Sunday, January 06, 2019

Dietary-resistant starch and glucose metabolism

Recent findings in animal models suggest that resistant starch is beneficial for both body weight regulation and glycaemic control. The purpose of this review is to summarize the current evidence and recommendations in humans. When resistant starch replaces available carbohydrate in a meal, postprandial glycaemia is reduced. There are some data to suggest that resistant starch may affect glycaemia even when the available carbohydrate portion remains constant; however, there is inconsistency in the literature. Recent animal data suggest that chronic resistant starch feeding upregulates glucagon-like peptide 1 expression in the large bowel with concomitant increases in neuropeptide expression in the hypothalamus, combining to result in weight loss and improvements in glycaemic control. However, to date there is no evidence for this in humans. Resistant starch may have a role in glycaemic control in healthy individuals and those with type 2 diabetes; however, there are limited interventional trials in humans to support this. There are no data concerning resistant starch feeding in human diabetes and as such no health recommendation can be made.
however, the reliability of this is questioned especi-
ally with the inclusion of newer fibres such as the
oligosaccharides [fructooligosaccharide (FOS), for
example, is soluble yet nonviscous]. Viscosity is a
physiochemical property referring to the thickening
which occurs when mixed with fluids, and the
viscosity and the fermentability of a fibre by the
colonic microbiota are much more likely to predict
the impact of ingestion on human health, and of
course on plasma glucose than solubility alone.
Despite the National Academy of Sciences Panel
for the definition of dietary fibre (2002) [3] recom-
mending that the terms soluble and insoluble
should be replaced by viscosity and fermentability,
this is slow to be adapted by both the research and
clinical communities.
Resistant starch is a nonviscous fibre which is
also fermentable. Resistant starch can be classified
into four subtypes depending on botanical source
andprocessing:RS1,starchgranulesembeddedin
indigestible plant material such as found in whole
grains;RS2,nativegranularstarchsuchasfoundin
raw potato or high-amylose maize, wheat etc; RS3,
crystallized starch made by alternative cooking–
cooling and RS4, chemically modified starch typ-
ically through esterification, cross-linking or trans-
glycosylation. Resistant starch is of considerable
interest to the food industry as humans can toler-
ate relatively large amounts without the usual
gastrointestinal symptoms, but also relating to
the ease of use within food fortification producing
high-fibre foods which may be acceptable to the
consumer.
Many studies clearly demonstrate that the blood
glucose response is reduced when digestible CHO is
replaced with resistant starch [4], which has formed
the basis of the recent European Food Standards
Agency (EFSA, ID 681, April 2011) [5
&
] claim for
RS2. The EFSA claim for a reduction in postprandial
glycaemic response when RS2 replaces digestible
starch was upheld, but there is insufficient evidence
for the effects of RS2 when glycaemic CHO remains
constant.
So where do we stand in the aftermath of this
claim?
(1) In the opinion of EFSA, the beneficial effects of
RS2 were not unique to this type of resistant
starch and might be expected from all types of
resistant starch. Are all resistant starch really
created equal?
(2) Investigating the role of adding resistant starch
to food without diluting the available CHO will
be important. There is insufficient human evi-
dence currently to either support or refute a
health claim.
(3) Investigating the chronic intake of resistant
starch in humans and the impact on glycaemia
is required. Improvements in glycaemia over
time will rely on ‘metabolic adaptation’ in both
gastrointestinal and nongastrointestinal tissues
such as muscle, adipose tissue, liver, etc.
ACUTE EFFECTS OF RESISTANT STARCH
INTAKE ON GLYCAEMIA AND
INSULINAEMIA
Resistant starch, as a nonviscous fibre, would not be
expected to delay gastric emptying in a similar way
to that observed with viscous fibres [6] or to reduce
postprandial glycaemia as a consequence; however,
the only study to have categorically investigated
this using appropriate methodology concluded that
RS3 significantly hastened the gastric emptying
rate [7]. Manipulating the amylose:amylopectin
ratio involves by default, changing the digestible
component and glycaemic index, which although
forming part of the recent EFSA claim, cannot be
used to assess resistant starch as a true functional
food ingredient. More recently, in line with the
deficiencies noted by EFSA, studies have been pub-
lished in which the available CHO has remained
constant, with the only difference being the resist-
ant starch component. Studies using resistant
starch from different sources are summarized in
Table 1 [8–11]. Of note is the lack of consistency
KEY POINTS
Resistant starch is a nonviscous, highly fermentable
dietary fibre which is well tolerated in both humans
and animal models.
