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Tain, Y. Fructose and Gut Microbiota. Encyclopedia. Available online: (accessed on 24 February 2024).
Tain Y. Fructose and Gut Microbiota. Encyclopedia. Available at: Accessed February 24, 2024.
Tain, You-Lin. "Fructose and Gut Microbiota" Encyclopedia, (accessed February 24, 2024).
Tain, Y. (2022, March 09). Fructose and Gut Microbiota. In Encyclopedia.
Tain, You-Lin. "Fructose and Gut Microbiota." Encyclopedia. Web. 09 March, 2022.
Fructose and Gut Microbiota

Fructose is a structural isomer of glucose and galactose. As eating a fructose-rich diet is becoming more common, the effects of maternal fructose intake on offspring health is of increasing relevance. The gut is required to process fructose, and a high-fructose diet can alter the gut microbiome, resulting in gut dysbiosis and metabolic disorders. 

fructose gut microbiota

1. Fructose and Gut Microbiota

Major functions of the gut microbiota include the maintenance of the structural integrity of the gut, host nutrient metabolism, regulation of immune homeostasis, xenobiotic and drug metabolism, and fermentation of non-digestible substrates [1]. It is becoming increasingly obvious that a loss of balance in gut microbiota, termed dysbiosis, is implicated in numerous human diseases. Gut microbiota-derived metabolites are key molecular mediators between the microbiota and the host [2]. Certain metabolites, notably bile acids, SCFAs, branched-chain amino acids, tryptophan derivatives, and trimethylamine N-oxide (TMAO), have been connected to the pathogenesis of metabolic disorders [2]. Emerging data have demonstrated an association between the fructose and gut microbiota dysbiosis in metabolic syndrome-related disorders [3][4]. Although prior research reports that the gut microbiota compositions differ between healthy subjects and patients with metabolic syndrome [5], the causality is still insufficiently demonstrated.

2. How Fructose Alters Gut Microbiota and Their Metabolites

The tight junctions form a selectively permeable barrier defending the host by avoiding the entry of intestinal microbes and their products. Chronic consumption of fructose is accompanied with a loss of intestinal tight junction proteins, resulting in elevated translocation of endotoxin [6]. A high-fructose diet fed to mice has been shown to result in the development of hyperglycemia, adiposity, dyslipidemia, endotoxemia, and glucose intolerance, which coincided with lost gut microbial diversity in these mice [7]. A high-fructose diet also altered gut microbiota compositions, characterized by a lower abundance of Bacteroidetes and a markedly increased proportion of Proteobacteria. Another study demonstrated that a high-fructose diet induced steatosis with dyslipidemia and was associated with decreased beneficial microbes Bifidobacterium and Lactobacillus [8].
Additionally, several lines of evidence indicate fructose is able to mediate microbiota-derived metabolites. First, SCFA levels in plasma from rats fed with a high-fructose diet were reduced [9]. Another line of evidence comes from metabonomic analysis. The metabolic profiling from high-fructose- and salt-fed rats showed the increase of TMAO in urine was associated with metabonomic progression axes, progressing from normal to insulin resistance and hypertension status [10]. This final status of hypertension is an observation regarding mice fed a HFCS-moderate fat diet and displayed anxio-depressive behavior coinciding with altered gut microbiota compositions and tryptophan metabolites [11]. Altogether, these studies indicate that fructose is able to induce gut microbiota dysbiosis in three ways: it disrupts the gut barrier triggering endotoxemia and inflammation; it alters gut microbial profile and diversity; and it influences key microbial metabolites.

