REVIEW

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Lactose, Maltose, and Sucrose in Health and Disease

Xin Qi* and Richard F Tester

perhaps honey, would not be found in

Scope: This review represents a focus on the structure and properties of the nature. It is thus sugary drinks have re-
common nutritional disaccharides (lactose, maltose, and sucrose) in health ceived most health-related concerns in
and disease. The aim is to provide a comprehensive reference source related the literature.
to the role of disaccharides in human nutrition.
Methods and results: Key reference sources are searched, including Web of
Science, PubMed, Science Direct, and Wiley Online, and key reference works
2. Structure and Properties
are selected to support the factual basis of the text where interpretations and
relevance of the works are discussed in the review. There are key nutritional The disaccharides lactose, maltose, and
sucrose are composed of galactose plus
health benefits of receiving dietary energy in the form of sugars, but equally
glucose, glucose only, and glucose plus
life-threatening issues exist associated with constant/excess consumption. fructose, respectively, which exist with
These issues are discussed together with genetic disorders, which impact specific bonding profiles: namely 𝛽-(1-
upon health associated with consumption of the disaccharides (e.g., specific 4) for lactose, 𝛼-(1-4) for maltose, and
disaccharide intolerance due to deficiency of relevant digestive enzymes). glucose-𝛼-(1-2)-𝛽-fructose for sucrose
Conclusions: As the three common dietary disaccharides (lactose, maltose, (Table 1). These configurations leave free
reducing ends (aldehyde groups in the
and sucrose) are consumed on a very regular basis in the human diet, it is
non-ring conformations) for the glucose
critical to understand insofar as possible their role in health and disease. This residues (C1) in lactose and maltose
review provides an insight into the structure and properties of these but loss of reducing power for sucrose
molecules in health and disease. as the potential reducing end (ketone)
of fructose (C2) is bonded to C1 of the
glucose residue.
Lactose is located within mammalian milk (“milk sugar”, pro-
1. Introduction vides energy for the baby when sucking), maltose within malted
This review “follows” a review on monosaccharides by the same (germinated) grains (although made by man during starch hy-
authors,[1] and readers are referred to that article to get further drolysis too and especially within high maltose syrups), and su-
insight into the positive and negative health-related issues asso- crose universally in plants as a carbon transfer molecule and en-
ciated with the constituent monosaccharides. In some situations, ergy reserve (especially, high concentration within sugar cane
the disaccharide molecules themselves provide gut (rather than and sugar beet). Maltose will also be generated in the gut dur-
systemic)-focused health-related issues while in other situations, ing starch digestion (which proceeds via the dextrinization of the
it is their constituent monosaccharides that have a deleterious starch molecules in the small intestine due to 𝛼-amylase). More
health impact. details regarding the sources of these disaccharides can be found
In terms of sugar-related health issues generally, it is im- in Table 2. Although the molecular weight of these three disac-
portant to recognize that energy is required by the body and charides is the same, their physical properties differ considerably
that sugars provide energy. The context of consumption is im- as shown in Table 3. The solubility and sweetness of sucrose is es-
portant however—for example, if sugars are consumed within pecially different in comparison with the other two disaccharides
fruit, other nutrients and digestive moderating tissues of the (Table 3).
fruit structure are co-consumed and thus the body has to extract Cooking of foods creates substantial transformation of the
the sugar from the fruit. On the other hand, sugary drinks pro- constituent molecules, including sugars. A reducing sugar con-
vide a more intense “dose” of sugar which, with the exception of denses with a free amino group (amino acid or proteins, es-
pecially the 𝜖-amino group of lysine, but also the 𝛼-amino
groups of terminal amino acids) to give a condensation prod-
uct which via the Amadori rearrangement product (ARP) devel-
Dr. X. Qi, Prof. R. F Tester
ops brown colored compounds, created through a number of
Glycologic Limited
Glasgow G4 0BA, UK complex reactions.[2,3] Sucrose (a non-reducing sugar) can only
E-mail: e.qi@glycologic.co.uk; r.f.tester@glycologic.co.uk brown, however, when pre-hydrolyzed to glucose and fructose.
