Ribose sugar and inflammation control -
It can be difficult to get enough from dietary sources, however. This natural sugar is available in health stores and online in supplement form as a powder, chewable tablet or capsule. You can take the powder in water or add it to other beverages, like smoothies, or mix it into kefir or yogurt.
Powder form is definitely a popular way to take it, but reading D-ribose reviews may help you to determine which supplement is best for your you. It is also a component of multi-ingredient supplements for energy. How much D-ribose should you take in supplement form?
Most makers of these supplements recommend doses between one to 10 grams per day. When should I take D-ribose? To improve the ability of people with coronary artery disease to exercise, the following D-ribose dosage by mouth has been studied: 15 grams four times daily taken one hour prior to exercise until the end of the exercise session.
In other words, take three grams every 10 minutes during exercises. This has been used to decrease muscle stiffness and cramps caused by exercising.
Ribose and deoxyribose are both five-carbon sugars that each contain 10 hydrogen atoms. The molecular formula of ribose is C 5 H 10 O 5, and the molecular formula of deoxyribose 2-deoxyribose is C 5 H 10 O 4.
Does DNA contain ribose? It is a component of RNA while deoxyribose is part of DNA. RNA stands for ribonucleic acid, and it is a complex compound that plays a vital role in cellular production of proteins.
It also replaces DNA deoxyribonucleic acid as a carrier of genetic codes in some viruses. The biggest difference between deoxyribose vs. ribose is one oxygen atom. Meanwhile, the deoxyribose in DNA is a modified sugar and lacks one oxygen atom. This single oxygen atom difference between the two sugars is key to distinguishing the two sugars within organisms.
For most people, D-ribose is typically safe by mouth on a short-term basis or when a health care provider administers it intravenously by IV. Are there any D-ribose dangers? Some potential side effects include upset stomach, diarrhea, nausea and headache.
Does ribose raise blood sugar? Actually, it may decrease blood sugar so, typically, people with hypoglycemia or diabetes should not take these type of supplements.
In addition, you should not take it two weeks prior to any surgery due to its possible blood sugar effects. Drugs known to moderately interact with this naturally occurring sugar include insulin and other antidiabetes drugs.
Other things that may have more minor interactions include alcohol, aspirin, choline magnesium trisalicylate Trilisate , propranolol Inderal and salsalate Disalcid. Check with your doctor before taking these supplements if you are pregnant, nursing, have an ongoing medical condition or currently take any medication.
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Axe on Youtube 2. Low levels of serum C-peptide, glucagon and insulin and brain insulin were also detected in diabetic rats Supplementary Figure 1D.
These data conformed to the requirements for using rats as a diabetic model, which was observed as D-glucose dysmetabolism. To investigate whether D-ribose dysmetabolism occurs in T1DM, we monitored urine D-ribose levels every other week. As shown in Figure 1A , the concentrations of urine D-ribose in diabetic rats were significantly higher than those in control rats P P P Figure 1B and 1C , respectively.
Together with the results above, these results indicated that T1DM rats exhibit D-glucose and D-ribose dysmetabolism. However, further investigation was needed to determine why D-ribose levels were increased in T1DM. Figure 1. Increase in the levels of D-ribose and related enzymes in type 1 diabetic rats.
Levels of D-ribose in urine were measured at different time intervals panel A. D-ribose levels in serum panel B and the brain panel C were determined within 3 days after dissection.
The expression and activity levels of ribokinase, transketolase TKT , 5-phosphoribosyl 1-pyrophosphate PRPP and glucose-6 phosphate dehydrogenase G6PD in the brain were measured with ELISA kits panel D and E. All values are expressed as the mean ± S.
TKT is a key enzyme in the nonoxidative branch of the pentose phosphate pathway PPP that is involved in the metabolism of D-ribose derivatives [ 33 , 34 ]. To investigate the mechanism of the D-ribose metabolic disorder in T1DM, we measured TKT expression and activity by ELISA.
As shown in Figure 1D and 1E , the expression and activity level of TKT were decreased remarkably in T1DM brain tissue. Other kinases, such as ribokinase, D-glucosephosphate dehydrogenase G6PD and ribose phosphate pyrophosphokinase PRPP , which also play roles in regulating D-ribose metabolism, did not show significant changes in expression or activity level in T1DM rats compared to control rats.
To demonstrate that TKT is linked to D-ribose dysmetabolism, we used BTMP to rescue the TKT change in T1DM rats since BTMP can increase the level of thiamine diphosphate and enhances TKT activity [ 35 ]. The results of the liver and kidney assays after BTMP treatment are shown in Supplementary Table 1.
As shown in Figure 2A , administration of BTMP increased brain TKT levels in both normal rats P P Figure 2B. Both the activity and expression Western blots of TKT in the liver and brain were significantly rescued after BTMP administration Supplementary Figure 2.
By contrast, D-ribose levels in both serum and brain were significantly decreased after BTMP administration Figure 2C , 2D. Under the experimental conditions, BTMP did not rescue or decrease FBG levels in T1DM rats Figure 2F.
However, BTMP could partially rescue the body weights of T1DM rats but not the forepaw tension or insulin levels in the brain and serum Supplementary Figure 3. That is, administration of BTMP can regulate the metabolism of D-ribose rather than D-glucose in rats via activation of TKT.
Figure 2. Effect of benfotiamine BTMP on the levels of D-ribose, D-glucose and TKT in T1DM rats. Conditions for the preparation of T1DM rats are shown in Figure 1.
The expression levels of transketolase TKT in the brain panel A and liver panel B were measured with ELISA kits. After 10 weeks of domestication, D-ribose levels in the serum panel C and brain panel D of rats were measured, and D-glucose levels were measured in the brain panel F. Fasting blood glucose FBG was measured every other week panel E.
According to McCrimmon and colleagues, both T1DM and T2DM are related to cognitive dysfunction [ 36 ]. Here, we investigated whether T1DM rats experienced cognitive impairment.
First, compared with control rats, T1DM rats showed significantly fewer correct alterations in the Y maze test Supplementary Figure 4A. In the Morris water maze test, the escape latency in the training session was significantly longer among T1DM rats Supplementary Figure 4B , and the percentage of time spent in the target quadrant in the probe trial was markedly lower for T1DM rats Supplementary Figure 4C.