3. The Impact of Maternal Fructose Diet on Gut Microbiome

Much of the work investigating the actions of fructose on gut microbiota has directly studied the fructose-fed animals, yet relatively little data exist on its programming effect on the offspring’s gut microbiota. A summary of animal studies demonstrating the association between gut microbiome, maternal high-fructose intake, and subsequent development of diseases in adult offspring is provided in Table 1 [12][13][14][15][16]. As shown in Table 1, rats were the dominant animal species being used. The major adverse outcome is hypertension [12][14][15][16].
Table 1. Maternal high-fructose diet-induced adult disease of developmental origins related to gut microbiota dysbiosis in animal models.
Animal Models Species/
Programming Mechanisms Related to Gut Microbiota Adverse Offspring Outcomes References
Maternal 60% fructose diet SD rat/M Decreased SCFA receptor GPR41 and GPR43 expression Hypertension [12]
Maternal 10% fructose water Wistar rat/F Reduced genera Lactobacillus and Bacteroides Adiposity, dyslipidemia, and insulin resistance [13]
Maternal 60% fructose diet SD rat/M Reduced genus Akkermansia abundance; Increased plasma TMA level Hypertension [14]
Maternal plus post-weaning 60% fructose diet SD rat/M Decreased abundance of genera LactobacillusLeuconostoc, and Turicibacter Hypertension [15]
Maternal 60% fructose diet and minocycline administration SD rat/M Reduced α-diversity, Decreased genera abundance of LactobacillusRuminococcus, and Odoribacter; Increased abundance of Akkermansia; Increased SCFA receptor expression Hypertension [16]
SCFA, Short-chain fatty acid. GPR, G protein-coupled receptor. TMA, Trimethylamine.
Adding 10% fructose to the drinking water of pregnant rats significantly altered the maternal microbiome [13]. Notably, there was a significant reduction in Lactobacillus and Bacteroides; both are commonly known as beneficial microbes. Their female offspring developed adiposity, dyslipidemia, and insulin resistance at 8 weeks of age. These findings were associated with a reduction in the expression of tight junction proteins in the offspring. Similarly, a maternal high-fructose diet also alters the microbiome in rat offspring. Maternal high-fructose diet-induced hypertension in adult male offspring is related to decreased genus Akkermansia abundance [14]. Another study showed adult offspring born to dams that received a 60% fructose diet during pregnancy and lactation displayed an increase in the Firmicutes to Bacteroidetes ratio [15], a microbial marker of hypertension [16]. A follow-up study identified that maternal plus post-weaning high-fructose diet programs caused hypertension and coincided with a decreased abundance of genera Lactobacillus, Leuconostoc and Turicibacter [15].
Moreover, a maternal high-fructose diet not only alters microbiota compositions but also their metabolites in adult offspring. An association has been found between maternal high-fructose-induced programmed hypertension and gut microbial metabolites, trimethylamine (TMA), and acetate [14]. TMA is a microbiota-derived precursor of TMAO. Like TMAO, TMA is emerging as a cardiovascular risk marker [17][18]. The major SCFAs produced are acetate, propionate, and butyrate. Evidence shows that SCFAs regulate BP via interacting with SCFA receptors, including G protein-coupled receptor 41 (GPR41), GPR43, and olfactory receptor 78 (Olfr78) [19]. Feeding mother rats with a 60% fructose diet causes elevation of BP in adult offspring, relevant to an increase in plasma acetate level and a decrease in renal GPR41 and GPR43 expression [12]. Considering acetate is a ligand for Olfr78 to induce vasoconstriction and GPR41 exhibits vasodilatory action [20], these findings suggest that SCFAs and their receptors may be involved in maternal high-fructose diet programs leading to hypertension in their offspring.
Abnormalities in early-life gut microbiota were related to a number of adverse offspring outcomes, including obesity [21][22], insulin resistance [21][23], dyslipidemia [23], nonalcoholic fatty liver disease [22], and cardiovascular disease (CVD) [23]. All of these diseases are connected with fructose-induced developmental programming. Limited information is available about the use of gut microbiota-targeted therapies to study other adult diseases programmed by maternal fructose consumption, such as obesity, liver steatosis, dyslipidemia, insulin resistance, and cardiovascular disease.
Using Lactobacillus as a probiotic intervention, previous studies demonstrated it slowed progression of liver steatosis [24] and type II diabetes [25] in fructose-fed rats and mice. Additionally, maternal Lactiplantibacillus plantarum WJL treatment prevented adult offspring against CVD [23]. Another study revealed that maternal oligofructose therapy attenuated hepatic steatosis and insulin resistance induced in adult offspring born to dams received high-sucrose/-fat diets [26]. At this point, these studies evaluating the effect of gut microbiota-targeted therapies have only examined the established disease model or developmental models programmed by other insults. There will be a growing need to examine their reprogramming effects in adult diseases related to maternal fructose-induced developmental programming.
Furthermore, prior research demonstrated that excess maternal fructose consumption that caused adverse fetal outcomes was related to increased placental uric acid levels, while treatment of mother mice with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels and improved fetal weights and serum triglycerides [27]. Given that uric acid is a key mediator in high-fructose intake-related disorders [28] and intestinal microbes like Lactobacillus and Pseudomonas are known to participate in the metabolism of uric acid [29], probiotics Lactobacilli with uric acid-lowering effects targeting the gut microbiota may be a potential therapy for fructose-induced programming in further research.

