While there is significant talk of fructose’s negative roles in the body and the harm that it causes us, this article will not delve into those details. We will simply attempt to learn a bit more about fructose and its relationship to our body. We will learn about the molecule itself, we will dive into the digestion and absorption of fructose, and we will discuss the various functions and regulation of fructose within the body; this is, simply, a background article on the molecule.
What is Fructose?
Fructose is a simple sugar found in several foods, with the most commonly associated being fruit . Fructose is also a ketose sugar, meaning it has a ketone group (carbon with a double bonded oxygen), as well as the rest of the sugar component to its structure . Fructose is, otherwise, very similar to glucose in that it is the same chemical makeup (C6H12O6), but rather than forming a 6 carbon ring as in glucose, it typically forms a 5 carbon ring . Like glucose, it comes in two main forms, L-fructose and D-fructose, and like glucose, our body only utilizes D-fructose . Since it is a monosaccharide (simple sugar), it is the most base form of sugar and is absorbable by the body; again, it shares this characteristic with glucose and with galactose – the other two common simple sugars .
Digestion & Absorption
Fructose, as we now know, is a simple sugar, so finding it in its monosaccharide form is less likely than finding it in its combination form like a sucrose disaccharide (glucose + fructose) . That means, then, that our body must break sucrose apart through chewing, then travels to the stomach and is effectively broken apart from its glucose counterpart, putting it in its absorbable state as a monosaccharide.
A mechanistic view of the intestinal wall. You can see fructose entering the intestinal cell wall via GLUT-5 and GLUT-2 transporters.
Now, once fructose enters the intestines, it is absorbed by the intestinal lumen by, primarily, two transporters – GLUT-2 and GLUT-5; GLUT-5 being the primary of the two . Then, once inside the epithelial cells, from the lumen, fructose follows similar transporter as glucose and galactose by moving across into the blood stream via GLUT-2 transporter . Fructose is also absorbed slower than glucose and is absorbed more quickly if ingested with glucose (a form in which it is already commonly found – sucrose); if consumed in isolation (monosaccharide form), there is a chance for stomach irritation as not all of the fructose is absorbed and will be passed into the large intestine and excreted (diarrhea) .
Function of Fructose?
Fructose, surprisingly (or maybe not so surprisingly), is not too different from glucose in its function. While it is true that glucose is what the body ultimately runs on (at least when discussing sugars), it seems that fructose is often simply used as energy via the conversion to glucose (using fructose-6-phosphate via gluconeogenesis) or via fructolysis to fructose-1-phosphate, as well as a tiny percentage (less than 1%) is converted to fatty acids via de novo lipogenesis, some is converted to lactate, and some is converted to glycogen via glycogenesis, although the conversion from fructose to glycogen is about half as efficient as glucose to glycogen . So, that said, fructose seems to primarily be absorbed in the liver by GLUT-2, and a small amount can also be absorbed by the muscle cells via the same transporter .
Clearly, fructose is a largely insulin independent energy system that is, in almost every case, less efficient at supplying energy than glucose alone.
Too much fructose?
Now, this is a topic in and of itself, but I thought we could discuss it, briefly, here. There is a lot of data around fructose, but the conclusions created based on that data are, well, inconsistent. It is even difficult to say what is “too much” fructose considering there is no minimum requirement and there are varying thoughts on the intake of fructose, but we can still discuss some of the effects of fructose on the body, even if we won’t specify an amount that would be considered a “line” for “too high” (we may do so in a more specialized article on the topic since it is so polarizing).
Okay, so here it is: As we know, fructose does not stimulate insulin, hence it was thought to be potentially beneficial for those with diabetes since a reliance on insulin wouldn’t be necessary. However, the issue with this was that fructose ingestion led to an increase in circulating triglycerides (fats) . So, something about fructose leads the body to undergo lipolysis, which may be largely due to the little to no insulin stimulation, and since insulin reduces lipolysis, having less insulin could have us see the body releasing fat uninhibited . Insulin also promotes the uptake of triglycerides from the body into the fat cells, so the lack of insulin may have a doubling effect; this may also be exacerbated by the fact that glucose has a feedback mechanism to tell the cells not to release triglycerides, but fructose metabolism does not, as well as some fructose being converted to triglycerides in the liver .
So, while this may be a deciding factor for why fructose could be seen as not favorable for consumption, that isn’t the whole story.
It seems that extremely high fructose intake (1.5g/kg of bodyweight), independent of weight gain, leads to substantial increase in triglycerides – this we know; however, other studies have shown that fructose intake increases triglycerides, but only acutely (for a week or two), not chronically (over 2 weeks) . So, how do we make sense of this?
Well, while others are not sure what to conclude on the matter, I would venture to bet that the ingestion of 100% fructose does increase triglycerides, even chronically, because the studies investigating this phenomenon have used high percentage fructose . However, those studies that used sucrose (glucose + fructose), and high fructose corn syrup (50-55% fructose) saw an initial increase in triglycerides, but did not see it chronically . So, this means that there is a relationship between pure fructose and chronic triglyceride levels as opposed to disaccharide ingestion of fructose (with glucose) – maybe the stimulation of insulin from the attached glucose plays some role long term? I am merely speculating, but the association is intriguing.