T1DM rats also showed fewer platform crossings than did control rats, but the difference was nonsignificant Supplementary Figure 4D. Representative images of the performance path of the rats are shown in Supplementary Figure 4E.
These results indicated that T1DM rats exhibited cognitive impairment, which was regarded as type 1 diabetic encephalopathy. In addition, rats with type 1 diabetic encephalopathy also showed anxiety behavior based on open field and elevated plus maze assays Supplementary Figure 5.
To demonstrate whether cognitive impairment in T1DM rats was linked to D-ribose dysmetabolism, we tested the cognitive ability of T1DM rats with BTMP gavage. In the Y maze test, BTMP-gavaged T1DM rats exhibited significantly more correct alterations than in T1DM rats without BTMP gavage Figure 3A.
In the Morris water maze test, T1DM rats gavaged with BTMP spent less time searching for the platform than did T1DM rats without BTMP gavage Figure 3B. After platform withdrawal, the time spent in the target quadrant and the number of platform crossings were significantly higher in the T1DM group gavaged with BTMP than in that without BTMP gavage Figure 3C , 3D.
These data suggested that the alleviation of cognitive impairment by treatment with BTMP is related to a decrease in D-ribose in STZ-induced T1DM rats. Figure 3.
Rescue of spatial learning and memory abilities in T1DM rats with BTMP. Animal groups and treatments were as described in Figure 2 except that rats were subjected to Y maze and Morris water maze tests. The accuracy of Y maze alternation was detected panel A. The escape latency panel B , percentage of time spent in the target quadrant panel C and number of platform crossings panel D were recorded.
Representative images of the performance path are shown panel E. As hyperphosphorylated Tau and the resultant neurofibrillary tangles and AGE are closely related to cognitive impairment [ 37 , 38 ], and high dose D-ribose treatment resulted in AGE aggregation and Tau hyperphosphrylation [ 39 ].
We wondered whether cognition-impaired T1DM rats exhibit Tau hyperphosphorylation and AGE accumulation along with a decrease in D-ribose. At the same time, markedly high AGE levels were detected in both the cortex and hippocampus.
These data suggest that T1DM rats suffer from Tau hyperphosphorylation as well as AGE accumulation in the brain. To investigate whether D-ribose dysmetabolism is linked to Tau hyperphosphorylation and AGE accumulation, we gavaged T1DM rats with BTMP and measured Tau phosphorylation and AGE levels.
As shown in Supplementary Figure 7 , AGE in both the cortex and hippocampus in BTMP-gavaged T1DM rats were significantly decreased compared with those without BTMP gavage. Furthermore, the results from the glycated serum protein GSP assay showed a marked decrease in GSP in T1DM rats after treatment with BTMP Supplementary Figure 7C.
These data demonstrated that D-ribose plays a role in AGE accumulation in T1DM rats. Along with the distinct decrease in AGE accumulation, Tau hyperphosphorylation was also reduced by BTMP administration. Tau phosphorylation levels AT8 and pSer in the cortex and hippocampus were significantly reduced, while nonphosphorylated Tau levels Tau-1 were increased in T1DM rats treated with BTMP compared with control rats Supplementary Figure 7.
That is, Tau hyperphosphorylation is related to the D-ribose dysmetabolism in T1DM rats. Neuronal loss is regarded as the most important pathological feature of age-related cognitive impairment. We performed immunochemical experiments to determine neuronal death in the brains of T1DM rats.
However, neuronal death in the brains of T1DM rats was greatly reduced by treatment with BTMP Figure 4A , 4B. The decrease in D-ribose induced by BTMP occurred with the amelioration of pathological features, such as AGE accumulation, Tau hyperphosphorylation and neuronal death.
These data suggested that D-ribose dysmetabolism is closely related to cognitive impairment and that BTMP can be used as a potential medicine to rescue cognitive impairment via a decrease in D-ribose levels.
Additionally, the anxious behavior was observably improved after BTMP administration in the open field and elevated plus maze assays Supplementary Figure 8. Figure 4. Nissl staining of hippocampal neurons of rats treated with BTMP. Animal groups and treatment were as described in Figure 2 except that hippocampal slices were prepared and stained with cresyl violet panel A.
Numbers of necrotic neurons were counted under a microscope as described in the Materials and Methods panel B. To detect the D-ribose level in T1DM patients, twenty-four participants 8 T1DM patients and 16 age-matched participants without diabetes mellitus were recruited for collection of fasting blood and morning urine.
The summarized characteristics of the participants are shown in Supplementary Table 2. We measured the concentrations of D-ribose in urine and serum by high-performance liquid chromatography HPLC. Figure 5. Comparison of D-ribose levels between T1DM patients and normal participants. D-ribose levels in serum panel A and urine panel B were measured by HPLC as previously described [ 17 ].
All values are shown as the mean ± S. T1DM results in long-term complications in the central nervous system, causing brain cellular dysfunction and cognitive deficits [ 40 ].
As reported in a recent study, T2DM patients suffer from D-ribose and D-glucose dysmetabolism [ 16 ]. In the present study, in addition to D-glucose, endogenous D-ribose was markedly increased in T1DM patients and STZ-induced T1DM rats, which also exhibited AGE accumulation and cognitive impairment accompanied with Tau hyperphosphorylation and neuronal death.
Administration of BTMP decreased D-ribose levels and AGE accumulation and improved cognitive ability in T1DM rats. BTMP also reduced Tau hyperphosphorylation, and neuronal death. All these data indicated that D-ribose dysmetabolism is associated with cognitive impairment in T1DM rat and that the administration of BTMP can ameliorate the loss of neurons and cognitive impairment via regulation of D-ribose.
As a very active aldose, D-ribose exists in urine [ 16 ], serum [ 41 ] and cerebrospinal fluid 0. AGE accumulation is one of the most important features in diabetes and its complications due to the high sugars levels [ 43 ].
The Panel considers that the effects observed in a subchronic toxicity study in Wistar rats could be the consequence of nutritional imbalances but that toxicological effects could not be ruled out [ 25 ]. In accordance with the Guidance for Industry, Center for Drug Evaluation and Research, U.
