Cereal β-glucans are dietary fibres primarily found in oats and barley, and have several positive effects on health, including lowering the postprandial glucose response and the improvement of blood cholesterol levels. Cereal β-glucans have a specific combination of β-(1→4) and β-(1→3) linkages into linear long-chain polysaccharides of high molecular weight. Due to their particular structure, cereal β-glucans generate viscosity within the intestinal tract, which is thought to be the main mechanism of action responsible for their positive health effects. However, cereal grains are rarely consumed raw; at least one cooking step is generally required before they can be safely eaten. Cooking and processing methods more generally will modify the physicochemical characteristics of β-glucans, such as molecular weight, extractability and the resulting viscosity. Therefore, the health impact of β-glucans will depend not only on the dose administered, but also on the ways they are processed or converted into food products. This review aims at summarizing the different parameters that can affect β-glucans efficacy to improve glucose and lipid metabolism in humans.

PCSK9 (Proprotein Convertase Subtilisin Kexin type 9) is a circulating protein that promotes hypercholesterolemia by decreasing hepatic LDL receptor protein. Under non interventional conditions, its expression is driven by sterol response element binding protein 2 (SREBP2) and follows a diurnal rhythm synchronous with cholesterol synthesis. Plasma PCSK9 is associated to LDL-C and to a lesser extent plasma triglycerides and insulin resistance. We aimed to verify the effect on plasma PCSK9 concentrations of dietary interventions that affect these parameters. We performed nutritional interventions in young healthy male volunteers and offspring of type 2 diabetic (OffT2D) patients that are more prone to develop insulin resistance, including: i) acute post-prandial hyperlipidemic challenge (n=10), ii) 4 days of high-fat (HF) or high-fat/high-protein (HFHP) (n=10), iii) 7 (HFruc1, n=16) or 6 (HFruc2, n=9) days of hypercaloric high-fructose diets. An acute oral fat load was also performed in two patients bearing the R104C-V114A loss-of-function (LOF) PCSK9 mutation. Plasma PCSK9 concentrations were measured by ELISA. For the HFruc1 study, intrahepatocellular (IHCL) and intramyocellular lipids were measured by ¹H magnetic resonance spectroscopy. Hepatic and whole-body insulin sensitivity was assessed with a two-step hyperinsulinemic-euglycemic clamp (0.3 and 1.0 mU.kg^-1.min^-1). HF and HFHP short-term diets, as well as an acute hyperlipidemic oral load, did not significantly change PCSK9 concentrations. In addition, post-prandial plasma triglyceride excursion was not altered in two carriers of PCSK9 LOF mutation compared with non carriers. In contrast, hypercaloric 7-day HFruc1 diet increased plasma PCSK9 concentrations by 28% (p=0.05) in healthy volunteers and by 34% (p=0.001) in OffT2D patients. In another independent study, 6-day HFruc2 diet increased plasma PCSK9 levels by 93% (p<0.0001) in young healthy male volunteers. Spearman’s correlations revealed that plasma PCSK9 concentrations upon 7-day HFruc1 diet were positively associated with plasma triglycerides (r=0.54, p=0.01) and IHCL (r=0.56, p=0.001), and inversely correlated with hepatic (r=0.54, p=0.014) and whole-body (r=−0.59, p=0.0065) insulin sensitivity. Plasma PCSK9 concentrations vary minimally in response to a short term high-fat diet and they are not accompanied with changes in cholesterolemia upon high-fructose diet. Short-term high-fructose intake increased plasma PCSK9 levels, independent on cholesterol synthesis, suggesting a regulation independent of SREBP-2. Upon this diet, PCSK9 is associated with insulin resistance, hepatic steatosis and plasma triglycerides.