Glycation end products or more usually “advanced glycation
The ORCID identification number(s) for the author(s) of this article end products (AGEs)” incorporate proteins or lipids that are gly-
can be found under https://doi.org/10.1002/mnfr.201901082 cated. Animal foods are often rich in these types of molecules,
DOI: 10.1002/mnfr.201901082 which may be generated further during food processing.

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Using sugar glycine models, the order of browning for differ-
ent sugars reported by Buera et al.[4] at pH 6 was xylose > glucose
> fructose > lactose > maltose > sucrose, reflecting the capacity
of the individual sugars to react with the amino groups of glycine.
It is well established that with respect to browning reactions with
different types of reducing sugars, pentoses react > hexoses >
disaccharides.[5]
3. Effects on Health
The effects on health include (in alphabetical order):
3.1. Acrylamide
During the thermal processing of food, when browning type re-
actions occur (discussed above), amino acids (asparagine espe-
cially) can react with reducing sugars to generate acrylamide.[3,6,7]
Acrylamide is a potential carcinogen and hence the growing con-
cern associated with acrylamide presence in food and the poten-
tial to cause (chronic especially) disease. Tumors may be created
at multiple sites in the body post consumption of acrylamide, as
has been shown, for example, in rodents.[8]
3.2. Advanced Glycation End Products
There are some associations/correlations of advanced glycation
end products with aging and disease states such as Alzheimer’s
disease, atherosclerosis, diabetes, and kidney disease. Only the
low-molecular-weight advanced glycation end products are ab-
sorbed actually from the diet. It is not understood if or how di-
etary advanced glycation end products may contribute to disease
and aging, or if only advanced glycation end products produced
within the body have the perceived health-related significance.
3.3. Blood Lipid Profile Debate
There is a relatively heated debate about the impact of ingested
sugars and, in particular, sucrose on blood lipid profiles. In some
reports, sucrose appears as a more favorable passive dietary com-
ponent with respect to impact on blood lipids than others. This
debate has been linked to the commercial interests of manufac-
turers of sucrose in some publications. The specific cause of con-
cern has been the development of coronary heart disease due
to sucrose consumption.[9] Cholesterol, low-density lipoprotein,
and high-density lipoprotein changes in the blood have been re-
viewed in detail by Jameel et al.[10] They discussed the role of fruc-
tose, glucose, and sucrose in this context and concluded that fruc-
tose has the greatest impact on blood lipids. Readers are referred
to, for example, the recent review of Kearns et al.[9] to understand
the detailed concerns with respect to fructose (and hence sucrose)
consumption on the generation of a negative blood lipid profile.
Hypertriglyceridemia due to sugar consumption is key to their
concerns, an issue discussed in detail as long ago as 1969.[11]
Some of these related issues are addressed with respect to other
health concerns below.
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Xin Qi obtained her Ph.D. in
Starch Chemistry in 2002. Since
then she has been working at
Glycologic Limited, developing
new technologies involving car-
bohydrates in the areas of food,
nutrition, and pharmaceuticals.
Richard Tester has run Glyco-
logic Limited since its creation
in 2002, having worked previ-
ously in the academic and in-
dustrial sectors for many years
on carbohydrate structures and
properties, plus their applica-
tions in food and drink, clinical
nutrition, and pharmaceutical
applications.
3.4. Cancer
Sugars, fructose in particular (and hence sucrose), are associated
with an increased risk of cancer.[9,12–14] Different forms of cancer
have been reviewed by these authors. In general, fructose, and
hence sucrose, provides the greatest cause of concern for trig-
gering different forms of cancer. Presumably, the sugars provide
energy in excess of basal requirements for cell replication and
growth. Fructose (and hence sucrose) have been linked especially
to the development of breast cancer in particular.[14]
3.5. Cognition
There are loose links between cognitive decline and sugar
intake, although there is a sense that cognition more broadly is
associated with a healthy diet.[7,15,16] Ginieis et al.,[17] however,
have indicated that “neuro-cognitive research has confirmed that
glucose, as a main energy substrate for the brain, can momen-
tarily benefit cognitive performances, particularly for memory
functioning.” This is not surprising in that glucose (which may
be derived from relevant disaccharides and starches of course) is
the key source of energy for the brain.[9,13,18] The brain requires
a constant drip-feeding of glucose from the diet. In fact, adult
brains require about 100 mg min−1 glucose and infants about
twice this amount.[15]
3.6. Glycemic Index
The glycemic index (GI) is a measure of the relative ability of a car-
bohydrate or carbohydrate containing drink or food to increase
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Table 1. Lactose, maltose, and sucrose disaccharide constituents.