Administration of an approximate dose 3. D-ribose can also give rise to Tau hyperphosphorylation and Aβ-like deposition in brain tissue and cause endoplasmic reticulum stress, which is toxic to cells and results in apoptosis [ 27 , 39 , 45 ]. Administration of D-ribose can increase hepatic triglyceride and water intake and decrease body weight in SD rats [ 24 ].
Furthermore, formaldehyde was regarded as a risk factor for age-related cognitive impairment [ 46 ]. These finding suggest that high dose D-ribose intake induces toxicity. A high level of D-ribose was also found in the urine of T2DM patients, suggesting the dysmetabolism of D-ribose in T2DM [ 16 ].
Therefore, speculation that D-ribose dysmetabolism is involved in type 1 diabetic encephalopathy and its pathogenesis is reasonable. T1DM rats showed a low level of TKT in brain tissue accompanied by a high level of D-ribose and pathological features of diabetic encephalopathy.
Because D-ribose can be converted from D-glucose through the PPP [ 48 , 49 ], we measured G6PD and ribokinase. However, G6PD and ribokinase did not show a marked change in T1DM rats except for TKT.
These results indicated that STZ-induced T1DM rats did not suffer from dysfunction in G6PD, a key enzyme in the D-glycolytic pathway. Many studies have shown that G6PD is upregulated [ 50 ] or downregulated [ 51 ] in STZ-induced DM rats. Epel demonstrated that the level of G6PD can be regulated by NADP, the critical factor in oxidative stress [ 52 , 53 ].
Many studies have also shown that the expression of G6PD regulates the generation of NADPH to alleviate oxidative stress [ 54 ], suggesting that G6PD would induce dynamic changes in DM.
Mendez et al. showed that neurons maintain the oxidation of G6PD through the PPP to sustain their antioxidant status [ 55 ]. In DM, apart from G6PD, TKT is also an important shunt key enzyme in the PPP [ 34 ]; thus, it makes sense that supplementation with BTMP, acting as a TKT activator [ 56 ], causes a reduction in oxidative stress and affects several anabolic reactions, which might also reduce the level of AGEs [ 57 , 58 ].
BTMP regulates the level of TKT that is directly involved in D-ribose metabolism [ 59 , 60 ]. In this studies, BTMP treatment upregulated TKT, decreased D-ribose levels and simultaneously rescued T1DM rats from diabetic-related encephalopathy but did not decrease D-glucose levels.
These data indicated that dysmetabolism of D-ribose with a decline in TKT function was involved in cognitive impairment in T1DM rats under the experimental conditions. Other laboratories also observed dynamic changes of TKT activity in different tissues in diabetes [ 61 , 62 ].
Consequently, TKT may be used as a potential drug target in the treatment of diabetic-related encephalopathy with high D-ribose levels. BTMP gives a relatively wide range of actions on a number of cellular targets [ 58 ] such as treatment of inflammatory [ 63 ], peritoneal dialysis [ 64 ] and Tauopathy [ 65 ].
BTMP also plays a role in the metabolism of D-glucose [ 66 ]. According to Hammes and colleagues, BTMP activates TKT and prevents the activation of multiple pathways of hyperglycemic damage, such as the hexosamine pathway, the AGE formation pathway and the diacylglycerol-protein kinase C pathway, in diabetic animals [ 56 ].
Though activation of TKT through BTMP is downstream of the D-ribose pathway, which may not be direct evidence, the current work at least showed that a decrease in D-ribose levels could help the amelioration of cognitive impairment.
In fact, BTMP is closely related to D-ribose metabolism. BTMP markedly ameliorates the impaired spatial cognitive ability of T1DM rats in the Y maze and Morris water maze. Administration of BTMP decreases D-ribose levels in the brain, blood and urine of T1DM rats. Chen and coworkers have indicated the correlation between D-ribose and the administration of BTMP in a ZDF rat animal model for diabetes [ 17 ].
Currently, a clinical trial on the treatment of cognitive impairment in Alzheimer's disease a pilot study with BTMP has been started and performed by Gibson and Jordan in the Burke Neurological Institute clinicaltrials.
Here, we would like to suggest that changes in D-ribose in blood and urine should be monitored and analysed in their clinical trials because BTMP can reduce D-ribose levels and ameliorate cognitive impairment in T1DM rats.
Neuronal loss may deteriorate cognitive ability. CA4 is a subfield of the hippocampus that is adjacent to the DG subfield [ 71 , 72 ]. The DG region, which is involved in long-term potentiation LTP and long-term memory, is associated with cognitive ability [ 73 , 74 ].
Here, we also found that T1DM rats showed anxiety-like behaviour Supplementary Figure 8. In previous studies, BTMP was also shown to counteract anxiety-like behaviour [ 77 , 78 ]. The current work suggests that dysregulated D-ribose acts as a novel metabolite in cognitive impairment in T1DM rats by triggering protein glycation, Tau hyperphosphorylation and neuronal loss.
This viewpoint is based on the following observations. First, T1DM rats demonstrated high levels of D-ribose in the serum, urine and brain. Second, T1DM patients also showed high levels of D-ribose in the urine and serum. Third, the expression and activity levels of TKT in the brain and liver of T1DM rats were reduced, which affected D-ribose metabolism [ 60 ].
Fourth, gavage of BTMP as the activator upregulated the expression of TKT in the brain and liver and decreased the levels of D-ribose but not those of D-glucose. Fifth, administration of BTMP suppressed D-ribose levels and rescued cognitive impairment in T1DM rats in both the Y maze and Morris water maze assays, which confirmed the influence of D-ribose dysmetabolism.
Sixth, in T1DM rats with cognitive impairment, AGE accumulation and Tau hyperphosphorylation in the hippocampus and cortex were closely related to D-ribose dysmetabolism. Finally, on the basis of previous work in this laboratory, AGE accumulation, Tau hyperphosphorylation and cognitive impairment were observed in a D-ribose-induced mouse model [ 27 , 79 ].
As described by other studies, both AGE [ 80 ] and Tau hyperphosphorylation [ 81 ] are associated with neuronal death [ 82 ] or loss [ 83 , 84 ], which can cause hippocampal atrophy [ 85 ] and result in cognitive impairment [ 86 , 87 ].