Background: The connection between gut microbiota and metabolism and its role in the pathogenesis of diabetes are increasingly recognized. The objective of this study was to quantitatively measure Bifidobacterium and Lactobacillus species, members of commensal bacteria found in human gut, in type 2 diabetic patients (T2D) patients from Southern China. Methods: Fifty patients with T2D and thirty control individuals of similar body mass index (BMI) were recruited from Southern China. T2D and control subjects were confirmed with both oral glucose tolerance test (OGTT) and HbA_1c measurements. Bifidobacterium and Lactobacillus species in feces were measured by real-time quantitative PCR. Data were analyzed with STATA 11.0 statistical software. Results: In comparison to control subjects T2D patients had significantly more total Lactobacillus (+18%), L. bugaricus (+13%), L. rhamnosum (+37%) and L. acidophilus (+48%) (P < 0.05). In contrast, T2D patients had less amounts of total Bifidobacteria (−7%) and B. adolescentis (−12%) (P < 0.05). Cluster analysis showed that gut microbiota pattern of T2D patients is characterized by greater numbers of L. rhamnosus and L. acidophillus, together with lesser numbers of B. adolescentis (P < 0.05). Conclusion: The gut microflora in T2D patients is characterized by greater numbers of Lactobacillus and lesser numbers of Bifidobacterium species.

Suspicion that fructose-containing caloric sweeteners (FCCS) may play a causal role in the development of metabolic diseases has elicited intense basic and clinical research over the past 10 years. Prospective cohort studies converge to indicate that FCCS, and more specifically sugar-sweetened beverages (SSBs), consumption is associated with weight gain over time. Intervention studies in which FCCS or SSB consumption is altered while food intake is otherwise left ad libitum indicate that increased FCCS generally increases total energy intake and body weight, while FCCS reduction decreases body weight gain. Clinical trials assessing the effects of SSB reduction as a sole intervention however fail to observe clinically significant weight loss. Many mechanistic studies indicate that excess FCCS can cause potential adverse metabolic effects. Whether this is associated with a long-term risk remains unknown. Scientific evidence that excess FCCS intake causes more deleterious effects to health than excess of other macronutrients is presently lacking. However, the large consumption of FCCS in the population makes it one out of several targets for the treatment and prevention of metabolic diseases.

Low glycemic index (GI) and/or low glycemic load (GL) are associated with decreased risks of type-2 diabetes and cardiovascular disease. It is therefore relevant to consider GI and GL in the early phases of the development of packaged foods and beverages. This paper proposes a model that predicts GI and GL from macronutrient composition, by quantifying both the impact of glycemic carbohydrates and the GI-lowering effects of nutrients such as proteins, fats and fibers. The precision of the model is illustrated using data on 42 breakfast cereals. The predictions of GI (r = 0.90, median residual = 2.0) and GL (r = 0.96, median residual = 0.40 g) compete well with the precision of the underlying in-vivo data (Standard Error SE = 3.5 for GI). This model can guide product development towards lowering GI and GL, before final confirmation by in vivo testing.

Summary: Background: Intakes of dietary sugars is a global concern, and many national and international organizations have set targets to limit consumption. However, it is unclear to what extent intakes of total and added sugars vary between geographies.Objectives: The aim of this study was to assess the differences in intakes of total and added sugars in 4 to 13‐year‐old children in China, Mexico and the United States. The secondary aim was to identify main sources of total and added sugars in the diets of these children.Methods: Secondary data analysis was conducted using the 2011 China Health and Nutrition Survey, 2012 Mexican National Health and Nutrition Survey, and 2009–2012 US National Health and Nutrition Examination Surveys. Total and added sugar intakes were calculated using the US Food Patterns Equivalents Database.Results: Mean intakes of total and added sugars were 26 and 9 g d⁻¹ among Chinese children, 92 and 55 g d⁻¹ among Mexican children, and 124 and 76 g d⁻¹ among US children, respectively. The top food sources of total sugars were fruits among Chinese children, and sugar‐sweetened beverages and milk‐based beverages among Mexican and US children.Conclusions: These data highlight the heterogeneity of food patterns worldwide and the need for adapted country‐specific public health recommendations on sugars.