Disaccharide Constituents Chemical name Bonding profile

Lactose Galactose plus glucose 𝛽-d-galactopyranosyl-(1→4)-d-glucose Galactose–glucose 𝛽-(1-4) bond

Maltose Glucose 𝛼-d-glucopyranosyl-(1→4)-d-glucose Glucose–glucose 𝛼-(1-4) bond
Sucrose Glucose plus fructose 𝛼-d-glucopyranosyl-(1→2)-𝛽-d-fructofuranoside Glucose–fructose glucose-𝛼-(1-2)-𝛽-fructose

Table 2. Examples of lactose, maltose, and sucrose sources. affect mood/activity. Some authors on the other hand have re-
ported a greater correlation and believe there is a connection be-
Disaccharide Natural sources Man-made sources tween ADHD and sugary drink consumption.[25]
Lactose Milk Milk(s); cheese; yoghurts;
ubiquitous ingredient in
different foods and drinks 3.8. Metabolic Disease
Maltose Malted grains Hydrolyzed starches; ubiquitous
(malt) ingredient in different foods and Metabolic disease is a combination of diseases related largely to
drinks; malt-containing drinks over consumption of food. It refers to cardiovascular disease, type
Sucrose Plants; fruits; Table sugar extracted from sugar 2 diabetes, and non-alcoholic fatty liver disease combined as dis-
vegetables beet or cane; ubiquitous cussed by Das[13] and Stanhope[28] and under the respective sec-
ingredient in different foods tions below. In common with other disease states linked to sugar
and drinks
excess, fructose/fructose containing sugar (sucrose) appears to
be of particular concern.
the concentration of glucose in the blood.[7,19] Foods are classi-
fied as high, medium, or low GI depending on their capacity to
3.8.1. Cardiovascular Disease
impact on the blood glucose.[20] A GI of ≥70 is considered as high
and ≤55 as low.
Cardiovascular disease (CVD) involves the heart and/or blood
The relative glycemic indices (GI) of different sugars are:
vessels and includes angina and myocardial infarction especially,
although many other disease states are included in the defini-
• Maltose 105 (high)
tion. There appears to be a positive correlation between blood
• Glucose 100 (high)
triglyceride (TG), very-low-density lipoprotein (VLDL), and low-
• Sucrose 65 (medium)
density lipoprotein (LDL) and sugar consumption (especially
• Lactose 46 (low)
fructose), inversely with high-density lipoprotein (HDL), as dis-
• Galactose 23 (low)
cussed elsewhere.[7,16,19,28–30] (See also the blood lipid discussion
• Fructose 19 (low)
section above.) The blood lipid profile as a consequence of excess
sugar consumption is thus a real risk factor and concern for the
The disaccharides tend to “sit” almost on average between the
development of cardiovascular disease.
GI of their constituent monosaccharides. This is not unexpected,
as the constituent monosaccharides are absorbed from the gut
into the blood stream. Note that when water is “added back” 3.8.2. Diabetes (Mellitus)
(water of hydrolysis) to maltose upon hydrolysis, the apparent
“amount” of free glucose increases and hence the GI of 105. Diabetes mellitus is evident when blood glucose control is
defective in the body and where i) fasting blood glucose is
> 7.0 mmol L−1 ; ii) glucose exceeds 11.1 mmol L−1 2 h after the
3.7. Hyperactivity—Attention Deficit Hyperactivity Disorder consumption of 75 g glucose; iii) other medical symptoms asso-
ciated with high blood glucose and/or; iv) glycated hemoglobin
Milich et al.[21] discussed the various relatively inconclusive re- (≥11.1 mmol L−1 ). Type 1 reflects loss of the insulin-producing
ports on a relationship between sugar consumption and attention beta cells in the pancreas (in most cases autoimmune in nature).