Therefore, D-ribose-induced neuronal loss may be an important contributor to cognitive impairment in T1DM rats. In conclusion, STZ-induced T1DM rats had high levels of D-ribose in their brain, serum and urine in addition to D-glucose.
TKT controlled D-ribose metabolism, and activation of TKT with BTMP decreased D-ribose levels, followed by a reduction in AGE formation, Tau hyperphosphorylation, neuronal death and cognitive impairment.
Thus, dysmetabolism of D-ribose is considered a novel pathological features in rats with T1DM and its complications. T1DM patients also show high levels of D-ribose. However, further investigations should be conducted on T1DM pathologies and complications related to D-ribose. Male SD rats ~8 weeks, weighing ~ g were provided by Vital River Laboratory Animal Technology Co.
The animals were housed in plastic cages measuring 45×30×26 cm 4 rats in each cage. Rats were maintained under standard laboratory conditions, i.
Background: D -ribose Foods that support cholesterol reduction an aldehyde sugar innflammation a necessary component Rbose all living cells. Numerous reports Cojtrol focused on D -ribose Riboxe in Ribose sugar and inflammation control models to assess the negative effects of D -ribose on cognition. However, the results across these studies are inconsistent and the doses and actual effects of D -ribose on cognition remain unclear. This systematic review aimed to evaluate the effect of D -ribose on cognition in rodents. Methods: The articles from PubMed, Embase, Sciverse Scopus, Web of Science, the Chinese National Knowledge Infrastructure, SinoMed, Wanfang, and Cqvip databases were screened.D-ribose, conhrol ubiquitous pentose compound found in all living Weight management aid, serves as a ijflammation constituent of Metabolism-boosting nutrients essential biomolecules, including Conttol, nucleotides, and Ribowe.
It plays a crucial role in various fundamental life processes. Cojtrol the cellular milieu, exogenously suggar D-ribose can undergo phosphorylation to yield ribosephosphate RP.
This RP compound serves a dual purpose: it not dugar contributes to sguar triphosphate ATP production Ribose sugar and inflammation control the nonoxidative phase of inflammxtion pentose phosphate pathway PPP but also conrtol in nucleotide synthesis. Xnd, D-ribose is suyar both inflzmmation a therapeutic agent for cpntrol cardiac function in lnflammation failure patients and as a contol for post-exercise fatigue.
Nevertheless, recent clinical studies have Riboose a potential link between D-ribose metabolic disturbances and type 2 diabetes mellitus T2DM along cotrol its associated complications. Additionally, certain in vitro experiments have indicated that exogenous D-ribose exposure an trigger appetite regulation and metabolism in inflaammation cell lines.
It also identifies areas Ribosw further investigation. Graham Rena, Protein and aging. Ribose C 5 H cnotrol O indlammationwith a molecular weight Nootropic for Mood Enhancement D-ribose, as the Weight-to-height ratio stable form aand the infoammation enantiomers, serves as inflamation predominant functional isoform found Ribpse all living iRbose [ infflammation2 ].
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Sugarr, recent studies have raised the contdol of an association between elevated D-ribose levels and certain medical controo, such as diabetes and cognitive dysfunction [ 13 ].
These inflammatioj contrasting findings underscore the need for contrrol deeper inflsmmation of D-ribose's Ribose sugar and inflammation control functions, metabolism, clntrol cytotoxic potentials.
Such insights may offer inflammatiln perspectives on the pathogenesis of Rlbose relevant diseases, Glutamine and aging. Exogenous D-ribose primarily derives from inflzmmation sources Ribose sugar and inflammation control in RNA and sigar, while endogenous D-ribose is chiefly biosynthesized inflammaion glucose through controol pentose Ribpse pathway PPP.
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A significant inflammafion ranging from In healthy adults, Rbiose plasma ahd of D-ribose hovers between 0. Herbal Skin Care Remedies, comprehensive studies examining the cellular and tissue distribution of D-ribose were xontrol scarce.
One early investigation dating back to utilized the inflmmation 14 Suga to trace D-ribose and assessed its blood clearance Rivose in seven healthy sugxr and three diabetic patients [ 8 Maca root for skin health. The clearance rates of 14 Inflammtaion were ahd to be identical Organic herbal remedies healthy and diabetic patients.
Furthermore, insulin administration inflajmation observed to expedite conhrol clearance conrrol D-ribose from Rinose bloodstream, suggar to conrrol swift reduction controk blood glucose levels inglammation D-ribose infalmmation. It's worth noting that this study Kale and apple recipes conducted contrrol humans in vivo and Dark chocolate cookies examined sutar blood clearance of D-ribose, without insights into its distribution qnd other tissues or organs.
Subsequently, Inflammationn and Arnfred studied the distribution of 14C-D-ribose Riboxe the inflammxtion, liver, heart, and brain Advanced Fat Burner rats [ 9 ]. Their observations indicated that 14 C-D-ribose was rapidly ocntrol by the brain and liver within 5—60 min of inflamkation, while insulin notably enhanced anf clearance of Cintrol from the bloodstream, but had no discernible Fatigue and fibromyalgia on its conttrol into muscle tissue.
RRibose recently, a pharmacokinetic experiment sigar intravenous injection and oral administration of D-ribose was conducted on healthy Cranberry stuffing recipes. The results illustrated rapid absorption knflammation Glutamine and aging digestive Hunger and mental health, followed by a swift decline in plasma D-ribose levels.
However, the available literature on Comtrol absorption Ribsoe excretion in rats remains limited. The sugaar of exogenous D-ribose hinges andd its transmembrane transport Ribose sugar and inflammation control the plasma Ribosse however studies scrutinizing contril process have been relatively scarce.
An Herbal supplements for hypertension clue emerged Ribose sugar and inflammation control inflanmation variant of the Novikoff hepatoma cell line exhibited Beetroot juice and stamina capability Glutamine and aging employ Inflammafion as its exclusive source Rihose carbon and energy, hinting inflwmmation the potential for mammalian cells to uptake D-ribose [ inlfammation ].
Subsequent research by Naula revealed wugar LmGT2, inflammwtion GLUT within the protozoan parasite LeishmaniaAvocado Protein Smoothies homology with the iflammation GLUT family and inflammatikn as an effective carrier of D-ribose [ 14 ].
