Non-glucose sugars are metabolized through specific enzymatic pathways in the body
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Peer-reviewed literature demonstrates that non-glucose dietary sugars such as fructose and galactose are processed through distinct enzymatic and fructolytic pathways that differ from standard glucose metabolism.
<h4>Background</h4>High fructose consumption has been suggested to contribute to several features of metabolic syndrome including insulin resistance, but to our knowledge, no previous meta-analyses have investigated the effect of fructose on insulin sensitivity in nondiabetic subjects.<h4>Objective</h4>We performed a systematic review and meta-analysis of controlled diet-intervention studies in nondiabetic subjects to determine the effect of fructose on insulin sensitivity.<h4>Design</h4>We searched MEDLINE, EMBASE, and the Cochrane Library for relevant trials on the basis of predetermined eligibility criteria. Two investigators independently performed the study selection, quality assessment, and data extraction. Results were pooled with the use of the generic inverse-variance method with random effects weighting and were expressed as mean differences (MDs) or standardized mean differences (SMDs) with 95% CIs.<h4>Results</h4>Twenty-nine articles that described 46 comparisons in 1005 normal-weight and overweight or obese participants met the eligibility criteria. An energy-matched (isocaloric) exchange of dietary carbohydrates by fructose promoted hepatic insulin resistance (SMD: 0.47; 95% CI: 0.03, 0.91; P = 0.04) but had no effect on fasting plasma insulin concentrations (MD: -0.79 pmol/L; 95% CI: -6.41, 4.84 pmol/L; P = 0.78), the homeostasis model assessment of insulin resistance (HOMA-IR) (MD: 0.13; 95% CI: -0.07, 0.34; P = 0.21), or glucose disposal rates under euglycemic hyperinsulinemic clamp conditions (SMD: 0.00; 95% CI: 20.41, 0.41; P = 1.00). Hypercaloric fructose (∼25% excess of energy compared with that of the weight-maintenance control diet) raised fasting plasma insulin concentrations (MD: 3.38 pmol/L; 95% CI: 0.03, 6.73 pmol/L; P < 0.05) and induced hepatic insulin resistance (SMD: 0.77; 95% CI: 0.28, 1.26; P < 0.01) without affecting the HOMA-IR (MD: 0.18; 95% CI: -0.02, 0.39; P = 0.08) or glucose disposal rates (SMD: 0.10; 95% CI: -0.21, 0.40; P = 0.54). Results may have been limited by the low quality, small sample size, and short duration (mostly <60 d) of included trials.<h4>Conclusions</h4>Short-term fructose consumption, in isocaloric exchange or in hypercaloric supplementation, promotes the development of hepatic insulin resistance in nondiabetic adults without affecting peripheral or muscle insulin sensitivity. Larger and longer-term studies are needed to assess whether real-world fructose consumption has adverse effects on insulin sensitivity and long-term outcomes.
BACKGROUND &AIMS
Dietary sugars are absorbed in the hepatic portal circulation as glucose, fructose, or galactose. The gut and liver are required to process fructose and galactose into glucose, lactate, and fatty acids. A high sugar intake may favor the development of cardio-metabolic diseases by inducing Insulin resistance and increased concentrations of triglyceride-rich lipoproteins.
METHODS
A narrative review of the literature regarding the metabolic effects of fructose-containing sugars.
RESULTS
Sugars' metabolic effects differ from those of starch mainly due to the fructose component of sucrose. Fructose is metabolized in a set of fructolytic cells, which comprise small bowel enterocytes, hepatocytes, and kidney proximal tubule cells. Compared to glucose, fructose is readily metabolized in an insulin-independent way, even in subjects with diabetes mellitus, and produces minor increases in glycemia. It can be efficiently used for energy production, including during exercise. Unlike commonly thought, fructose when ingested in small amounts is mainly metabolized to glucose and organic acids in the gut, and this organ may thus shield the liver from potentially deleterious effects.
CONCLUSIONS
The metabolic functions of splanchnic organs must be performed with homeostatic constraints to avoid exaggerated blood glucose and lipid concentrations, and thus to prevent cellular damages leading to non-communicable diseases. Excess fructose intake can impair insulin-induced suppression of glucose production, stimulate de novo lipogenesis, and increase intrahepatic and blood triglyceride concentrations. With chronically high fructose intake, enterocyte can switch to lipid synthesis and accumulation of triglyceride, possibly causing an enterocyte dysfunction.