deficit hyperactivity disorder (ADHD). Others in more recent re- Type 2 reflects insulin resistance (of tissue) in the body with per-
ports took a similar inconclusive cause versus effect view.[7,22,23] haps reduced insulin production. Body mass is correlated with
Johnson et al.[24] took the same view as the other authors based insulin resistance.[31] The effect of specific sugars rather than ex-
essentially on existing data but discussed the issues in the context cess calories per se on the development of type 2 diabetes is the
of neurotransmitter signaling. They indicated that “…chronic ef- subject of much debate and in many cases conflicting opinion.
fects of excessive sugar intake may lead to alterations in mesolim- This lack of a coherent picture has been reviewed by Laville and
bic dopamine signaling, which could contribute to the symptoms Nazare.[32]
associated with ADHD.” They also reported that ADHD “may Different sugars have different impacts on blood glucose (see
be associated with a disruption in dopamine signaling whereby sections above), where lactose has a consistently lower impact
dopamine D2 receptors are reduced in reward-related brain re- in this respect post ingestion than sucrose in test diets.[33] Fruc-
gions.” Hence, in this context, circulating nutrients/drugs may tose (and hence sucrose) is of particular focus and concern with

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Table 3. Physical properties of lactose, maltose, and sucrose.
Disaccharide Melting point [°C] Molecular weight [g mol−1 ]
Lactose 203 342.3
Maltose 102 342.3
Sucrose Decomposes at 186 342.3
respect to the development of type 2 diabetes in individuals.[34]
It is apparent from previous sections and Paper 1 in this series[1]
how fructose in particular impacts negatively on health. Monto-
nen et al.[35] reported that a “combined intake of fructose and
glucose was associated with the risk of type 2 diabetes but no
significant association was observed for intakes of sucrose, lac-
tose, or maltose.” According to Rippe et al.[16] however, “…sin-
gling out added sugars as unique culprits for metabolically based
diseases such as obesity, diabetes and cardiovascular disease ap-
pears inconsistent with modern, high quality evidence and is
very unlikely to yield health benefits.” Janket et al.[36] indicated
that “intake of sugars does not appear to play a deleterious role
in primary prevention of type 2 diabetes.” Hence, the respec-
tive role of sugars versus (excess) calorie consumption in terms
of type 2 diabetes development is, according to some groups,
less clear cut than other groups’ report. The overall role of (dif-
ferent) sugars with respect to an association with the develop-
ment of diabetes (type 2) has been discussed in further detail by
others.[7,16,28–30]
3.8.3. Non-Alcoholic Related Fatty Liver
This disease state reflects a buildup of fat in the liver and is as-
sociated most often with obesity. Sugar consumption (especially
fructose) is associated negatively with the development/presence
of fatty liver, which correlates with an excess accumulation of fat
in the individual liver hepatocyte cells.[7,16,28–30,37]
Das[13] discussed the specific issue of fructose (sucrose) con-
sumption in comparison with glucose to cause fatty liver and has
indicated all fructose consumed in the diet is taken up by the
liver and converted to fat rapidly. However, glucose remains in
the bloodstream for some time and is used either for energy pro-
duction or conversion to glycogen. When energy demands are
met, only then it is converted to fat.
Hence, glucose has a more positive energy profile than fruc-
tose in terms of handling and storage in the liver and throughout
the body.
3.8.4. Monosaccharides Versus Disaccharides
In a sense, disaccharides do not impact on metabolic dis-
ease directly as they have to be converted to their constituent
monosaccharides in the gut, and it is the monosaccharides them-
selves which are the causative agents of the conditions. Read-
ers are referred to a previous publication by these authors on
monosaccharides[1] for more details.
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Density [g cm−3 ] Solubility [g L−1 ] Sweetness (relative to sucrose = 1) Energy [kcal g−1 ]
1.525 190 (25 °C) 0.2 3.75
1.540 1080 (20 °C) 0.4 3.75
1.587 2000 (25 °C) 1 3.75
3.9. Non-Ingested Fate of Disaccharides as a Point of Nutritional
Reference
In normal health, disaccharides are not absorbed through the gut
but are converted by the digestive enzymes to their constituent
monosaccharides which are absorbed.