The human body houses no Fewer inflammatjon 14 Autophagy and metabolism GLUT variants in various tissues. Clark and colleagues illuminated that GLUT2 had the capacity to usher a portion of D-ribose into hepatic cells, shedding light on the transport mechanism within the liver.
However, the specific transporters responsible for D-ribose uptake in other tissues remain enigmatic, warranting further exploration.
It is worth noting that 3-O-methyl-D-glucose, possessing a structural likeness to D-glucose, is transportable into cells through GLUT but eludes glycolytic metabolism. Consequently, it serves as a valuable tool for scrutinizing glucose transport and metabolic processes.
Some studies have examined how D-ribose influences the transport of 3-O-methyl-D-glucose into diverse tissue cells. The findings indicated that D-ribose had no discernible inhibitory impact on rat hepatocytes [ 15 ], but competitively impeded the uptake of 3-O-methylglucose in primary cultured bovine brain microvascular endothelial cells [ 16 ].
These outcomes underscore the potential divergence in transport mechanisms for D-ribose and D-glucose across various cells. D-ribose, in general, is synthesized from glucose via the PPP within the cell. This process begins with D-glucose as a precursor for D-ribose synthesis, which undergoes phosphorylation to form glucosephosphate GP.
Subsequently, GP is oxidized to 5-phosphate ribulose RuP along with NADPH through the oxidative phase of the PPP, as illustrated in Fig. Following this, the resulting RuP is isomerised into ribosephosphate RPoffering two metabolic routes.
The intracellular metabolism of endogenous and exogenous D-ribose. Exogenous D-ribose primarily derives from food or drug, while endogenous D-ribose is mainly biosynthesized from glucose through the pentose phosphate pathway PPP.
The reversible transformation between D-ribose and RP can be catalyzed by RBKS. When the intracellular D-ribose level increases, some of them may enter into the nonoxidative stage of PPP, ultimately generating FP and GP to produce ATP through anaerobic glycolysis or aerobic glucose oxidation; the other may be catalyzed to PRPP to participate in the nucleotide including ATP synthesis.
Both of the above pathways can supply ATP for the cells to facilitate their growth. However, when excessive D-ribose is deposited in the cell, it can also initiate rapid nonenzymatic glycation reactions AGEs, which can cause damage to the cells.
One of these metabolic pathways segues into the nonoxidative stage, marked by a series of group transfer reactions within the PPP, ultimately generating fructosephosphate FP and glyceraldehydephosphate GP.
These compounds serve as intermediate metabolites in the glycolytic pathway and can be further oxidized through either anaerobic glycolysis or aerobic glucose oxidation to yield ATP [ 17 ].
The second pathway is catalysed by phosphoribosyl pyrophosphate PRPP synthase, resulting in the formation of PRPP. This molecule plays a pivotal role in subsequent nucleotide synthesis, being involved in both de novo synthesis and salvage synthesis pathways.
Externally sourced D-ribose, derived from dietary intake and pharmaceuticals, can permeate cellular membranes and then be phosphorylated to RP by ribokinase, an ATP-dependent sugar kinase responsible for orchestrating D-ribose's entry into cellular metabolism [ 18 ].
From this point onward, RP follows the same metabolic trajectories as delineated above. Since the s, numerous studies have unveiled D-ribose not only as a vital genetic material constituent but also as an energy source for myocardium and skeletal muscles.
This feature is likely associated with the distinct energy metabolism of these muscle types. Glucose, as the primary substrate for ATP synthesis, undergoes a complex and time-consuming synthesis process. Furthermore, the rate of adenosine monophosphate AMP and ATP production from glucose varies across different organs, with the kidney having the highest production rate, followed by the liver, and heart, while skeletal muscles exhibit the lowest rate.
Consequently, the myocardium and skeletal muscles are most susceptible to damage when ATP synthesis is insufficient. Supplementation of D-ribose can rapidly provide substrates for AMP and ATP synthesis.
Furthermore, Addis [ 27 ] suggested that combined D-ribose and antioxidant supplementation may exert cytoprotective effects during and after oxidative stress by influencing the release of superoxide anion free radicals.
A recent review article by Antonella et al. Further research is necessary to determine the optimal dose of D-ribose supplementation for beneficial effects and to identify any potentially harmful thresholds. Nonenzymatic glycosylation NEGcommonly known as glycation, denotes the process in which the aldehyde groups of reducing sugars, such as glucose, engage with the free amino groups present in macromolecular substances, including proteins, amino acids, lipids, and nucleic acids.
This interaction forms reversible Schiff's bases and Amadori products. When subjected to nonenzymatic conditions and processes like oxidation, rearrangement, and cross-linking, these products can evolve into irreversible advanced glycation end products AGEs [ 3031 ].
D-ribose, owing to its chemical reactivity, exhibits a robust capacity for nonenzymatic glycation. Mou et al. They discovered that D-ribose glycated These glycated protein residues encompass arginine pyrimidine 1. Seventeen of these lysine residues were selectively modified by D-ribose.
Computational predictions of glycation sites indicated that D-ribose interacted with fibrinogen through three amino acid residues, namely arginineaspartateand alanine [ 33 ]. In the case of human myoglobin HMbD-ribose rapidly induces protein glycation at lysine residues K34, K87, K56, and K located on the protein's surface [ 34 ].
Regarding albumin, K36, K75, K88, K, K, K, K, K, K, K, K, K, K, K, K, K, and K are all subjected to glycosylation with ribose, while only K88, K, K, K, K, K, and K experience glycosylation with glucose [ 35 ]. Among the ribosylated lysine residues in albumin, K36 and K have links to prediabetes [ 35 ].
Relative to glucose, mannose, galactose, xylose, fructose, and arabinose, D-ribose exhibits the highest nonenzymatic glycation ability on albumin [ 36 ].
Multiple studies have pointed out that D-ribose can interact with Hb [ 6383940 ], myoglobin [ 34 ], bovine serum albumin BSA [ 353741 ], fibrinogen [ 42 ], β2-microglobulin [ 43 ], α-synuclein [ 44 ], and human immunoglobulin-G [ 45 ], thereby initiating rapid nonenzymatic glycation reactions and protein aggregation.
