Fructose conversion to glucose & triglycerides

[sungvimil]

This study shows that fructose can be converted to glucose in children (fig. 6).
http://www.pnas.org/content/87/14/5449.full.pdf

[Iris]

I remember time back when RRM wrote about fructose conversion to glucose, but can´t find it.

I would like to know if I am correct when stating that fructose can be converted to glucose by the liver with the objective of raising blood sugar levels, and not necessarily enter the lipogenic route. This assertion is present in any biochemistry book, but I would like to know if RRM or anyone else is familiar with human studies showing this.

If this is true, then all the ¨health experts¨ talking about fructose toxicity are ignoring simple biochemistry facts, since the danger would be from excessive fructose consumption. On the other hand, eating fructose when you need the energy will not be converted to fatty acids, and will not produce decreased NO synthesis (high blood prerssure), excessive urea formation (gout) and ROS generation (oxidative damage), as those Dr. Lustig argues.
http://www.youtube.com/watch?v=dBnniua6 ... r_embedded

Thanks.

You mean this topic? viewtopic.php?t=2028&highlight=fructose+glucose

[RRM]

I would like to know if I am correct when stating that fructose can be converted to glucose by the liver with the objective of raising blood sugar levels, and not necessarily enter the lipogenic route.

Yes, directly and indirectly (via glycogen)
Glucose can be metabolised anywhere in the body.
Fructose however can only be metabolized in the liver.
Depending on the level of glucose in the blood and the level of glycogen in the liver,
in the liver fructose is converted into glucose

fructose > fructose-1-phosphate > dihydroxyacetone phosphate (DHAP) + glyceraldehyde-3-phosphate (GA-3-P) > fructose-1,6-biphosphate > glucose-6-phosphate > glucose

glycogen

fructose > fructose-1-phosphate > dihydroxyacetone phosphate (DHAP) + glyceraldehyde-3-phosphate (GA-3-P) > fructose-1,6-biphosphate > glucose-6-phosphate > glucose-1-phosphate > glycogen

or fatty acids (and triglycerides).
In the pathways described above, there is a third product besides DHAP and GA-3-P, which is glyceraldehyde (GA), but there its is converted into GA-3-P anyway.
In the pathway below however, this GA (together with some of the DHAP) is converted into glycerol instead,
which (together with the fatty acids) forms triglycerides.

fructose > fructose-1-phosphate > dihydroxyacetone phosphate (DHAP) + glyceraldehyde-3-phosphate (GA-3-P) (+ GA) > phosphoenolpyruvate > pyruvate > Acetyl CoA > fatty acids

The glycogen in the liver repletes the glucose in the blood

glycogen > glucose-1-phosphate > glucose-6-phosphate > glucose

When the glycogen depot in the liver is filled up (400 kcal) and not used for keeping up the blood glucose level,
then the fructose will be converted into fatty acids.

Dietary fructose is best absorbed in the presence of about as much glucose.
(which is naturally the case in fruits)
Glucose directly inhibits appetite, thus ensuring that also not too high quantities of fructose enter the blood stream, which prevents the production of triglycerides by the liver.
Indeed the danger would be from excessive fructose consumption,
achieved by consuming much fructose and little glucose.

On the other hand, eating fructose when you need the energy will not be converted to fatty acids...

Indeed, and this overconsumption is prevented by the glucose.

fructose can be converted to glucose by the liver with the objective of raising blood sugar levels, ... I would like to know if RRM or anyone else is familiar with human studies showing this.

Keeping up blood glucose levels is a process that is top prioritized,
because if they get too low, you will faint almost immediately, and eventually die.
So that processes like the conversion of fructose into glucose, will have a very high priority when required.
Survival over anything else.
No study required for this.

[sungvimil]

Thanks RRM for the detailed response!

Because of your vast knowledge, you are without the shadow of a doubt the guy to turn on when someone needs a clarification about biochemistry!

Is all your knowledge a result of reading biochemistry text books or from other places also?