On a side note, fructose seems to drop leptin levels, which may be indicative of the body’s inability to recognize it readily on its own . This may be one of the main mechanisms (along with lack of insulin) that leads fructose to generally be less satiating . However, some individuals do see a rise in ghrelin, but this is not generalizable, so based on the interactions listed, it seems that pure fructose leans more toward being less satiating than glucose . Again, though, high fructose corn syrup (55% fructose), seems to be as satiating as sucrose (glucose + fructose), so if fructose is paired with glucose, the increased hunger may be offset .
More on this particular subject will be written, but for now, it is understandable to think fructose is a confusing subject for many as the evidence is rather nuanced.
Too little fructose?
No such thing. Unlike glucose, we do not need to consume fructose. Admittedly, nutritionally, we do not need to consume glucose, either, but we need the molecule glucose in our system at all times, be that through the body’s synthesis of glucose or ingestion of glucose through nutrition. However, physiologically speaking, fructose has no necessary role.
In general, fructose is not too different from its brother, glucose. It has some interesting differences, aside from its different shape that set it apart; like, it fails to stimulate the release of insulin and debatably increases triglycerides in the blood. However, it can also be converted to useful glucose for the cells. It is likely that pure fructose may have deleterious effects, but as it is almost never consumed in pure form, the real investigation should be in its popularized presentation – roughly 50% of the ingested nutrient. In this form, it seems to be far less negative than its pure form, and this may be, at least biochemically, why there is debate if fructose is dangerous or not. While we did not investigate this directly, there are clear differences in its effect based on its presentation.
Writer: Nicolas Verhoeven
 Carbohydrates - Fructose. (n.d.). Retrieved from http://chemistry.elmhurst.edu/vchembook/543fructose.html
 D-Fructose | C6H12O6 - PubChem. (n.d.). Retrieved from https://pubchem.ncbi.nlm.nih.gov/compound/D-fructopyranose#section=Top
 Carbohydrate Structure and Function. (n.d.). Retrieved from
 monosaccharide. (n.d.). Retrieved from
 FILE NOT FOUND. (n.d.). Retrieved from https://www.rpi.edu/dept/bcbp/molbiochem/MBWeb/mb1/part2/sugar.htm
 Noelting, J., & DiBaise, J. K. (2015). Mechanisms Of Fructose Absorption. Clinical and Translational Gastroenterology, 6(11), e120. doi:10.1038/ctg.2015.50
 Absorption of Monosaccharides. (n.d.). Retrieved from http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_sugars.html
 Sun, S. Z., & Empie, M. W. (2012). Fructose metabolism in humans – what isotopic tracer studies tell us. Nutrition & Metabolism, 9(1), 89. doi:10.1186/1743-7075-9-89
 Teff, K. L., Elliott, S. S., Tschöp, M., Kieffer, T. J., Rader, D., Heiman, M., … Havel, P. J. (2004). Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women. The Journal of Clinical Endocrinology & Metabolism, 89(6), 2963-2972. doi:10.1210/jc.2003-031855
 Dimitriadis, G., Mitrou, P., Lambadiari, V., Maratou, E., & Raptis, S. A. (2011). Insulin effects in muscle and adipose tissue. Diabetes Research and Clinical Practice, 93, S52-S59. doi:10.1016/s0168-8227(11)70014-6
 Akhavan, T. (2007). Effects of glucose-to-fructose ratios in solutions on subjective satiety, food intake, and satiety hormones in young men. American Journal of Clinical Nutrition, 86(5), 1354-1363. Retrieved from
 Le, K. A. (2006). A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans. American Journal of Clinical Nutrition, 84(6), 1374-1379. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17158419
 Tappy, L., & Le, K. (2010). Metabolic Effects of Fructose and the Worldwide Increase in Obesity. Physiological Reviews, 90(1), 23-46. doi:10.1152/physrev.00019.2009
 Williams, H. R., & Landau, B. R. (1972). Pathways of fructose conversion to glucose and glycogen in liver. Archives of Biochemistry and Biophysics, 150(2), 708-713. doi:10.1016/0003-9861(72)90089-6
 Stanhope, K. L. (2008). Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. American Journal of Clinical Nutrition, 87, 1194-1203. Retrieved from http://ajcn.nutrition.org/content/87/5/1194.full.pdf+html
 Swanson, J. E. (n.d.). Metabolic effects of dietary fructose in healthy subjects. American Journal of Clinical Nutrition, 55(4), 851-856. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/1550068
 Stanhope, K. L., Schwarz, J. M., Keim, N. L., Griffen, S. C., Bremer, A. A., Graham, J. L., … Havel, P. J. (2009). Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation, 119(5), 1322-1334. doi:10.1172/jci37385
 Moran, T. H. (2009). Fructose and Satiety. Journal of Nutrition, 139(6), 1253S-1256S. doi:10.3945/jn.108.097956