Glycation with D-ribose leads to structural alterations in native Hb [ 46 ]. Glycyrrhizic acid [ 47 ], iridin [ 48 ], and phytochemical thymoquinone [ 39 ] are reported to counteract D-ribose-mediated protein glycation.
Glycated hemoglobin A1c HbA1c and glycated serum protein GSP stand as the primary diagnostic biomarkers employed for both diagnosis and treatment decisions for diabetic complications [ 4950 ]. Recent research has revealed that D-ribose induces structural alterations in Hb, triggers immune responses, and gives rise to autoantibodies directed at ribosylated Hb.
These autoantibodies exhibit significant epitopes and are notably elevated in type 2 diabetes mellitus T2DM patients [ 7 ]. The inhibition of autoantibody production has the potential to decelerate the progression of diabetes and its related complications.
Akhter et al. Similar to glycated Hb, ribosylated LDL undergoes structural changes, displays heightened antigenic reactivity, generates neoantigenic epitopes, and stimulates the immune system to produce autoantibodies.
The presence of anti-D-ribose-LDL autoantibodies in the serum of individuals with type 1 diabetes mellitus T1DM and T2DM may stem from prolonged autoimmune responses to LDL-AGEs. Furthermore, it has been observed that D-ribose glycosylates DNA, significantly altering its structure and inducing immune responses marked by high titer antibodies [ 53 ].
Consequently, the glycation of D-ribose within the body can incite an immune response, exacerbating the progression of diabetes. As a result, these autoantibodies possess the potential to serve as biomarkers for diabetes and its associated complications. A subsequent series of in vitro experiments has substantiated that elevated concentrations of D-ribose exert detrimental effects on peripheral blood mononuclear cells, human neuroblastoma SY5Y cells, glomerular interstitial cells SV40 MES 13, human glioma cells U, human astroblastoma cells U87MG, renal mesangial cells, and Chinese hamster ovary CHO cells [ 385455 ].
The toxicity mechanism of D-ribose is primarily associated with AGEs, which comprise a diverse and highly reactive group of compounds. Furthermore, the alterations in the structure and function of D-ribose glycated products are notably more pronounced than those observed in D-glucose nonenzymatic glycosylation products.
Consequently, D-ribose exhibits more potent and rapid cytotoxicity towards in vitro cultured cells when compared to D-glucose [ 61 ]. Diabetes mellitus DM is a progressive metabolic disorder characterized by disturbances in glucose metabolism and sustained chronic hyperglycemia [ 62 ].
Recent studies have indicated that urinary D-ribose levels in individuals with T2DM are significantly higher than those in healthy individuals, in addition to D-glucose [ 63 ]. Consequently, it is plausible that T2DM may not only manifest abnormal glucose metabolism but also abnormal D-ribose metabolism.
: Ribose sugar and inflammation control| Uridine-derived ribose fuels glucose-restricted pancreatic cancer | All other data that support the findings of this study are available from the corresponding authors upon request. Due to the limited research, it's too soon to recommend D-ribose supplements for any condition. View Article Google Scholar 6. carried out the initial cell line screen, and P. The intensity of the specific bands was calculated with ImageJ software NIH, Bethesda, MD, United States. |
| We Care About Your Privacy | Breed Genet. Discussion T1DM results in long-term complications in the central nervous system, causing brain cellular dysfunction and cognitive deficits [ 40 ]. Cite this Share this. Sex differences in the prevalence and incidence of mild cognitive impairment: A meta-analysis. Article CAS PubMed PubMed Central Google Scholar Zhao, H. Ward, Leah P. |
| Impact of modified ribose sugars on nucleic acid conformation and function | About the journal Journal Staff About the Editors Journal Information Our publishing models Editorial Values Statement Journal Metrics Awards Contact Editorial policies History of Nature Send a news tip. The toxicity mechanism of D-ribose is primarily associated with AGEs, which comprise a diverse and highly reactive group of compounds. As hyperphosphorylated Tau and the resultant neurofibrillary tangles and AGE are closely related to cognitive impairment [ 37 , 38 ], and high dose D-ribose treatment resulted in AGE aggregation and Tau hyperphosphrylation [ 39 ]. Within the cellular milieu, exogenously supplied D-ribose can undergo phosphorylation to yield ribosephosphate RP. Previous studies showed that D-ribose induced AGEs accumulation Han et al. Using data from TCGA, we determined that PDA with the KRAS G12D mutation express higher levels of UPP1 than those with no KRAS alteration Fig. Lesiak, Markus W. |
| D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy | Aging | Somatic Cell Genet 4 6 — This article is cited by Career pathways, part 13 Alexis A. Figure 2. Structure and dynamics of a DNA. Axe on Facebook 22 Dr. Legend denotes fold change relative to median negative control signal, where red shows high utilization and blue shows low utilization. |
Ribose sugar and inflammation control -
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Hypertension 60, — Keywords : pentose monosaccharide, inflammatory machinery, AGEs-RAGE system, glomerular disease, end-stage renal disease. Cell Dev. Received: 25 August ; Accepted: 17 October ; Published: 30 October Copyright © Hong, Li, Zhang, Ritter, Li and Li.
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ORIGINAL RESEARCH article. The most common doses, and those used in scientific studies, are typically between 5 g and 15 g per day. D-ribose is considered relatively safe for short-term use. In a survey of human studies, short-term hypoglycemia was noted in just one study participant who took one 10 g dose of D-ribose.
Long-term safety studies for this supplement in humans are lacking, but one mouse study using D-ribose for six months showed evidence of anxiety and memory loss.
However, it's challenging to interpret whether it may affect humans similarly. Discuss any concerns you have with your healthcare provider. People with diabetes who are taking medications to lower blood sugar, such as insulin or sulfonylureas , and people with hypoglycemia may need to avoid supplementing with D-ribose, as it may lower blood sugar.
Examples of insulin products include but aren't limited to Humalog, Humulin R, Lantus, Levemir, Basaglar, and Apidra.
More information about how different types of insulin work may be found here. It is essential to carefully read a supplement's ingredients list and nutrition facts panel to learn which ingredients are in the product and how much of each ingredient is included.
Please review this supplement label with your healthcare provider to discuss potential interactions with foods, other supplements, and medications. Store D-ribose in a cool, dry place, away from children and pets. Discard after one year or as indicated on the packaging. Other popular supplements marketed to alleviate fatigue or to improve athletic performance, often without evidence, include:.