Disaccharides do not exist in the blood stream. Weber et al.[26]
infused 10 g of lactose, sucrose, or maltose in adults and found
no rise in blood glucose where a mean of 8.7 ± 1.89 g lactose and
6.3 ± 1.39 g sucrose was excreted in a 24-h urine sample. Only a
very small quantity (0.11 ± 0.03 g) of the maltose was recovered in
the urine, indicating that unlike the other disaccharides, the mal-
tose was metabolized. Clearly, this is a very unnatural situation
where the gut was bypassed, where the key constituent enzymes
are located that convert disaccharides to monosaccharides.
As a matter of interest, there are unusual situations where dis-
accharides do appear in the blood stream and urine, and these are
not related to digestive disorders. One such example is drug users
which inject medications intended for oral consumption only.[27]
Here, the disaccharide excipients (carriers) of the oral drug for-
mats are injected into the blood and appear consequently in the
urine.
3.10. Obesity
Consumption of excess calories compared to their utilization
in the body leads to obesity. Overweight/obese body states re-
flect excess fat within the body leading to considerable health is-
sues. The body mass index (BMI) is calculated from a person’s
weight (kg) divided by the square of height in meters (m2 ). A BMI
of >25 represents excess weight and >30 obesity. The calories
within the diet may be consumed as different types of carbohy-
drates (sugars and amorphous starches). Sugar excesses are asso-
ciated extensively with obesity.[7,16,19,28–30,38,39] A diet rich in fruc-
tose (including sucrose) does in particular, according to some au-
thors, contribute to the onset and treatment-resistance of obesity
and obesity-related complications.[28–30,37–39] Fructose and thus
sucrose (over consumption) seem to be particularly problematic
in terms of excess bodyweight and hence growing concerns over
fructose utilization in drinks.[38] Later articles by some of the
authors[30] are not so heavily focused on fructose but more gener-
ally on the reduction of dietary calories (in the form of soft drinks
especially).
3.11. Osmotic Diarrhea
Excess intake of sugary drinks can cause (osmotic) diarrhea.[40]
This type of diarrhea can also be caused by congenital
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abnormalities associated with enzyme deficiencies (which will be
discussed later). The retention of water in the intestinal lumen
due to the osmotic pressure of the unabsorbed disaccharide, plus
sodium ion equilibrium, is the most important causative mecha-
nism of diarrhea with respect to disaccharide malabsorption.[41]
3.12. Satiety
Sugars promote satiety (“feeling full”), which leads to the con-
sumer reducing food intake. There are different physiological
and psychological elements to satiety. Although this response oc-
curs after eating, it cannot be due entirely to effect(s) on blood glu-
cose concentration.[42] Ochoa et al.[43] have discussed a range of
physiological mechanisms whereby different sugars might con-
trol and regulate satiety. Not all forms of drinks and food are
treated in the same way by the body. Liquid and solid foods may
impact differently on satiety and the role of the carbohydrate
needs to be viewed in this context.[7] Fructose may be less sati-
ating than glucose.[15,43]
3.13. Transit Through the Digestive System
Lactose, maltose, and sucrose can all be cariogenic, depending on
the consumption (amount, form, frequency, etc.) profile[15,44–47]
and the oral tooth hygiene procedures in place.
When experimental animals have been fed glucose, lactose,
maltose, or sucrose, there has been no clear distinction be-
tween the efficacy of the individual sugars for the creation of
periodontal syndrome in certain studies.[48] Studies reported by
other authors,[49] however, have shown that maltose encourages
the growth of Streptococcus mutans and formation of plaques less
than sucrose and especially less than lactose. This is contrary to
the commonly held view that lactose is far less cariogenic than
other sugars. Presumably, sugars in the diet are non-deleterious
in the mouth before tooth formation (as in babies), but once
teeth were in place, any sugars may become detrimental to tooth
health. The primary health measures for reducing caries risk,
from a nutritional perspective, are i) the consumption of a bal-
anced diet and ii) adherence to dietary guidelines and the dietary
reference intakes.[44] Clearly, oral hygiene is also of critical im-
portance.
Unless the disaccharides are malabsorbed (see above and be-
low), they will enter the blood stream after digestive enzyme hy-
drolysis as monosaccharides. If not, osmotic diarrhea will be ini-
tiated in the small intestine (see above and below). Thereafter,
any disaccharides not absorbed will enter the colon and ferment
causing great discomfort. Hydrogen, methane, and carbon diox-
ide gases will be generated. If the load is excessive, excretion of
the disaccharides in the feces will occur.
