What is fructose & how is it absorbed

Fructose exists in foods either as a monosaccharide (free fructose) or as a unit of a disaccharide (sucrose). Free fructose is absorbed directly by the intestine. When fructose is consumed in the form of sucrose, it is digested (broken down) and then absorbed as free fructose. As sucrose comes into contact with the membrane of the small intestine, the enzyme sucrase catalyzes the cleavage of sucrose to yield one glucose unit and one fructose unit, which are then each absorbed. After absorption, it enters the hepatic portal vein and is directed toward the liver.

The mechanism of fructose absorption in the small intestine is not completely understood. The majority of research supports the claim that fructose absorption occurs on the mucosal membrane via facilitated transport involving GLUT5 transport proteins. Since the concentration of fructose is higher in the lumen, fructose is able to flow down a concentration gradient into the enterocytes, assisted by transport proteins. Fructose may be transported out of the enterocyte across the basolateral membrane by either GLUT2 or GLUT5, although the GLUT2 transporter has a greater capacity for transporting fructose.

Capacity and rate of absorption

The absorption capacity for fructose in monosaccharide form ranges from less than 5g to 50g (per individual serving) and adapts with changes in dietary fructose intake. Studies show the greatest absorption rate occurs when glucose and fructose are administered in equal quantities. When fructose is ingested as part of the disaccharide sucrose, absorption capacity is much higher because fructose exists in a 1:1 ratio with glucose. It appears that the GLUT5 transfer rate may be saturated at low levels, and absorption is increased through joint absorption with glucose.

Fructose Malabsorption

Fructose malabsorption, or also called dietary fructose intolerance (DFI), is a digestive disorder in which the absorption of fructose in the small intestine is impaired. This leads to several abdominal symptoms like bloating, pain, nausea and cramps. For some time, the public didn’t know of this disease and physicians often overlooked it. Today we know, that almost 40% of the population are suffering from some kind of fructose malabsorption, 30% of these people show the typical symptoms.

Fructose malabsorption is sometimes called “fructose intolerance”. This term is misleading, as there is a disease called Hereditary Fructose Intolerance (HFI) which is even more serious. This is discussed in more depth further on.

What is wrong in case of fructose malabsorption?

In the case of fructose malabsorption the protein GLUT5, which is involved in the absorption of fructose along the entire small intestine, is impaired. Meaning the absorption of fructose is reduced. The remaining fructose reaches the colon and is rapidly fermented by intestinal bacteria, as shown in the figure above.

This bacterial fermentation results in the formation of hydrogen, carbon dioxide, methane and short-chain fatty acids (e.g. butyric and acetic), which causes abdominal symptoms like bloating, pain, and cramps.

Furthermore, untreated fructose malabsorption leads to a proliferation of intestinal bacteria and yeast, which metabolize the fructose. This worsens the symptoms over time.

The amount of tolerated fructose varies greatly among FrucMals. Some people may be able to ingest modest amounts of fructose without experiencing any problems, while others show symptoms even after very small amounts.

Hereditary Fructose Intolerance (HFI)

Besides fructose malabsorption, which can occur suddenly and as a result of external influences, there is also another fructose-related disease. It is called hereditary fructose intolerance. In contrast to fructose malabsorption, which is based on an impaired GLUT5 fructose transporter, hereditary fructose intolerance is a rare life-threatening disorder of the fructose metabolism within the human body. HFI is usually diagnosed in early childhood.

A genetic defect causes a deficiency in the fructose-1-phosphate aldolase B activity. This deficiency leads to the accumulation of fructose-1-phosphate, a derivative of fructose, within the liver. And this, in turn, causes severe toxic symptoms after fructose ingestion, such as serious hypoglycemia with tremors, vomiting, and disorientation. In the worst case, it can lead to convulsion and coma.

If too much fructose becomes a problem

In principle, every human being whether or not affected by fructose malabsorption can only consume a certain amount of fructose. Normally, the body does not have difficulty in reducing normal amounts of fructose. However, if large quantities of fructose enter the body over the long term, it may be unhealthy even for people who do not have fructose incompatibility.

In the early 1970s, the US food industry began to replace cane sugar on a large scale with HFCS (High Fructose Corn Syrup). Fructose has since been found in sweets, ready meals and also in many calorie-reduced foods. Overall, per-capita consumption of fructose has risen by about 20 percent in recent decades.

Sorbitol tolerance and fructose malabsorption

Industrially produced, calorie-reduced foods often contain sorbitol, which belongs to the group of sugar alcohols, in addition to fructose. As with fructose, it is a so-called sugar substitute. Even with a sorbitol tolerance or sorbitol intolerance, the degradation process in the small intestine is disturbed, so that the sugar can not be recycled or not sufficiently.

The body reacts with indigestion. If you suffer from fructose malabsorption, you should also completely remove sorbitol from your diet.

Xylose Isomerase, how does it work?

Xylose Isomerase is an enzyme that promotes the conversion of fructose into easily absorbable glucose, in the small intestine. A scientific double bind study conducted in 2012 by Sciotec Diagnostic Technologies, Austria. Found that orally administered dose of 43.12mg Xylose Isomerase significantly improved symptoms (Nausea and abdominal pain) in 84% of patients that ingested 25g fructose.  

An abstract from the 2012 study

BACKGROUND: Incomplete resorption of fructose results in increased colonic hydrogen production and is a frequent cause of abdominal symptoms. The only treatment available is diet.

AIM: To study whether orally administered xylose isomerase (XI), an enzyme that catalyses the reversible isomerisation of glucose and fructose, can decrease breath hydrogen excretion in patients with fructose malabsorption.

METHODS: Patients received 25g fructose in 100mL water together with either placebo or XI capsules. Primary endpoint was the reduction in breath hydrogen excretion, as assessed by the area under the breath hydrogen curve over 4 h (AUC). A secondary endpoint was the reduction in abdominal pain, bloating and nausea assessed on a visual analogue scale (VAS, range: 0-10). A P value <0.05 was considered statistically significant.

RESULTS: Sixty-five patients in whom fructose malabsorption had been diagnosed by positive breath hydrogen test within the previous year, were included in the study [15 males, 50 females; mean age 43.3 (s.d. = 14.4), range: 21-73 years]. The median AUC was 885 ppm/240 min in the XI group compared to 2071 ppm/240 min in the placebo group (P = 0.00). Median scores for abdominal pain (0.7 vs. 1.3) and nausea (0.2 vs. 0.6), but not for bloating (P = 0.053), were significantly improved after XI (P = 0.009 and P = 0.005) as compared with placebo.

CONCLUSIONS: Oral administration of xylose isomerase significantly decreased breath hydrogen excretion after ingestion of a watery fructose solution. Nausea and abdominal pain were significantly improved by xylose isomerase.