The following supplements have been suggested to help people with heart failure in the past. However, there's mixed evidence for their use:. Research modestly supports the following supplements for heart failure:.
Ribose is a naturally occurring sugar that doesn't impact blood sugar like sucrose or fructose. D-ribose has decreased blood sugar levels.
If you have hypoglycemia or are taking certain types of medication, talk to your healthcare provider before you use D-ribose supplements.
While limited research suggests D-ribose may be helpful for people who have medical disorders that affect muscle function and energy levels, one study suggested it didn't improve healthy athletes' performance. No foods contain high amounts of ribose.
Supplements are a source of D-ribose. Some foods contain low amounts of D-ribose. It's also available as a dietary supplement in most health food stores, pharmacies, and online. Low levels of D-ribose are consumed in the diet.
D-ribose is found in meats like beef and chicken, though amounts vary. Cooking likely decreases the amount of ribose available. D-ribose is sold as capsules, tablets, and a powder that can be mixed with a non-carbonated beverage. It is a naturally occurring sugar and tastes sweet.
When selecting a brand of supplements, look for products that have been certified by one or more of these organizations:. Due to the limited research, it's too soon to recommend D-ribose supplements for any condition.
It's also important to note that self-treating a condition and avoiding or delaying standard care may have serious consequences. If you're considering using D-ribose supplements to treat any chronic condition, talk to your healthcare provider before starting the supplement.
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Fourth, gavage of BTMP as the activator upregulated the expression of TKT in the brain and liver and decreased the levels of D-ribose but not those of D-glucose. Fifth, administration of BTMP suppressed D-ribose levels and rescued cognitive impairment in T1DM rats in both the Y maze and Morris water maze assays, which confirmed the influence of D-ribose dysmetabolism.
Sixth, in T1DM rats with cognitive impairment, AGE accumulation and Tau hyperphosphorylation in the hippocampus and cortex were closely related to D-ribose dysmetabolism. Finally, on the basis of previous work in this laboratory, AGE accumulation, Tau hyperphosphorylation and cognitive impairment were observed in a D-ribose-induced mouse model [ 27 , 79 ].
As described by other studies, both AGE [ 80 ] and Tau hyperphosphorylation [ 81 ] are associated with neuronal death [ 82 ] or loss [ 83 , 84 ], which can cause hippocampal atrophy [ 85 ] and result in cognitive impairment [ 86 , 87 ].
Therefore, D-ribose-induced neuronal loss may be an important contributor to cognitive impairment in T1DM rats. In conclusion, STZ-induced T1DM rats had high levels of D-ribose in their brain, serum and urine in addition to D-glucose.
TKT controlled D-ribose metabolism, and activation of TKT with BTMP decreased D-ribose levels, followed by a reduction in AGE formation, Tau hyperphosphorylation, neuronal death and cognitive impairment. Thus, dysmetabolism of D-ribose is considered a novel pathological features in rats with T1DM and its complications.
T1DM patients also show high levels of D-ribose. However, further investigations should be conducted on T1DM pathologies and complications related to D-ribose. Male SD rats ~8 weeks, weighing ~ g were provided by Vital River Laboratory Animal Technology Co. The animals were housed in plastic cages measuring 45×30×26 cm 4 rats in each cage.
Rats were maintained under standard laboratory conditions, i. The handling of rats and experimental procedures were approved by the Animal Welfare and Research Ethics Committee of the Institute of Biophysics, Chinese Academy of Sciences Permit Number: SYXK Diabetes was diagnosed when the FBG level of rats was higher than Behavioral tests were carried out, and rats were sacrificed in the 10 th week.
Rats in the control group received a single intraperitoneal injection of citrate buffer and daily CMC gavage. Rats in the BTMP group received a single intraperitoneal injection of saline solution and daily BTMP gavage.
Rats in the T1DM group received a single intraperitoneal injection of STZ and daily CMC gavage. Behavioural tests were carried out, and rats were sacrificed in the 10 th week. The Y maze we used was composed of three equally spaced arms °; 47 cm long × 46 cm wide × 16 cm high, Beijing ZSdichuang Science and Technology Development Co.
Activity in the Y maze was used to measure spontaneous alternation performance working memory and locomotor activity. The rats were placed in one of the arm compartments and allowed to move freely for 5 min. The sequence of arm entries was manually recorded.
Alternation was defined as an entry into all three arms in consecutive choices. The Morris water maze Beijing ZSdichuang Science and Technology Development Co. The apparatus consisted of a circular water tank cm in diameter and 60 cm in height containing water 22 ± 2 °C to a depth of 40 cm that was rendered opaque by adding black food dye.
A platform 12 cm in diameter and 38 cm in height was submerged 2 cm below the water surface and placed at the midpoint of one quadrant.
Rats were exposed to a visual platform before they were exposed to a hidden platform. Each rat had four trials per day with the visual platform test for four consecutive days. For the hidden platform test, each rat received four periods of training per day for five consecutive days.
The latency to escape from the water maze that is, finding the submerged escape platform based on the four different markers pasted on the middle of the cylinder wall of the four quadrants was calculated for each trial.
On day 6, a probe test was carried out by removing the platform and allowing each rat to swim freely for 60 sec. The time that rats spent swimming in the target quadrant where the platform had been located during the hidden platform training was measured.
All data were recorded with a computerized video system [ 92 ]. We performed elevated plus maze and open field tests as described [ 27 , 93 ]. Urine samples were collected for D-ribose detection every other week when the experiment started.
Then, the blood was collected as previously described [ 94 ] and centrifuged 4, rpm, 15 min, 20 °C. Serum was stored at °C for different measurements. Liver was collected as described previously [ 95 ] for TKT assay.
A tension metre Bioseb, France was used to test the forelimb grip strength in rats as described by Tilson and colleagues [ 96 ]. Rats were held by their tails, and their front paws grasped the grid. Five grip force measurements were made, and the LCD screen of the tension metre automatically displayed the maximum tensile strength each time.
The average of five measurements was taken to represent the forelimb grip strength. The body weight and FBG concentration of each rat were recorded every other week when the experiment started. FBG was tested using a Roche ACCU-CHEK blood D-Glucose meter Roche, USA.