Resistant starch lowers glycaemia when it replaces the
available carbohydrate portion of a meal; this has
formed the basis of a recent European Food Standards
Agency (EFSA) health claim.
There are limited data in humans for resistant starch
reducing glycaemia, when the available carbohydrate
portion of a meal is not reduced.
There is no evidence for an improvement in
postprandial glycaemia following chronic feeding of
resistant starch in humans.
Resistant starch does improve insulin resistance in
humans following chronic feeding, through a
mechanism involving changes to both adipose tissue
and muscle metabolism.
There are no data on the effects of resistant starch
feeding in human diabetes.
Dietary-resistant starch and glucose metabolism Robertson
1363-1950 ß2012 Wolters Kluwer Health | Lippincott Williams & Wilkins www.co-clinicalnutrition.com 363



between the results obtained in terms of both post-
prandial glucose and insulin. Bodinham et al. [8]
found no impact on glycaemia using HAM-RS2, but
a significant reduction in the corresponding insulin
secretion during a meal tolerance test, whereas
in direct contrast to this Hallstro
¨met al. [9] found
a reduction in glycaemia and an elevation in post-
prandial insulinaemia feeding elevated-amylose
wheat (EAW). Could there be intrinsic differences
between resistant starch derived from maize rather
than wheat? The association between blood glucose
and insulin levels are not always straightforward
and potentially masked when samples are taken at
15 or 30min intervals. The glucose measured is a
balance between absorption, clearance and hepatic
release, which cannot be disentangled using simple
methodology.
CHRONIC EFFECTS OF RESISTANT
STARCH ON GLUCOSE CONTROL
Resistant starch has been fed to humans and animal
models in relatively large quantities, from a variety
of grains. Zhou et al. (2010) fed large doses (30%
HAM-RS2 diet) of RS2 to healthy rats and found that
there was less ‘fluctuation’ in the glucose and insu-
lin concentrations. In a more recent study, Brites
et al. [12] fed both resistant starch from maize and
wheat, again to healthy rats. Wheat-resistant starch
bread led to a significantly lower glucose response
than standard wheat bread, although it is not clear
as to whether the glycaemic index of the diets was
controlled. There was no effect of maize-resistant
starch on glucose levels. Zhu et al. [13] investigated
the effects of a high-amylose rice (HA2 transgenic
rice) compared to a wild-type; however, there was
no effect on fasting glucose or insulin levels after
4 weeks (postprandial data not measured). Recent
work in rat models documented a reduction in
jejunal alpha-glucosidase activity following 2-week
feeding of maize-resistant starch [14] which might
explain lower postprandial glucose digestion and
absorption of the available CHO portion when
resistant starch is present, although the effects of
starch source and the mechanism underlying this
effect are unknown. How does this compare to work
from humans? There is very little data in humans
following the chronic consumption of resistant
starch, where the glycaemic load/glycaemic index
of the diet is controlled. Pivotal work in 2005 [15] in
healthy individuals following 30 g maize RS2 per day
for 4 weeks found no effect on either fasting of
postprandial glucose levels, although insulin levels
were significantly reduced. It would appear from the
literature that there has not been a single study
feeding resistant starch chronically to humans
and measuring postprandial metabolism in over
6 years. Our own work in 2010, confirmed that there
was no effect of 40 g/day for 8 weeks in patients with
metabolic syndrome [16
&
] on fasting glucose or
insulin. It is clear that more work in humans is
warranted in order to translate the accumulating
animal literature.
IS RESISTANT STARCH INVOLVED IN THE
INCRETIN EFFECT?
There is consistent animal data demonstrating
the effects of resistant starch intake on endocrine
activity within the gastrointestinal tract [17] and
associated neuropeptide expression within the
arcuate nucleus (ARC) of the hypothalamus [18].
Both glucagon-like peptide 1 (GLP-1) and glucose-
dependent insulinotrophic polypeptide (GIP) are
still considered the most potent incretin signals
from the gastrointestinal tract. Although 50% of
GLP-1 secretion occurs directly from the colon,
secretion occurs immediately following a meal but
is degraded rapidly to the inactive form, GLP-1
(9–36). Plasma total GLP-1 is increased in healthy
rats fed resistant starch for 10 days [19], although
interestingly without the expected effects on either
Table 1. Are all resistant starch cereal grains equal in terms of glycaemic impact?
Grain Sample size Dosing Impact on glycaemia
Bodinham et al.
2010 [8]
Type 2 resistant starch
from high-amylose
maize (HAM-RS2)
Human. n¼20, randomized
design, GL controlled.
