Ribose sugar and diabetes management -
The female subjects were objectively and subjectively evaluated at 14 and 28 days while applying the lotion on a daily basis. What did they find? After 14 days, there was a significant reduction of After 28 days, total wrinkle surface area remained at Overall, 67 percent of the subjects thought their skin looked more glowing and radiant after the treatment.
These results show that this natural carbohydrate is a potential anti-aging supplement for skin health. What foods are high in ribose? It can be found in the following food sources :. 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. 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.
Here, we show that streptozotocin STZ -induced T1DM rats showed cognitive impairment in both Y maze and Morris water maze assays, accompanied with D-ribose was significantly increased in blood and urine, in addition to D-glucose. The expression and activity of transketolase TKT , an important enzyme in the pentose shunt, were decreased in the brain, indicating that TKT may be involved in D-ribose metabolism in T1DM.
Support for these change was demonstrated by the activation of TKT with benfotiamine BTMP treatment. Decreased D-ribose levels but not D-glucose levels; markedly reduced AGE accumulation, Tau hyperphosphorylation, and neuronal death; and improved cognitive ability in T1DM rats were shown after BTMP administration.
In clinical investigation, T1DM patients had high D-ribose levels in both urine and serum. Our work suggests that D-ribose is involved in the cognitive impairment in T1DM and may provide a potentially novel target for treating diabetic encephalopathy.
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 ]. T1DM can affect different organs and result in many complications; among these complications, diabetic encephalopathy is diabetes-induced brain damage [ 2 ].
As early as , diabetes was recognized to lead to cognitive dysfunction [ 3 ]. Because an increasing number of people are diagnosed with T1DM or type 2 diabetes mellitus T2DM , diabetic encephalopathy has become widely recognized [ 4 — 6 ]. Patients with diabetic encephalopathy show both mental and physical symptoms, including an altered mental state, cognitive decline, memory lapses, and changes in personality [ 2 , 7 ].
Compared with people without diabetes mellitus, people with diabetes are at higher risk of cognitive decline and dementia, such as Alzheimer's disease [ 8 ]. Although many pathomechanisms, such as alterations in the vascular supply of the brain and the interaction between insulin and the brain [ 9 ], have been proposed for diabetes mellitus, the most attention has been paid to T2DM in ageing people [ 10 ].
Unlike T2DM, T1DM is one of the most frequent chronic diseases in children and can start at any age. Some children with T1DM may be at high risk of cognitive deficits, especially those diagnosed at earlier ages [ 11 , 12 ].
Middle-aged and older adults are also at increased risk for cognitive decline [ 13 , 14 ]; however, the risk factors for cognitive decline in adults with T1DM have remained unclear thus far [ 15 ]. Therefore, identifying the risk factors of T1DM-related cognitive impairment is important.
D-glucose is a long-standing major molecular biomarker for both T1DM and T2DM. However, recent studies have shown that in addition to D-glucose, D-ribose plays a role in T2DM [ 16 , 17 ]. As a key component of intracorporal biomolecules, including RNA, ATP and riboflavin, D-ribose participates in numerous biochemical processes [ 18 — 20 ] and has an active role in the glycation of protein, producing advanced glycation end products AGE [ 21 , 22 ].
In particular, D-ribose is an important contributor to glycated haemoglobin HbA1c [ 17 ] and glycated serum protein [ 23 ], showing the linkage between aldopentose and diabetes. Intraperitoneal injection with D-ribose 3. bw, once daily elicited a significant increase in triglyceride in Sprague-Dawley SD rat liver [ 24 ].
As described by the European Food Safety Authority [ 25 ], toxicological effects could not be ruled out, although the use of D-ribose in nutritional supplement is considered acceptable. Especially in cognitive impairment, ribosylation-induced Tau protein aggregation is highly cytotoxic to neuronal cells [ 26 ].
Long-term gavage of D-ribose can also cause cognitive impairment in mice [ 27 ]. Increasing evidence suggests that D-ribose is closely related to T2DM and even diabetic complications.
However, the relationship between D-ribose and cognitive impairment in T1DM has not yet been investigated. The streptozotocin STZ -injected rats is a common animal model used in T1DM studies [ 28 , 29 ].
T1DM is associated with neurocognitive dysfunction and astrogliosis [ 30 ]. Furthermore, metabolic analyses revealed that T1DM mainly affects metabolic pathways involved in mitochondrial energy failure and impairs the antioxidative system [ 31 ].
In the present study, we observed that T1DM patients had abnormally increased levels of D-ribose in blood and urine. STZ-induced T1DM rats exhibited cognitive impairment and had high levels of D-ribose in blood and urine, along with AGE formation, Tau hyperphosphorylation and neuronal death. Transketolase TKT was demonstrated to be an important enzyme in regulating D-ribose metabolism in T1DM-related encephalopathy rats.
Interestingly, elevation of TKT by benfotiamine BTMP rescued D-ribose dysmetabolism, followed by decreases in AGE accumulation, Tau hyperphosphorylation, and neuronal death, as well as the rescue of cognitive impairment in T1DM rats.
Rats injected with citrate buffer pH 4. Rats were maintained for 10 weeks; during this period, their fasting blood glucose FBG , body weight and forepaw tensions were monitored every other week Supplementary Figure 1A — 1C.
FBG levels in diabetic rats markedly increased after STZ injection, while body weight and tension decreased. 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.
People with certain medical conditions may experience benefits from D-ribose supplements, including improved exercise performance and recovery of muscle cell energy stores after intense exercise. However, benefits in healthy, active individuals are unsupported by science, and more research is needed.
If you fall into one of the specific groups discussed in this article, you may want to consider D-ribose supplements. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.
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Dosage and Side Effects.
D-ribose is elevated in Ribose sugar and diabetes management patients and can be managekent in the onset of encephalopathy. Managemenh Albany NY. Copyright viabetes Yu et al. Sutar is an open-access article distributed Ribose sugar and diabetes management the terms of the Managwment Commons Attribution CC BY 3. Although many mechanisms have been proposed for diabetic encephalopathy in type 2 diabetes mellitus T2DMthe risk factors for cognitive impairment in type 1 diabetes mellitus T1DM are less clear. Here, we show that streptozotocin STZ -induced T1DM rats showed cognitive impairment in both Y maze and Morris water maze assays, accompanied with D-ribose was significantly increased in blood and urine, in addition to D-glucose.
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