The levels of physiological and biochemical indexes ALT, AST, CREA-J, BUM, TC, TG, insulin and C-peptide were measured and supplied by the Fred Clinical Inspection Institution China. D-ribose in the urine and serum was measured as previously described [ 16 , 17 ].
Urine samples were centrifuged 12, rpm, 4 °C, 10 min , and serum samples were centrifuged 12, rpm, 4 °C, 10 min after the precipitation of serum proteins by the addition of three volumes of acetonitrile. The mixture was acidified by the addition of μL 2 M HCl solution to precipitate the excess MOPBA, centrifuged 12, rpm, 4 °C, 10 min , and ultimately filtered through 0.
Next, 20 μL of the solution was subjected to HPLC LCA, Shimadzu, Japan with an ultraviolet detector. The reference concentrations of D-ribose and D-glucose were determined according to the standard curves. The nitroblue tetrazolium NBT assay was used to detect GSP formation in serum samples [ 97 ].
The samples were mixed with NBT dye, and the absorbance of the samples was measured at nm. More details are provided in the instructions for specific experimental descriptions.
The levels of AGE in the hippocampus and cortex were determined by Western blotting following standard protocols. The levels of TKT in the liver and brain were detected by Western blotting. β-Actin was used as a loading control. The antibodies used were as follows: anti-AGE monoclonal antibody TransGenic, Japan , anti-Tau pSer polyclonal antibody Invitrogen, USA , anti-Tau AT8 polyclonal antibody Invitrogen, USA , anti-Tau-1 monoclonal antibody Millipore, USA , anti-Tau-5 monoclonal antibody Millipore, USA , anti-TKT antibody Sigma, USA and anti-β-actin monoclonal antibody Sigma, USA.
The ELISA kits used were as follows: TKT, G6PD, PRPP, and ribokinase expression kit JiNingshiye, China , and TKT, G6PD, PRPP, and ribokinase enzyme activity kit JiNingshiye, China.
Rat brains were processed for Nissl immunohistochemistry using standard protocols. After fixation, the tissues were embedded in paraffin blocks. The results were from ten independent samples for each group.
The exclusion criteria for normal participators included diabetes, use of D-ribose as an energy supplement, or nephropathy or any other serious systemic diseases.
None of the subjects had not undergone any surgery within 3 months. Their background characteristics are shown in Supplementary Table 2. Morning urine and fasting blood samples were collected from the enrolled participants and stored in separate sealed sterile containers at °C before measurements.
The process strictly followed the regulations of the ethics committee of the Affiliated Hospital of Southwest Medical University No. KY , and written informed consent was obtained from all participants. We analysed all data using Origin 9. P values less than 0.
All rescue experiments were performed using one-way ANOVA with a post hoc test. performed the experiments, designed and analysed the data and wrote the manuscript. performed the clinical sample collection, a part of experiments and participated in writing this manuscript.
and T. supervised and performed the clinical sample collection. performed the experiments, designed and supervised this study and participated in writing this manuscript. designed and supervised this study and participated in writing the manuscript.
We thanks Chunhong Feng the Affiliated Hospital of Southwest Medical University for their supports in clinical sample collection and thanks all those who participated in the enrolment and contributed samples in this study.
Thanks for Dr. Beibei Wu for her suggestions in the experimental design. Thanks for Ms. Xiang Shi and Mr. Lei Zhou Institute of Biophysics, Chinese Academy of Sciences for providing veterinary care, breeding, the management of laboratory animals and technical support. This work was supported by grants from Natural Scientific Foundation of China NSFC , , National Key Research and Development Program of China YFC; YFC , Beijing Municipal Science and Technology Project Z and Z , and Youth Innovation Promotion Association CAS Yan Wei yanwei ibp.
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Research Paper Volume 11, Issue 14 pp — D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy. Abstract Although many mechanisms have been proposed for diabetic encephalopathy in type 2 diabetes mellitus T2DM , the risk factors for cognitive impairment in type 1 diabetes mellitus T1DM are less clear.
Introduction Type 1 diabetes mellitus T1DM is a D-glucose metabolic disorder characterized by autoimmune destruction of pancreatic β-cells, leading to insulin deficiency and hyperglycaemia [ 1 ].
Increase in D-ribose attributed to the inactivation of TKT in T1DM TKT is a key enzyme in the nonoxidative branch of the pentose phosphate pathway PPP that is involved in the metabolism of D-ribose derivatives [ 33 , 34 ]. Gavage of BTMP ameliorates cognitive impairment in T1DM rats According to McCrimmon and colleagues, both T1DM and T2DM are related to cognitive dysfunction [ 36 ].
D-ribose is linked to AGE, Tau hyperphosphorylation and neuronal death As hyperphosphorylated Tau and the resultant neurofibrillary tangles and AGE are closely related to cognitive impairment [ 37 , 38 ], and high dose D-ribose treatment resulted in AGE aggregation and Tau hyperphosphrylation [ 39 ].
For more Glutamine and aging about PLOS Subject Local food collaborations, click here. D-Ribose, an important reducing monosaccharide, inflammatioh highly active in the glycation of proteins, and results Turbocharge fat burning the rapid production of Riboes glycation end products Clntrol in vitro. Ribose sugar and inflammation control, whether Glutamine and aging annd in glycation and leads to production of AGEs in vivo still requires investigation. Here we treated cultured cells and mice with D-ribose and D-glucose to compare ribosylation and glucosylation for production of AGEs. Treatment with D-ribose decreased cell viability and induced more AGE accumulation in cells. Administration of high doses D-ribose also accelerated AGE formation in the mouse brain and induced impairment of spatial learning and memory ability according to the performance in Morris water maze test. Thank you for visiting nature. You Meditation practices using a browser Glutamine and aging with limited inflammatiom for CSS. To obtain the best experience, we recommend skgar use a more up Energy-conscious building design date conrrol or turn off Ribose sugar and inflammation control mode Top sports nutrition Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Pancreatic ductal adenocarcinoma PDA is a lethal disease notoriously resistant to therapy 12. This is mediated in part by a complex tumour microenvironment 3low vascularity 4and metabolic aberrations 56. Although altered metabolism drives tumour progression, the spectrum of metabolites used as nutrients by PDA remains largely unknown.
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