were determined in 8–12 subjects in each of seven centres using the method recommended by FAO/WHO. Data analysis was performed centrally. Setting: University departments of nutrition. Subjects: Healthy subjects (28 male, 40 female) were studied. Results: The GI values of the five foods did not vary significantly in different centres nor was there a significant centre×food interaction. Within-subject variation from two centres using venous blood was twice that from five centres using capillary blood. The s.d. of centre mean GI values was reduced from 10.6 (range 6.8–12.8) to 9.0 (range 4.8–12.6) by excluding venous blood data. GI values were not significantly related to differences in method of glucose measurement or subject characteristics (age, sex, BMI, ethnicity or absolute glycaemic response). GI values for locally obtained bread were no more variable than those for centrally provided foods. Conclusions: The GI values of foods are more precisely determined using capillary than venous blood sampling, with mean between-laboratory s.d. of approximately 9.0. Finding ways to reduce within-subject variation of glycaemic responses may be the most effective strategy to improve the precision of measurement of GI values.

Published meta-analyses indicate significant but inconsistent incident type-2 diabetes (T2D)-dietary glycemic index (GI) and glycemic load (GL) risk ratios or risk relations (RR). It is now over a decade ago that a published meta-analysis used a predefined standard to identify valid studies. Considering valid studies only, and using random effects dose–response meta-analysis (DRM) while withdrawing spurious results (p < 0.05), we ascertained whether these relations would support nutrition guidance, specifically for an RR > 1.20 with a lower 95% confidence limit >1.10 across typical intakes (approximately 10th to 90th percentiles of population intakes). The combined T2D–GI RR was 1.27 (1.15–1.40) (p < 0.001, n = 10 studies) per 10 units GI, while that for the T2D–GL RR was 1.26 (1.15–1.37) (p < 0.001, n = 15) per 80 g/d GL in a 2000 kcal (8400 kJ) diet. The corresponding global DRM using restricted cubic splines were 1.87 (1.56–2.25) (p < 0.001, n = 10) and 1.89 (1.66–2.16) (p < 0.001, n = 15) from 47.6 to 76.1 units GI and 73 to 257 g/d GL in a 2000 kcal diet, respectively. In conclusion, among adults initially in good health, diets higher in GI or GL were robustly associated with incident T2D. Together with mechanistic and other data, this supports that consideration should be given to these dietary risk factors in nutrition advice. Concerning the public health relevance at the global level, our evidence indicates that GI and GL are substantial food markers predicting the development of T2D worldwide, for persons of European ancestry and of East Asian ancestry.