Highlights • Ethylene metabolism regulated flavonoid (and sugar) contents and composition.• Ethylene induced anthocyanin and reduced flavonol and flavan-3-ols in plum fruit.• Anthocyanins positively correlate with sucrose and galactose metabolic pathways.• Flavonol and flavan-3-ols associated with sorbitol, fructose, and glucose contents.
D-tagatose is a rare sugar found in nature that contains less than one-third of sucrose's calories while maintaining 92% of its sweetness. Owing to its physiological properties, such as lowering blood sugar, preventing obesity, anti-caries, and regulation of intestinal flora, it is being used as a new kind of healthy sweetener. This paper conducts a systematic review of advances in its biosynthesis research, focusing on the catalytic mechanisms of key enzymes and the multi-substrate conversion strategies. Specifically, by analyzing L-Arabinose Isomerase (L-AI), the study compares enzymatic conversion pathways for various substrates, including monosaccharides (D-galactose, D-fructose, D-glucose, etc.), disaccharides (lactose, sucrose), and maltodextrin. This study thoroughly examines the advantages and limitations of each pathway in terms of reaction efficiency, substrate cost, and industrial adaptability. The goal of this research is to provide guidance for D-tagatose's industrial manufacturing, advancing its efficient biosynthesis and commercial application.
There is much interest in the role of sweeteners such as table sugar (sucrose) and high-fructose corn syrup in obesity and metabolic disease. Both sweeteners consist of glucose and fructose, two six-carbon isomeric sugars. Whereas glucose ingestion may promote obesity through its effects to stimulate insulin secretion, fructose has unique metabolic effects that promote triglyceride synthesis and fat accumulation. These effects arise from fructose's well-known role as a signal of metabolic plenty. Under modern conditions of overnutrition, chronic excess fructose drives features of metabolic syndrome. Emerging evidence further links fructose to cancer and dementia. Here we review the biochemical, molecular and physiological distinctions between fructose and glucose, as well as the endogenous fructose pathway that makes fructose from glucose. Through this Review, we highlight the role of fructose not only as a caloric source, but also as a regulator of metabolic health and disease.
Bacterial cellulose (BC) is a high-purity biopolymer with significant potential for sustainable material applications. However, its production remains limited by the metabolic behavior and compositional complexity of available carbon substrates. Simple sugars such as fructose, glucose, and sucrose support BC synthesis but differ in their metabolic pathways and associated byproduct formation, which can influence medium pH and cellulose biosynthesis. Across refined substrates, fructose generally outperforms glucose, producing the most favorable balance between productivity and structure. Reported fructose-based yields range from 1.55 to 6.29 g/L depending on the composition. In media containing hexoses, such as fructose, and three-carbon compounds, such as glycerol and pyruvate, biosynthesis proceeds via the pentose phosphate pathway. Additionally, pyruvate can be further metabolized via gluconeogenesis coupled with the tricarboxylic acid cycle, producing more BC precursors. In contrast, glucose-based yields are limited primarily by oxidation to gluconic acid, and sucrose often shows slower or lower initial production due to delayed metabolism, depending on the medium’s composition. Interestingly, structural trends showed that yield and structural quality are not always coupled. Fructose-based BC can reach around 90% to 92% crystallinity index (CrI) and is associated with lower porosity and larger nanoribbon networks, while sucrose-based BC can reach up to a 95.2% CrI despite s
Fructose and high-fructose corn syrup (HFCS) have become central to the debate on metabolic health and the rising prevalence of type 2 diabetes. Chemically, fructose is a monosaccharide found naturally in fruits and honey, whereas HFCS is an industrially produced sweetener composed of varying proportions of free fructose and glucose. While fructose has unique metabolic effects, its impact is comparable to other sugars when consumed in excess. HFCS is widely used in processed foods and sugar-sweetened beverages (SSBs) due to its high sweetness and low production cost. However, its metabolic effects remain a topic of scientific and public health concern. Animal and human studies suggest that excessive fructose consumption contributes to metabolic disturbances, including insulin resistance, impaired glucose tolerance, and increased fat accumulation in the liver through <i>de novo</i> lipogenesis (DNL). Unlike glucose, fructose bypasses key regulatory steps in glycolysis, leading to unregulated hepatic uptake and lipid synthesis. Epidemiological studies have reported a higher prevalence of type 2 diabetes in countries with greater HFCS availability, independent of obesity rates. Despite this, there remains controversy regarding whether HFCS is a direct contributor to diabetes or if overall energy intake plays a more significant role. This study aims to analyze the chemical composition of fructose and HFCS and their potential role in the development of type 2 diabetes. Additionally, it briefly discusses the global policy measures, such as sugar taxation and public health interventions, aimed at reducing sugar consumption and mitigating diabetes risk.
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