Current perspectives on global sugars consumption: definitions, recommendations, population intakes, challenges and future direction

Currently there is considerable emphasis on the relationship between dietary sugars consumption and various health outcomes, with some countries and regions implementing national sugar reduction campaigns. This has resulted in significant efforts to quantify dietary sugars intakes, to agree on terms to describe dietary sugars and to establish associated recommendations. However, this information is infrequently collated on a global basis and in a regularised manner. The present review provides context regarding sugars definitions and recommendations. It provides a global review of the available data regarding dietary sugars intake, considering forms such as total, free and added sugars. A comprehensive breakdown of intakes is provided by age-group, country and sugars form. This analysis shows that free sugars intakes as a percentage of total energy (%E) are the highest for children and adolescents (13-14%E) and the lowest for older adults (8%E). This trend across lifecycle stages has also been observed for added sugars. The available data also suggest that while some reductions in sugars intake are observed in a few individual studies, overall intakes of free/added sugars remain above recommendations. However, any wider conclusions are hampered by a lack of detailed high quality data on sugars intake, especially in developing countries. Furthermore, there is a need for harmonisation of terms describing sugars (ideally driven by public health objectives) and for collaborative efforts to ensure that the most up-to-date food composition data are used to underpin recommendations and any estimates of intake or modelling scenarios.

Loss of intestinal ChREBP impairs absorption of dietary sugars and prevents glycemic excursion curves

Increased sugar consumption is a risk factor for features of the metabolic syndrome including obesity, hypertriglyceridemia, insulin resistance, diabetes, and nonalcoholic fatty liver disease. The gut epithelium, which plays a central role in dietary sugar digestion, absorption and metabolism has emerged a key actor of metabolic disorders. While the transcription factor ChREBP (Carbohydrate response element binding protein) has been established as a key player of the adaptive reprograming of cellular metabolism in various tissues upon glucose or fructose challenge, its specific contribution to the regulation of blood glucose upon dietary sugar intake was not previously addressed. We demonstrate here that ChREBP is abundantly expressed in the proximal gut epithelium, where carbohydrate digestion and absorption primarily occur and in particular L cells, which produce the glucoincretin GLP-1. The inducible deletion of ChREBP specifically in the mouse gut epithelium (ChΔGUT mice) resulted in the reduction of early glycemic excursion upon oral glucose load. Surprisingly, despite being associated with reduced GLP-1 production, loss of gut ChREBP activity significantly dampened glucose transepithelial flux, and thereby delayed glucose distribution to peripheral tissues. Among the underlying mechanisms, we unveil that ChΔGUT mice show an impaired expression of key intestinal hexose (glucose, galactose, fructose) transporters and metabolic enzymes as well as brush border dissacharidases. In agreement, intestinal ChREBP deficiency was accompanied by a precocious intolerance to both high-lactose and high-sucrose diets concomitant with mild galactose and severe fructose malabsorption syndromes. Altogether, our study demonstrates that, by transcriptionally orchestrating local digestion and absorption of dietary sugars, ChREBP activity in the mouse gut epithelium controls glucose appearance rate into systemic circulation and prevents against intolerance to mono- and disaccharides.

Degradation of the low-calorie sugar substitute 5-ketofructose by different bacteria

There is an increasing public awareness about the danger of dietary sugars with respect to their caloric contribution to the diet and the rise of overweight throughout the world. Therefore, low-calorie sugar substitutes are of high interest to replace sugar in foods and beverages. A promising alternative to natural sugars and artificial sweeteners is the fructose derivative 5-keto-D-fructose (5-KF), which is produced by several Gluconobacter species. A prerequisite before 5-KF can be used as a sweetener is to test whether the compound is degradable by microorganisms and whether it is metabolized by the human microbiota. We identified different environmental bacteria (Tatumella morbirosei, Gluconobacter japonicus LMG 26773, Gluconobacter japonicus LMG 1281, and Clostridium pasteurianum) that were able to grow with 5-KF as a substrate. Furthermore, Gluconobacter oxydans 621H could use 5-KF as a carbon and energy source in the stationary growth phase. The enzymes involved in the utilization of 5-KF were heterologously overproduced in Escherichia coli, purified and characterized. The enzymes were referred to as 5-KF reductases and belong to three unrelated enzymatic classes with highly different amino acid sequences, activities, and structural properties. Furthermore, we could show that 15 members of the most common and abundant intestinal bacteria cannot degrade 5-KF, indicating that this sugar derivative is not a suitable growth substrate for prokaryotes in the human intestine. Key points • Some environmental bacteria are able to use 5-KF as an energy and carbon source. • Four 5-KF reductases were identified, belonging to three different protein families. • Many gut bacteria cannot degrade 5-KF.

Salivary protein glycopatterns for natural regulation of oral microbiota

The oral microbiota is the direct precursor of dental caries and periodontitis, which are the most common microbial-induced diseases worldwide. The distinct microenvironment at the oral barrier breeds unique microbial communities, which are regulated by host factors (inflammation or dietary sugars)1. Increasing evidence indicates that dysbiosis of oral microbial communities is associated with many human diseases2-5. Our studies demonstrated that human disease could induce different alterations in salivary protein glycopatterns6. However, the relationship between salivary protein glycopatterns and oral microbial communities is unknown. Here, we report that altered salivary protein glycopatterns, namely, fucosylated or sialylated structures induced by gastric cancer (GC) or type 2 diabetes mellitus (T2DM), respectively, are also drivers of dysbiosis of oral microbial communities and ultimately dental caries and periodontitis. The fucosylated neoglycoproteins and sialic acid (SA) α2-3 galactose (Gal) structure can inhibit the growth or/and adhesion of Aggregatibacter segnis and Candida albicans from the oral cavity of patients with GC and T2DM, respectively. These findings provide a novel theory that dynamic communities of oral microbiota are regulated naturally by host salivary protein glycopatterns, having important implications for developing new carbohydrate drugs for oral and body health.