48 g HAM-RS given
acutely over
two meals.
No effects on plasma glucose.
Significantly lowers insulin
levels.
Hallstro
¨met al.
2011 [9]
High-amylose wheat
(EAW)
Human, n¼14, randomized and
balanced for available starch.
7.7 g RS Reduced glucose, elevated
insulin levels.
Li et al.
2010 [10]
GM RS-enriched rice Human, n¼16, compared to
wild-type (WT) rice
8 g RS Lower glucose and insulin
compared with WT.
Al-Tamimi et al.
2010 [11]
Chemically modified
RS4
XL
Human, n¼13, balanced for
available carbohydrate
20 g Lower glucose and insulin
levels.
GL, glycaemic load; GM, genetically modified; RS, resistant starch; WT, wild-type.
Carbohydrates
364 www.co-clinicalnutrition.com Volume 15 Number 4 July 2012

glucose or insulin levels. Proglucagon gene expres-
sion is also increased in both the caecum and colon
in vivo with short-chain fatty acids (SCFA) capable of
changing the gene expression in vitro in an STC-1
cell line, indicating the importance of fermentation
per se. Rodents have an enormously enlarged cae-
cum compared to their human counterparts and
combined with the larger doses of resistant starch
used, can these effects be translated into humans? At
the moment, no. The lack of chronic feeding studies
in humans has been highlighted. Resistant starch
would need to be fed for a long enough period in
humans not only for changes in the microflora to
become evident, but also for changes in tissue gene
expression. If we consider the lifespan of the two
species, 10 days in a rat may equate to 1 year in
human terms. Indeed, work using other fibres in
humans (wheat) has established that it may take
9–12 months for the effects on SCFAs and GLP-1 to
become evident [20]. Currently, the longest feeding
study in humans has been 12 weeks. Resistant starch
may impact on GLP-1 secretion in humans; how-
ever, currently there are no data to support this.
Although GIP is an incretin with potent effects
on insulin secretion, more recent findings have
linked high levels of GIP to impaired fat metabolism
[21] and the development of obesity. In addition,
GIP is released primarily from the upper gastro-
intestinal tract following the absorption of glucose
and long-chain fatty acids, and so the direct link
with fermentation is not clear. However, a recent
study in C57BL/6J mice fed a high-fat diet supple-
mented with resistant starch for 4 weeks found that
RS4 significantly reduced the postprandial GIP
response, whereas RS2 did not [22]. The explanation
for this is unclear but could be linked to a reduction
in nutrient absorption from the duodenum and
jejunum. Resistant starch feeding has been shown
to reduce GIP mRNA expression in the jejunum and
ileum in both healthy [23] and Goto-Kakizaki rats
[24]. This may be potentially explained by a
reduction in histone (H3 and H4) acetylation, reduc-
ing the transcriptional activity [24]. There is very
limited data on GIP levels following resistant starch
feeding in humans, so clear work is needed in this
area.
RESISTANT STARCH AND INSULIN
SENSITIVITY
In terms of the long-term effects of resistant starch
for the prevention of type 2 diabetes (primary pre-
vention Table 2) [25], changes in tissue insulin
sensitivity in hepatic and peripheral (adipose and
muscle) are important targets. Acute (single meal)
and semi-acute (overnight to next day) investi-
gations in themselves cannot answer this question,
any beneficial effect observed acutely with resistant
starch feeding must be maintained long-term and
involve true metabolic change. Resistant starch
feeding in humans increases the insulin sensitivity
[15,16
&
], when measured by the hyperinsulinae-
mic–euglycaemic clamp technique, which is con-
sidered to be the gold standard. Metabolic change in
humans is evident as reduced adipose tissue lipolysis
[15], increased uptake of glucose into skeletal
muscle [15], reduced triglyceride storage within
muscle [16
&
], increased uptake of SCFA into both
muscle and adipose [15], and increased meal
fat oxidation. Additionally, in animal models as
reduced lipogenic enzyme [14] and lipogenesis in
adipose tissue [26], reduced adipocyte size [27],
increased hepatic fatty acid oxidation [22] and
upregulation of fatty acid catabolism-related liver
enzymes [22]. Many of these effects are likely to be
directly or indirectly related to the SCFA produced
following fermentation. Despite all the beneficial
effects of resistant starch found, there have been
no effects reported on either systemic inflammation
(hsCRP, etc.) or vascular function.