4. Related Diseases/Disorders
The disaccharides need to be hydrolyzed to their constituent
monosaccharides (in the small intestine) for the body to be able
to absorb and metabolize them. The monosaccharides are then
transferred across the gut epithelia by transporter systems.[1]
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Some disaccharides can be digested by man and can thus gen-
erate calories while other molecules pass through the small in-
testine.
4.1. Lactose
Lactase or 𝛽-galactosidase is a small intestine brush-border-
based/located enzyme which converts lactose into galactose and
glucose. Without this enzyme, the constituent monosaccharides
cannot be made available to the intestinal monosaccharide trans-
porters and hence enter the blood stream from the gut.[50–52] Ba-
bies would thus not be able to utilize this undigested disaccha-
ride for energy and growth. Congenital lactase deficiency leads to
osmotic diarrhea and lack of growth, caused by the undigested
lactose remaining in the digestive system. Late-onset lactase de-
ficiency (primary lactase deficiency) becomes prevalent later in
life.[53]
According to Heyman,[50] the following terms apply to lactose
intolerance/malabsorption/deficiency conditions:
• “Lactose intolerance is a clinical syndrome of one or more
of the following: abdominal pain, diarrhea, nausea, flatu-
lence, and/or bloating after the ingestion of lactose or lactose-
containing food substances.”
• “Lactose malabsorption is the physiologic problem that mani-
fests as lactose intolerance and is attributable to an imbalance
between the amount of ingested lactose and the capacity for
lactase to hydrolyze the disaccharide.”
• “Primary lactase deficiency is attributable to relative or abso-
lute absence of lactase that develops in childhood at various
ages in different racial groups and is the most common cause
of lactose malabsorption and lactose intolerance. Primary lac-
tase deficiency is also referred to as adult-type hypolactasia, lac-
tase non-persistence, or hereditary lactase deficiency.”
• “Secondary lactase deficiency is lactase deficiency that results
from small bowel injury, such as acute gastroenteritis, persis-
tent diarrhea, small bowel overgrowth, cancer chemotherapy,
or other causes of injury to the small intestinal mucosa, and
can present at any age but is more common in infancy.”
• “Congenital lactase deficiency is extremely rare; teleologically,
infants with congenital lactase deficiency would not be ex-
pected to survive before the 20th century, when no readily ac-
cessible and nutritionally adequate lactose-free human milk
substitute was available.”
• “Developmental lactase deficiency is now defined as the rela-
tive lactase deficiency observed among preterm infants of less
than 34 weeks’ gestation.”
The incidence of lactose intolerance in human is about
1/60 000 newborn babies, although probably around 70% of peo-
ple have a reduced ability to digest lactose after infancy.[50,52–55]
Nature would not have intended, it is assumed, adults to con-
sume milk from other animals or products made from milk.
Some cultures consume very little milk or milk-derived products.
Non-white populations are more affected with this recessive trait
than other ethnic groups.[51,54,56,57] For babies with lactase defi-
ciency, avoidance of lactose in the diet is critical so that they can
maintain health and survive. As an alternative to mammalian
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milk, they (babies) can drink either plant-based (soya) “milk”
(soya bean particles suspended in water and usually sweetened
with sucrose) or lactase-treated mammalian milks.[53] Different
plant-based products are available on the market.
4.2. Maltose
Maltose occurs in mature plants[58] although it tends to be as-
sociated with biosynthesis in germinated grains, especially bar-
ley, which is used for malt (malted barley of the malting pro-
cess) production.[59] Maltose is produced commercially as a sugar
by industrial processing (hydrolysis) of starch. Maltase activity
is conferred by different enzyme activities in the human small
intestine[60–69] as discussed below.
Maltase-glucoamylase (called also maltase commonly and
maltase-𝛼-glucosidase) is located in the brush border of the small
intestine and hydrolyses both i) maltose and ii) linear 𝛼-(1-4)
chains (of starch) to glucose; accounting for about 20% of the
small intestine’s “maltase” activity.[67,69] The dual activity of this
“double-headed” enzyme (within two separate domains for ac-
tivities (i) and (ii)) plays a critical role in amorphous starch di-
gestion. Consequently, the enzyme plays a crucial role in the
regulation of postprandial glucose homeostasis.[62] Historically,
the “maltase” activity of this enzyme was referred to as maltase
II and III activity.[63,68,70]
The incidence of maltase-glucoamylase deficiency disease in
humans is probably around 2% of children presenting with
Scheme 1. Malabsorption and maldigestion relevant to disaccharides (adapted from the text of ref. [77]).
