Intestinal Fructose and Glucose Metabolism in Health and Disease

Merino, Beatriz; Fernández-Díaz, Cristina M; Cózar‐Castellano, Irene; Perdomo, Germán

doi:10.3390/nu12010094

Cited by 67 publications

(51 citation statements)

References 284 publications

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“…High consumption of fructose, one of the critical risk factors contributing to the development of NAFLD, increases gut permeability and alters the microbiota composition in the gastrointestinal tract and therefore promotes bacterial translocation and metabolic endotoxemia resulting in lipid accumulation and low-grade inflammation leading finally to hepatic steatosis and metabolic disease. Low doses of fructose are cleared by the small intestine, but high doses of fructose saturate the absorption and catabolism of fructose leading to fructose spill-over not only to the liver [ 42 ] but also to the colonic microbiota, which further metabolizes fructose [ 43 ]. The resulting metabolites become an energy source for bacteria and influence the gut environment [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

et al. 2020

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High consumption of fructose and high-fructose corn syrup is related to the development of obesity-associated metabolic diseases, which have become the most relevant diet-induced diseases. However, the influences of a high-fructose diet on gut microbiota are still largely unknown. We therefore examined the effect of short-term high-fructose consumption on the human intestinal microbiota. Twelve healthy adult women were enrolled in a pilot intervention study. All study participants consecutively followed four different diets, first a low fructose diet (< 10 g/day fructose), then a fruit-rich diet (100 g/day fructose) followed by a low fructose diet (10 g/day fructose) and at last a high-fructose syrup (HFS) supplemented diet (100 g/day fructose). Fecal microbiota was analyzed by 16S rRNA sequencing. A high-fructose fruit diet significantly shifted the human gut microbiota by increasing the abundance of the phylum Firmicutes, in which beneficial butyrate producing bacteria such as Faecalibacterium, Anareostipes and Erysipelatoclostridium were elevated, and decreasing the abundance of the phylum Bacteroidetes including the genus Parabacteroides. An HFS diet induced substantial differences in microbiota composition compared to the fruit-rich diet leading to a lower Firmicutes and a higher Bacteroidetes abundance as well as reduced abundance of the genus Ruminococcus. Compared to a low-fructose diet we observed a decrease of Faecalibacterium and Erysipelatoclostridium after the HFS diet. Abundance of Bacteroidetes positively correlated with plasma cholesterol and LDL level, whereas abundance of Firmicutes was negatively correlated. Different formulations of high-fructose diets induce distinct alterations in gut microbiota composition. High-fructose intake by HFS causes a reduction of beneficial butyrate producing bacteria and a gut microbiota profile that may affect unfavorably host lipid metabolism whereas high consumption of fructose from fruit seems to modulate the composition of the gut microbiota in a beneficial way supporting digestive health and counteracting harmful effects of excessive fructose.

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Section: Discussionmentioning

confidence: 99%

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

et al. 2020

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“…As a central organ involved in regulating energy homeostasis, the liver coordinates interactions with other organs that are critical for the maintenance of energy homeostasis. Dietary sugars such as fructose move from the small intestine into the blood circulation by means of a passive transport process throughout the apical border of enterocytes that is triggered by members of the facilitative glucose/fructose transporter (GLUT) family such as GLUT5 ( Merino et al, 2019 ) ( Figure 4 ). Thereafter, the sugar is transported toward the liver via the hepatic portal vein where it activates the production of glucose and lipid synthesis.…”

Section: The Way How Fructose Influences Non-alcoholic Fatty Liver DImentioning

confidence: 99%

Fructose and Non-Alcoholic Steatohepatitis

Roeb

Weiskirchen

2021

Front. Pharmacol.

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Background: The excessive consumption of free sugars is mainly responsible for the high prevalence of obesity and metabolic syndrome in industrialized countries. More and more studies indicate that fructose is involved in the pathophysiology and also in the degree of disease of non-alcoholic fatty liver disease (NAFLD). In epidemiologic studies, energy-adjusted higher fructose consumption correlates with NAFLD in overweight adults. In addition to glucose, fructose, as an equivalent component of conventional household sugar, appears to have negative metabolic effects in particular due to its exclusive hepatic metabolism. Liver-related mortality is strictly associated with the degree of fibrosis, whereas the most common cause of death in patients suffering from NAFLD and non-alcoholic steatohepatitis (NASH) are still cardiovascular diseases. In this review article, we have summarized the current state of knowledge regarding a relationship between fructose consumption, liver fibrosis and life expectancy in NASH.Method: Selective literature search in PubMed using the keywords ‘non-alcoholic fatty liver’, ‘fructose’, and ‘fibrosis’ was conducted.Results: The rate of overweight and obesity is significantly higher in both, adult and pediatric NASH patients. The consumption of free sugars is currently three times the maximum recommended amount of 10% of the energy intake. The current literature shows weight gain, negative effects on fat and carbohydrate metabolism and NASH with hypercaloric intake of fructose.Conclusions: Excessive fructose consumption is associated with negative health consequences. Whether this is due to an excess of energy or the particular metabolism of fructose remains open with the current study situation. The urgently needed reduction in sugar consumption could be achieved through a combination of binding nutritional policy measures including taxation of sugary soft drinks. Previous studies suggest that diet-related fructose intake exceeding the amount contained in vegetables and fruits lead to an increase of hepatic lipogenesis. Thus, further studies to clarify the protective contribution of low-fructose intake to positively influence NAFLD in industrial population are urgently required.

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“…Indeed, high-fructose feeding in mice (30% ( w / v ) fructose in the drinking water or 30% fructose or 60% sucrose (% kcal) in chow) resulted in more severe NAFLD phenotypes compared to isocaloric high-glucose feeding [ 35 , 36 , 37 ]. The explanation for this difference is based on the notion that glucose and fructose metabolism are quite different [ 38 , 39 , 40 ]. Once glucose is absorbed by the small intestine, it mostly bypasses the liver and is distributed to the whole body, including organs that avidly take up glucose (e.g., skeletal muscle, adipose tissues, and the brain).…”

Section: Hepatic Fructose Metabolism and Nafldmentioning

confidence: 99%

Organismal Fructose Metabolism in Health and Non-Alcoholic Fatty Liver Disease

Skenderian

Park

Jang

2020

Biology

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NAFLD has alarmingly increased, yet FDA-approved drugs are still lacking. An excessive intake of fructose, especially in liquid form, is a dietary risk factor of NAFLD. While fructose metabolism has been studied for decades, it is still controversial how fructose intake can cause NAFLD. It has long been believed that fructose metabolism solely happens in the liver and accordingly, numerous studies have investigated liver fructose metabolism using primary hepatocytes or liver cell lines in culture. While cultured cells are useful for studying detailed signaling pathways and metabolism in a cell-autonomous manner, it is equally important to understand fructose metabolism at the whole-body level in live organisms. In this regard, recent in vivo studies using genetically modified mice and stable isotope tracing have tremendously expanded our understanding of the complex interaction between fructose-catabolizing organs and gut microbiota. Here, we discuss how the aberrant distribution of fructose metabolism between organs and gut microbiota can contribute to NAFLD. We also address potential therapeutic interventions of fructose-elicited NAFLD.

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Intestinal Fructose and Glucose Metabolism in Health and Disease

Cited by 67 publications

References 284 publications

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

Fructose-Induced Intestinal Microbiota Shift Following Two Types of Short-Term High-Fructose Dietary Phases

Fructose and Non-Alcoholic Steatohepatitis

Organismal Fructose Metabolism in Health and Non-Alcoholic Fatty Liver Disease

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