5 replies to this topic

[rongqiaohe]

We have found that the concentration of D-ribose is abnormally high in the urine of type 2 diabetics. This suggests that type 2 diabetics suffer from not only disorders in D-glucose metabolism, but also in D-ribose metabolism. Our paper is online as follows:

http://www.pibb.ac.c...20130341&flag=1

[niner]

Thanks for the paper, rongqiaohe. I think people here will find this interesting. We've had two reports of people on low carb diets developing some sort of metabolic dysfunction after using D-ribose. If that's not enough reason to avoid ribose, your results showing the high AGE-forming potential of ribose are another reason.

Abstract of pibb paper linked above:

In 1815, the French chemist Michel Eug?ne Chevreul (1786-1889) discovered that the sweetness in the urine of diabetics comes from grape sugar or D-glucose. Diabetes mellitus (DM) is considered as a group of metabolic diseases characterized by hyperglycemia (high concentration of blood D-glucose) resulting from defects in insulin secretion, insulin action, or both. On the other hand, D-ribose as an energetic enhancer was found to decrease the concentration of blood D-glucose, and thus "Oral administration of D-ribose in diabetes mellitus" was ever described by Steinberg and colleagues (1970). As described previously in this laboratory, D-ribose rapidly glycates proteins, such as BSA, neuronal Tau and α-synuclein, producing advanced glycation end products (AGEs) with severe cytotoxicity, leading to dysfunction and cell death, in vitro and in vivo. Intraperitoneal injection of D-ribose into mice significantly increases their glycated serum protein and blood AGEs though the concentration of D-glucose became slightly decreased, suggesting that D-ribose is much easier to produce AGEs than D-glucose in vivo. Here, using 4-(3-Methyl-5-oxo-2-pyrazolin-1-yl) benzoic acid (MOPBA) coupled with HPLC, we determined the concentration of uric D-ribose of type 2 diabetic patients (n=30) and the age-matched healthy controls (n=30). The results show that the yield of the derivative of MOPBA-ribose is linearly correlated with the concentration of D-ribose (r²=0.999) with a recovery of 99%. The isolated fractions of D-ribose and D-glucose from urine of type 2 diabetic patients through HPLC were analyzed by mass spectrometry, and the results showed that the fractions contained 569.19 u compound (C₂₇H₂₉N₄O₁₀, D-ribose), and 599.20 u compound (C₂₈H₃₁N₄O₁₁, D-glucose) respectively. The concentration of uric D-ribose of Type 2 diabetics (male (134.28±35.09) μmol/L, female (97.33±23.68) μmol/L) was significantly (P < 0.001) higher than that of the age-matched healthy control (male (35.99±5.64) μmol/L, female (33.72±6.27) μmol/L). Under the experimental conditions, the uric D-glucose level of the patients was also markedly (P < 0.001) higher than the control. Further analyses showed a marked increase in the level of uric D-ribose from either male (P < 0.001) or female (P < 0.001), but a significant difference of the uric levels between male and female could not be observed (P > 0.05). The high levels of uric D-ribose and D-glucose of the patients suggest that type 2 diabetic patients are not only suffered from D-glucose metabolism disorders, but also from D-ribose metabolism disorders.

[rongqiaohe]

Thanks for the paper, rongqiaohe. I think people here will find this interesting. We've had two reports of people on low carb diets developing some sort of metabolic dysfunction after using D-ribose. If that's not enough reason to avoid ribose, your results showing the high AGE-forming potential of ribose are another reason.

Abstract of pibb paper linked above:

In 1815, the French chemist Michel Eug?ne Chevreul (1786-1889) discovered that the sweetness in the urine of diabetics comes from grape sugar or D-glucose. Diabetes mellitus (DM) is considered as a group of metabolic diseases characterized by hyperglycemia (high concentration of blood D-glucose) resulting from defects in insulin secretion, insulin action, or both. On the other hand, D-ribose as an energetic enhancer was found to decrease the concentration of blood D-glucose, and thus "Oral administration of D-ribose in diabetes mellitus" was ever described by Steinberg and colleagues (1970). As described previously in this laboratory, D-ribose rapidly glycates proteins, such as BSA, neuronal Tau and α-synuclein, producing advanced glycation end products (AGEs) with severe cytotoxicity, leading to dysfunction and cell death, in vitro and in vivo. Intraperitoneal injection of D-ribose into mice significantly increases their glycated serum protein and blood AGEs though the concentration of D-glucose became slightly decreased, suggesting that D-ribose is much easier to produce AGEs than D-glucose in vivo. Here, using 4-(3-Methyl-5-oxo-2-pyrazolin-1-yl) benzoic acid (MOPBA) coupled with HPLC, we determined the concentration of uric D-ribose of type 2 diabetic patients (n=30) and the age-matched healthy controls (n=30). The results show that the yield of the derivative of MOPBA-ribose is linearly correlated with the concentration of D-ribose (r²=0.999) with a recovery of 99%. The isolated fractions of D-ribose and D-glucose from urine of type 2 diabetic patients through HPLC were analyzed by mass spectrometry, and the results showed that the fractions contained 569.19 u compound (C₂₇H₂₉N₄O₁₀, D-ribose), and 599.20 u compound (C₂₈H₃₁N₄O₁₁, D-glucose) respectively. The concentration of uric D-ribose of Type 2 diabetics (male (134.28±35.09) μmol/L, female (97.33±23.68) μmol/L) was significantly (P < 0.001) higher than that of the age-matched healthy control (male (35.99±5.64) μmol/L, female (33.72±6.27) μmol/L). Under the experimental conditions, the uric D-glucose level of the patients was also markedly (P < 0.001) higher than the control. Further analyses showed a marked increase in the level of uric D-ribose from either male (P < 0.001) or female (P < 0.001), but a significant difference of the uric levels between male and female could not be observed (P > 0.05). The high levels of uric D-ribose and D-glucose of the patients suggest that type 2 diabetic patients are not only suffered from D-glucose metabolism disorders, but also from D-ribose metabolism disorders.

Dear Dr. Moderator,
Thank you very much for your message! I think that D-ribose plays some role in type 2 diabetes mellitus. Our work is going on and we will provide another evidence for this viewpoint.
Thanks a lot again,
The the best regards,
Rongqiao He

[docmaas]

Can anyone assess the likelihood  of  niacinimide riboside breaking down into the form of ribose that results in AGEs?  

[zorba990]

This is interesting. Life Extension reccomends fairly large doses for heart patients, so I wonder what their take on the risks are.

http://www.lifeexten...ur-Life/Page-01

[Heisok]

This is interesting. Life Extension reccomends fairly large doses for heart patients, so I wonder what their take on the risks are.

http://www.lifeexten...ur-Life/Page-01

 

zorba990, I had the same question, but held off. I have taken 5 gms off and on since about the time LEF started recommending it. The manufacturer brand they sell Bioenergy RIBOSE which I started buying elsewhere cheaper.  I never identified any adverse effects, and one of the warnings about it's use is lowered blood glucose. My last purchase was from a bulk powder seller without a manufacturer identified. I wonder about purity, so I am a little concerned. It is fluffier.