Energy From Fructose

[Carl Fredrik Ahl]

Hi,

I wonder if fructose can be converted to energy (ATP) like glucose can. How does fructose differ from glucose?

 

[YaDinghus]

4 minutes ago, Carl Fredrik Ahl said:

Hi,

I wonder if fructose can be converted to energy (ATP) like glucose can. How does fructose differ from glucose?

 

There is a slight chemical difference in the structure, but they are both C6H12O6. Glucose builds a ring with 6 links (one of them O) and one appendage(CH2OH), while fructose is a ring with 5 links (one of them again O) and two appendages (as above). But our cells can process fructose as well as glucose or galactose. It's the absorption in the colon that is problematic for some folks

[Carl Fredrik Ahl]

11 hours ago, YaDinghus said:

There is a slight chemical difference in the structure, but they are both C6H12O6. Glucose builds a ring with 6 links (one of them O) and one appendage(CH2OH), while fructose is a ring with 5 links (one of them again O) and two appendages (as above). But our cells can process fructose as well as glucose or galactose. It's the absorption in the colon that is problematic for some folks

Oh ok, thx for the answer. Is that any difference on how fast the body can use the fructose as energy and can fructose create the same amount of ATP as glucose can? Are there any other differens with fructose and glucose other than that some people have problem with the absorbstion in the colon as you say? 

[John Cuthber]

I'm fairly sure the body can convert fructose to glucose.

[StringJunky]

6 hours ago, Carl Fredrik Ahl said:

Oh ok, thx for the answer. Is that any difference on how fast the body can use the fructose as energy and can fructose create the same amount of ATP as glucose can? Are there any other differens with fructose and glucose other than that some people have problem with the absorbstion in the colon as you say? 

It seems that fructose malabsorption is a function of over-consumption rather than an inherent fault in the colon. The fructose should be fully absorbed by the small intestine but is easily overloaded and excess fructose is carried to and  metabolised by colon bacteria, which will produce gasses much faster than the usual slower-metabolised food constituents.

Quote

Fructose is mostly absorbed in the small intestine through GLUT-5 transporter mediated facilitative diffusion. This is an energy independent process and consequently its absorptive capacity is carrier limited4 Glucose promotes intestinal fructose absorption by solvent drag and passive diffusion2, 5. However, excessive dietary intake of fructose as a monosaccharide can easily overwhelm the absorptive capacity of the small intestine leading to incomplete absorption of fructose (fructose malabsorption). The unabsorbed fructose can serve as an osmotic load and is thereby rapidly propelled into the colon, where its contact with anaerobic flora causes fermentation and production of gas, bloating and diarrhea6 (dietary fructose intolerance). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994910/

 

[Carl Fredrik Ahl]

2 hours ago, John Cuthber said:

I'm fairly sure the body can convert fructose to glucose.

Yes correct

[BabcockHall]

Fructose enters into glycolysis differently from glucose; it comes in later.  IIRC there is an aldolase that is distinct from the aldolase that we associate with glycolysis, but the details escape me at the moment.  Therefore, the regulatory controls which govern early glycolytic enzymes such as hexokinase and phosphofructokinase-1 are bypassed.  Although glucose 6-phosphate and fructose 6-phosphate are easily interconverted by phosphohexoseisomerase, IIRC this is not the point at which the pathway from fructose joins glycolysis.

[BabcockHall]

In muscles and kidneys, hexokinase converts fructose into fructose 6-phosphate and enters into the hexose phosphate pool at this point; it can be converted into fructose 1, 6-bisphosphate (the first committed step of glycolysis) or be converted into glucose 6-phosphate.  However, in liver fructokinase converts fructose into fructose 1-phosphate, which is cleaved into glyceraldehyde and dihydroxyacetone phosphate (DHAP) by an aldolase.  DHAP is converted into glyceraldehyde 3-phosphate GAP by triosephosphate isomerase and enters into glycolysis in this way.  Glyceraldehyde is separately phosphorylated to GAP and continues through glycolysis. 

Edited July 2, 2018 by BabcockHall
adde information on fructose 6-phosphate

[CharonY]

If you talk about ATP production from sugars, you should be aware of two mechanisms. One is substrate-level phosphorylation (e.g. direct transfer from a phosphate group to ADP to form ATP) and the second, major component, which is respiration. The former happens for example in the latter steps of glycolysis (i.e. from 1,3- bishphosphoglycerate and PEP). If fructose is introduced via Fru-6P or glyceryladehyde-3P (both of which cost and ATP) the pathway is exactly the same at that point as when you started with glucose.

The latter requires synthesis of NADH. which happens mostly in the TCA cycle. Thus substrates that enter it, can contribute to ATP production via that pathway. For possibilities of substrate level phosphorylation, see above post. While not related to ATP production per se, the formation of glyceraldehyde is another deviation, which often branches of to tracylglycerol synthesis rather that phosphorylation (which costs an ATP) and introduction into glycolysis. 

[BabcockHall]

There is controversy concerning whether or not a diet high in fructose is healthy.  I cannot evaluate this question without a great deal more study, but I found a few links for those wishing to pursue the topic.

Fructose metabolism in humans – what isotopic tracer studies tell us https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533803/

Fructose, but not glucose, impairs insulin signaling in the three major insulin-sensitive tissues https://www.nature.com/articles/srep26149

Fructose Consumption in the Development of Obesity and the Effects of Different Protocols of Physical Exercise on the Hepatic Metabolism 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409744/

[StringJunky]

11 minutes ago, BabcockHall said:

There is controversy concerning whether or not a diet high in fructose is healthy.  I cannot evaluate this question without a great deal more study, but I found a few links for those wishing to pursue the topic.

Fructose metabolism in humans – what isotopic tracer studies tell us https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533803/

Fructose, but not glucose, impairs insulin signaling in the three major insulin-sensitive tissues https://www.nature.com/articles/srep26149

Fructose Consumption in the Development of Obesity and the Effects of Different Protocols of Physical Exercise on the Hepatic Metabolism 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5409744/

It also suspected to cause increased visceral adiposity ('belly fat') compared to glucose.

Quote

Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance.

Abstract

PURPOSE OF REVIEW:
Based on interim results from an ongoing study, we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance. From these results and a review of the current literature, we present two potential sequences of events by which fructose consumption may contribute to metabolic syndrome.

RECENT FINDINGS:
The earliest metabolic perturbation resulting from fructose consumption is postprandial hypertriglyceridemia, which may increase visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver. With insulin resistance, VLDL production is upregulated and this, along with systemic free fatty acids, increase lipid delivery to muscle. It is also possible that fructose initiates hepatic insulin resistance independently of visceral adiposity and free fatty acid delivery. By providing substrate for hepatic lipogenesis, fructose may result in a direct lipid overload that leads to triglyceride accumulation, novel protein kinase C activation, and hepatic insulin resistance.

https://www.ncbi.nlm.nih.gov/pubmed/18196982