Table 2. American Diabetes Association nutrient recommendations and interventions for diabetes
ADA recommendation for dietary fibre ADA position on resistant starch
Primary recommendation for the
prevention of diabetes
Individuals at high risk of diabetes should be
encouraged to achieve the USDA
recommended fibre intake of 14 g/1000 kcal.
Secondary recommendation for
the management of diabetes
As for the general public, people with
diabetes are encouraged to consume a
variety of fibre containing foods. However,
evidence is lacking to recommend a higher
fibre intake in people with diabetes.
There are no published long-term
studies in patients with diabetes
to prove benefits from the use of
resistant starch.
Tertiary recommendation for the
prevention of diabetes
complications.
None
ADA, American Diabetes Association. Data from [25].
Dietary-resistant starch and glucose metabolism Robertson
1363-1950 ß2012 Wolters Kluwer Health | Lippincott Williams & Wilkins www.co-clinicalnutrition.com 365



RESISTANT STARCH AND THE
MANAGEMENT OF TYPE 2 DIABETES
Despite all the potentially beneficial effects of
resistant starch noted in insulin-sensitive tissues,
there is not a single study in patients with type 2
diabetes to investigate the potential role of resistant
starch on glucose control (secondary management,
Table 2) [25]. There is also limited animal data in
this area.
Zhou et al. [19] fed resistant starch for 10 days
to the streptozotocin (STZ)-induced mouse model
of diabetes. Postprandial glycaemia was reduced
following resistant starch feeding, although insulin
and C-peptide were not measured. Zhu et al. [13]
fed HA2 high-amylose rice to this same mouse
model acutely and found no significant lowering
ofglucoselevels,despitethehigh-resistantstarch
rice having a lower glycemic load. This model of
chemically induced diabetes results in selective loss
of the beta cells without insulin resistance and as
such may be a more appropriate model of type 1
diabetes [28]. As such, the implication would be
that resistant starch feeding impacts directly on
beta-cell function.
Goto-Kakizaki rats fed resistant starch for 10
weeks were found to have an increased pancreatic
beta-cell density, although without an increase in
overall pancreatic insulin content [29]. Interestingly
though, pups born to these Goto-Kakizaki resistant
starch-fed dams did have a significantly higher
pancreatic insulin content, but no difference in
beta-cell density. Both dams and pups had lower
fasting glucose concentration, but postprandial
glucose was unaffected. Is there any evidence for
an effect of resistant starch on beta-cell function in
humans? At the moment, no. However, other fibres
(rye) have been shown to significantly increase first-
phase insulin secretion when fed to women with
metabolic syndrome for 8 weeks [30]. Although, as
rye contains bioactive compounds that resistant
starch does not (phenolic acids and tannins), results
cannot simply be extrapolated. Translating the
current animal data to humans could be potentially
important. The loss of the first-phase insulin
secretion is one of the earliest detectable defects
in the development of type 2 diabetes, it would be
interesting to speculate that resistant starch intake
could enhance beta-cell function or protect against
beta cell loss. Clearly, human data are now required.
CONCLUSION
The following unanswered questions should be
studied in-depth before a role of resistant starch
in human glucose metabolism can be attributed:
(1) Is there an impact of resistant starch in human
type 2 diabetes?
(2) Does resistant starch affect human beta-cell
function?
(3) Will longer term human feeding studies (>1 year
in length) reveal more about the true meta-
bolic effects of resistant starch on glucose
regulation?
A clear pattern is emerging within the animal
data for the potential importance of dietary-resist-
ant starch in metabolic health; however, the trans-
lational literature is lagging far behind. Perhaps
because of dosage issues, lifespan, anatomy or just
species differences, current evidence suggests that
animal models are failing to mimic humans in terms
of the metabolic effects of resistant starch. Ad libitum
resistant starch feeding in rodent models consist-
ently leads to weight and fat loss [17,18,29,31,32];
however, in humans there is no evidence for this
[15,16
&
]. With this caveat for the extrapolation of
animal data to humans, the need for high-quality
human clinical trials cannot be substituted by
animal models.
Acknowledgements
M.D.R. receives funding from Diabetes UK, the European
Foundation for the study of Diabetes (EFSD), BBSRC and
St Marks Foundation.
Conflicts of interest
There are no conflicts of interest.
REFERENCES AND RECOMMENDED
READING
Papers of particular interest, published within the annual period of review, have
been highlighted as:
&of special interest
&& of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (p. 405).
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Dietary-resistant starch and glucose metabolism Robertson
1363-1950 ß2012 Wolters Kluwer Health | Lippincott Williams & Wilkins www.co-clinicalnutrition.com 367




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