[RRM]

Textbooks are great for getting a good overview,
and when you need more specific info, you best get it online,
thanks to google.

[Kasper]

Dietary Fructose Inhibits Intestinal Calcium Absorption and Induces Vitamin D Insufficiency in CKD
Renal disease leads to perturbations in calcium and phosphate homeostasis and vitamin D metabolism. Dietary fructose aggravates chronic kidney disease (CKD), but whether it also worsens CKD-induced derangements in calcium and phosphate homeostasis is unknown. Here, we fed rats diets containing 60% glucose or fructose for 1 mo beginning 6 wk after 5/6 nephrectomy or sham operation. Nephrectomized rats had markedly greater kidney weight, blood urea nitrogen, and serum levels of creatinine, phosphate, and calcium-phosphate product; dietary fructose significantly exacerbated all of these outcomes. Expression and activity of intestinal phosphate transporter, which did not change after nephrectomy or dietary fructose, did not correlate with hyperphosphatemia in 5/6-nephrectomized rats. Intestinal transport of calcium, however, decreased with dietary fructose, probably because of fructose-mediated downregulation of calbindin 9k. Serum calcium levels, however, were unaffected by nephrectomy and diet. Finally, only 5/6-nephrectomized rats that received dietary fructose demonstrated marked reductions in 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 levels, despite upregulation of 1{alpha}-hydroxylase. In summary, excess dietary fructose inhibits intestinal calcium absorption, induces marked vitamin D insufficiency in CKD, and exacerbates other classical symptoms of the disease. Future studies should evaluate the relevance of monitoring fructose consumption in patients with CKD.

http://jasn.asnjournals.org/cgi/content ... 09080795v1

[gianni]

Conclusions of results of scientific experiments should be logical. The Wiki article states results of tests done on rats as though it would apply to humans, but then cleary says that "some human experiments have failed to show.....". Later it states that fructose is hypothesized to cause obesity in humans. Then it says it may cause water retention, may cause blah blah blah, and may cause blah blah blah. It finishes up by saying that they now have some "reports" that do show such things, so maybe it might help to actually look those up and see if they followed a logical scientific procedure or not. But I wouldn't take the wiki article seriously.

I am going to see if I can find out more about fructose chelating with minerals. It may be a temporary bond that is fairly soluble.

The second abstract seems unbelievably misleading to me. First of all, the experiments were done on rats, and as mentioned in Wiki, rats don't seem to respond the same as humans do to fructose. It wraps it all up at the end when it says that "future studies should evaluate relevance of monitoring fructose comsumption in patients with CKD". Something doesn't sound right to me.

Let's see. Where can we find some humans who have been eating fructose for a long time? We could ask them if it is causing obesity, elevated LDL and cholesterol, and if they have come down with metabolic syndrome.

I have been reading about uric acid for a little over a year now, and I do believe that uric acid would be more so the actual root cause of most of the issues listed in these studies.

Some things to google:

Uric acid forms very insoluble compounds with calcium, copper, and zinc.
Uric acid for sure is involved in renal disorders.
Uric acid involved in diabetes.
Uric acid + water retention.

I could go on forever, I've found it involved in so many different things.

Uric acid + fruit
A lot of studies are coming out saying that fructose raises serum uric acid levels, but if you go back to studies done before big pharma took over the world, you will find studies done on humans which show that fruit brings uric acid stores into the blood because it raises the ph of the blood. This is not a bad thing. This helps the body get rid of uric acid.


Betsy

[RRM]

excess dietary fructose inhibits intestinal calcium absorption, induces marked vitamin D insufficiency in CKD, and exacerbates other classical symptoms of the disease.

Inhibiting calcium absorption is not necessarily a bad thing.
The absorption of calcium needs to be regulated (up and down) in accordance with total calcium intake and calcium requirements.

Also, this is about excess dietary fructose.
How do you get to that?
By consuming fructose syrup? (or similar)

And, CDK is a disease.
In lots of diseases, consuming a specific nutrient may exacerbate symptoms of that disease.