4. How Gut Microbiota Links to Common Mechanisms Underlying Fructose-Induced Developmental Programming

In addition to gut microbiota dysbiosis, a number of mechanisms are proposed to be involved in fructose-induced developmental programming and the resulting adult disease. These molecular mechanisms include oxidative stress, aberrant renin–angiotensin system (RAS), nutrient sensing signals, epigenetic regulation, arachidonic acid metabolism pathway, etc. [30][31][32][33][34].

4.1. Oxidative Stress

The fetus is extremely sensitive to oxidative damage during development because of its low antioxidant capacity [35]. A maternal high-fructose diet has been shown to induce various features of metabolic syndrome in adult offspring. Among them, dyslipidemia [36], insulin resistance [37], and hypertension [33][34] have been related to oxidative stress. Oxidative stress can reduce nitric oxide (NO) production by enhancing asymmetric dimethylarginine production (ADMA, an endogenous inhibitor of NO synthase) [38]. Increased plasma ADMA levels and decreased NO bioavailability have been reported in maternal fructose diet-induced programmed hypertension [39].
Conversely, antioxidants can reduce oxidative stress and prevent adult disease of developmental origins [40]. Melatonin is an antioxidant. Its use in pregnancy and lactation has shown to have beneficial effects on hypertension programmed by maternal high-fructose consumption [39]. Because fructose-induced developmental programming induces various features of metabolic syndrome targeting different organs, there is still a lack of reliable data on which organ-specific redox-sensitive signals are responsible for fructose-triggered programming processes.
Fructose-induced developmental programming, apart from oxidative stress, has been linked to gut microbiota. Gut microbial communities have been shown to trigger redox signaling and maintain host–microbiota homeostasis [41]. When an imbalance in the redox state occurs, inflammatory responses may mediate collateral tissue damage and end organ dysfunction [41]. Therefore, oxidative stress seems to work together with gut microbiota behind fructose-induced developmental programming. Attention will be needed to be paid to understanding how gut microbiota interrelates with oxidative stress to trigger organ-dependent programming processes, and whether interventions targeting gut microbiota in pregnancy may also reduce oxidative stress to prevent adult progeny against adult disease of developmental origins.