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chronic diarrhea.[71] The enzyme deficiency and more especially
the associated diarrhea can be treated by eliminating starch (and
starch derivatives) from the diet.[71]
Sucrase-isomaltase (debranching enzyme or isomaltase) is lo-
cated in the brush border of the small intestine in common with
maltase-glucoamylase. The two-domain complex (which origi-
nated biochemically as one single polypeptide) has sucrase and
maltase activity in one domain (about 80% of small intestine
“maltase” activity), while in the other domain it has 𝛼-(1-6) de-
branching activity.[67,69] The two domain activities have been re-
ferred to as maltase Ib and maltase Ia, respectively.[63,70,72]
The incidence of primary sucrase-isomaltase deficiency dis-
ease is typically 1/500 to 1/2000 (of live births), although in some
populations the incidence is higher.[53,72–74]
Treatment (of chronic diarrhea, abdominal pain, and bloating)
is achieved by restricting sucrose and starch in the diet.[53,72–75]
However, this can be quite challenging as starch provides a large
proportion of dietary calories.[65] A secondary (transient) form of
the disease exists[74,76] with the same symptoms as the primary
form.
4.3. Sucrose
Sucrase-isomaltase deficiency has been discussed above. Dis-
orders of fructose metabolism have also been discussed
elsewhere.[1] Often ailments associated with sucrose con-
sumption are focused on the fructose moiety, although both
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Scheme 2. Examples of malabsorption syndromes relevant to disaccharides (adapted from the text of ref. [77]).
monosaccharides provide calories (which in excess can lead to
a range of diseases as discussed before).
4.4. Maldigestion Versus Malabsorption
Clark and Johnson[77] provided a very good definition of these in-
terrelated conditions as follows: “Malabsorption is impaired ab-
sorption of nutrients caused by any disruption in the process of
normal absorption. Impaired digestion of nutrients within the
intestinal lumen or at the brush border membrane can also in-
terfere with nutrient absorption. This is known as maldigestion.
Malabsorption and maldigestion differ pathophysiologically but
the processes of digestion and absorption are interdependent.
Therefore, in clinical practice, malabsorption refers to deficien-
cies in the process of both absorption and digestion.” These con-
cepts are highlighted in Scheme 1. In terms of specific malab-
sorption states that can affect disaccharide digestion/absorption,
examples of these are represented in Scheme 2. Clearly, a
number of factors can interplay to affect the digestion and sub-
sequent metabolism of disaccharides.
4.5. Gut Permeability Studies with Disaccharides to Identify
Disease
Previously (above), it was discussed that disaccharides do not en-
ter the blood stream via the gut as disaccharides themselves; they
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are converted to monosaccharides in the brush border of the gut
and absorbed thus. Disaccharides can be used therefore to mea-
sure the permeability of the gut to identify disease states of the
gut. Sucrose[78] has, for example, been used for this purpose.
5. Conclusions
The three common dietary disaccharides lactose, maltose, and
sucrose as themselves and their constituent monosaccharides
(galactose and glucose, glucose and glucose, glucose and fruc-
tose, respectively) provide health benefits (calories) but are also
associated with health issues due namely to:
1) their role as calorific sources and metabolic substrates;
2) health/disease states associated with the consumption of the
disaccharides as nutritional sources, for example, obesity, os-
motic diarrhea, tooth decay, and satiety;
3) disease states caused by processing induced modification, for
example, the generation of acrylamide;
4) congenital defects associated with metabolism.
Much is known about these disaccharides, although many
health-related issues associated with their consumption are still
largely misunderstood.
© 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
www.advancedsciencenews.com
Conflict of Interest
The authors declare no conflict of interest.
Keywords
gut health, lactose, maltose, metabolism, sucrose
Received: October 17, 2019
Revised: January 14, 2020
Published online: April 5, 2020
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