4.2. Aberrant RAS

The RAS is closely connected with adult disease of developmental origins [42]. The RAS is composed of different angiotensin peptides with diverse biological actions mediated by distinct receptors [43]. In general, activation of the classical axis of ACE/angiotensin II (ANG II)/ANG II type 1 receptor (AT1R) triggers vasoconstriction, oxidative stress, and inflammation. Maternal high-fructose diet-induced hypertension is relevant to the aberrant activation of RAS, represented by increases in (pro)renin receptor, angiotensinogen, and angiotensin-converting enzyme (ACE) in the kidneys (minocycline). In contrast, the non-classical RAS, composed mainly by the ACE2/angiotensin-(1-7) (Ang-(1-7))/Mas receptor (MasR)/ANG II type 2 receptor (AT2R), can counterbalance the adverse effects of ANG II. In the high-fructose diet plus 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure model, 3,3-dimethyl-1-butanol (DMB) therapy protected against hypertension coinciding with decreased AT1R and increased AT2R protein abundance [44]. Emerging evidence suggests a bidirectional interaction between the gut microbiome and RAS; gut microbiota-derived metabolites can modulate the gut RAS, while alterations in RAS shape microbiota composition and metabolic activity [45]. Considering maternal fructose consumption altered gut microbiota and the RAS concurrently, more work is required to explore the interaction between gut microbiome and the RAS implicating the pathogenesis of fructose-induced developmental programming.

4.3. Nutrient-Sensing Signals

During fetal development, nutrient-sensing signals regulate fetal metabolism in response to maternal nutritional status [46]. Accordingly, disturbed nutrient-sensing signals in pregnancy have a distinctive role in the pathogenesis of adult disease of developmental origins [47]. A number of signals, including silent information regulator transcript (SIRT), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptors (PPARs), and PPARγ coactivator-1α (PGC-1α), are related to developmental programming [48]. SIRT1 and AMPK can mediate deacetylation and phosphorylation of PGC-1α, respectively. The downstream signaling effect of PGC-1α is PPARγ, which governs the expression of specific sets of PPAR target genes involved in hypertension of developmental origins [49]. In a maternal and post-weaning high-fructose diet rat model, renal mRNA expression of AMPK, PGC-1α, and PPARs were shown to decrease [15]. On the contrary, resveratrol, an AMPK activator, can mediate these nutrient-sensing signals to activate PPAR target genes and thereby protect offspring against metabolic syndrome-related programmed processes [15]. Additionally, maternal insulin therapy, shown to prevent the elevation of BP in adult offspring born to fructose-fed dams, was associated with enhanced phosphorylated AMPKα2 protein levels [15]. These observations suggest a potential connection between nutrient-sensing signals and gut microbiota underlying fructose-induced developmental programming.

4.4. Epigenetic Regulation

The epigenetic modification of genes has emerged as a key mechanism for developmental programming [50]. These modifications include DNA methylation, histone modification, and noncoding RNAs, all of which control gene activation or silencing [51]. A previous work recognized significant alterations of renal transcriptome in 1-day-old male offspring exposed to maternal high-fructose intake by using next-generation RNA sequencing (NGS) analysis [33]. In total, 2706 differential expressed genes (DEGs) (1214 up- and 1492 down-regulated genes) were identified. Among them, Cyp2c23, Hpgds, Ptgds and Ptges belonging to arachidonic acid metabolism were involved in maternal high-fructose diet-induced hypertension [34]. Moreover, a number of genes regulating fructose metabolism, fatty acid metabolism, glycolysis/gluconeogenesis, and insulin signaling appear to be regulated by a maternal high-fructose diet in different organs at 1 day of age in follow-up study [52]. Notably, a maternal high-fructose diet induces differential alterations of gene expression in the brain, kidney, heart, and urinary bladder in progeny. NGS results suggest that epigenetic regulation may be involved in the developmental programming of various adult diseases in an organ-specific manner. Additionally, maternal fructose exposure altered the miR-206 expression level in offspring liver that increased promoter methylation at Lxra gene [51][53]. Gut microbiota and their metabolites have shown the ability of epigenetic programming of multiple host tissues [54]. The SCFAs can form acetyl-CoA, the substrate for histone acetyltransferase (HAT) enzymes. Further, butyrate is a known histone deacetylase (HDAC) inhibitor. Both scenarios could affect histone modification. Thus, maternal fructose diet-related gut dysbiosis induces epigenetic programming of offspring genes, and corresponding epigenetic mechanisms together with associated gut microbes await further elucidation.


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