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Current Research on the Effects of Non-Digestible Carbohydrates on Metabolic Disease

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Metabolic diseases (MDs), including cardiovascular diseases (CVDs) and diabetes, occur when the body’s normal metabolic processes are disrupted. Behavioral risk factors such as obesity, physical inactivity, and dietary habits are strongly associated with a higher risk of MD. However, scientific evidence strongly suggests that balanced, healthy diets containing non-digestible carbohydrates (NDCs), such as dietary fiber and resistant starch, can reduce the risk of developing MD. In particular, major properties of NDCs, such as water retention, fecal bulking, viscosity, and fermentation in the gut, have been found to be important for reducing the risk of MD by decreasing blood glucose and lipid levels, increasing satiety and insulin sensitivity, and modifying the gut microbiome. Short chain fatty acids produced during the fermentation of NDCs in the gut are mainly responsible for improvement in MD. However, the effects of NDCs are dependent on the type, source, dose, and duration of NDC intake, and some of the mechanisms underlying the efficacy of NDCs on MD remain unclear. In this review, we briefly summarize current studies on the effects of NDCs on MD and discuss potential mechanisms that might contribute to further understanding these effects.
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Citation: Chanmuang, S.; Nguyen,
Q.-A.; Kim, H.-J. Current Research on
the Effects of Non-Digestible
Carbohydrates on Metabolic Disease.
Appl. Sci. 2022,12, 3768. https://
doi.org/10.3390/app12083768
Academic Editor: Andrea Salvo
Received: 28 February 2022
Accepted: 5 April 2022
Published: 8 April 2022
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applied
sciences
Review
Current Research on the Effects of Non-Digestible
Carbohydrates on Metabolic Disease
Saoraya Chanmuang 1, Quynh-An Nguyen 2and Hyun-Jin Kim 1, 2, *
1Department of Food Science and Technology, Institute of Agriculture and Life Science,
Gyeongsang National University, Jinju 52828, Korea; c.saoraya@gmail.com
2Division of Applied Life Sciences (BK21 Four), Gyeongsang National University, Jinju 52828, Korea;
an.ngqnh@gmail.com
*Correspondence: hyunjkim@gnu.ac.kr; Tel.: +82-55-772-1908; Fax: +82-55-772-1909
Abstract:
Metabolic diseases (MDs), including cardiovascular diseases (CVDs) and diabetes, occur
when the body’s normal metabolic processes are disrupted. Behavioral risk factors such as obesity,
physical inactivity, and dietary habits are strongly associated with a higher risk of MD. However,
scientific evidence strongly suggests that balanced, healthy diets containing non-digestible carbohy-
drates (NDCs), such as dietary fiber and resistant starch, can reduce the risk of developing MD. In
particular, major properties of NDCs, such as water retention, fecal bulking, viscosity, and fermenta-
tion in the gut, have been found to be important for reducing the risk of MD by decreasing blood
glucose and lipid levels, increasing satiety and insulin sensitivity, and modifying the gut microbiome.
Short chain fatty acids produced during the fermentation of NDCs in the gut are mainly responsible
for improvement in MD. However, the effects of NDCs are dependent on the type, source, dose,
and duration of NDC intake, and some of the mechanisms underlying the efficacy of NDCs on MD
remain unclear. In this review, we briefly summarize current studies on the effects of NDCs on MD
and discuss potential mechanisms that might contribute to further understanding these effects.
Keywords:
cardiovascular diseases; diabetes; dietary fiber; non-digestible carbohydrates; metabolic
disease; short chain fatty acid
1. Introduction
Metabolic disorders occur when the normal processes of macronutrients, such as
proteins, carbohydrates, and lipids, in the human body are disrupted by various factors
resulting in dysfunctions, including atherogenic dyslipidemia, insulin resistance, hyperten-
sion, and obesity [
1
]. Individuals with these dysfunctions are at high risk for developing
metabolic diseases (MD), such as cardiovascular diseases (CVD) and diabetes [
2
], both of
which are the most common cause of death globally [
3
]. The most important behavioral risk
factors of MD are obesity, physical inactivity, and dietary habits [
1
]. In particular, several
clinical trials and epidemiological studies suggest that dietary patterns characterized by
high consumption of sugars, fat, and salt and low consumption of polyunsaturated fatty
acids, vegetables, fruit, and fiber are strongly associated with a higher risk of MD [
4
].
Studies over the past decade using multiple genetic and diet-induced animal models have
shown that insulin and leptin signaling cascades and the brain and its central nervous
system are strongly involved in key metabolic signaling pathways of MD [
5
9
]. However,
some of the mechanisms underlying the pathogenesis of MD are still unclear [
10
] and the
use of drug therapies developed for the treatment of MD are also limited due to various side
effects [
11
]. Therefore, physical activity, weight control, and diet control are very important
to suppress the development of MD [
12
14
]. In particular, scientific evidence accumulated
over the last few decades strongly suggests that balanced healthy diets rich in fruits, veg-
etables, legumes, whole grains, fish, nuts, and low-fat dairy products can decrease the
risk of MD [
15
,
16
]. Consumption of certain plants, seaweeds, and fermented food-derived
Appl. Sci. 2022,12, 3768. https://doi.org/10.3390/app12083768 https://www.mdpi.com/journal/applsci
Appl. Sci. 2022,12, 3768 2 of 18
compounds is known to have excellent health effects in preventing and suppressing the de-
velopment of MD [
17
,
18
]. Among these compounds, non-digestible carbohydrates (NDCs),
mainly represented by resistant starch and dietary fiber, have received considerable at-
tention as one of the most important components of MD development because of their
numerous physiological advantages [
19
]. Many clinical and animal studies revealed that
high intake of NDCs increased intestinal viscosity, fecal bulking, and production of short
chain fatty acids (SCFAs) via gut fermentation, resulting in improving blood glucose, lipid,
and insulin levels, reducing energy intake, and promoting satiety [
19
]. It was released that
these physiological changes due to the high intake of NDCs were strongly correlated with
suppression of the incidence of MD. Moreover, many meta-analysis results have confirmed
the correlation between intake of NDCs and MD incidence [
20
]. However, their correlation
was different according to the type, source, dose, and duration of NDC intake [
21
] and
some of the mechanisms underlying the efficacy of NDCs on MD remain unclear.
Therefore, the aim of this review is to discuss how NDCs regulate the incidence of MD,
including obesity, diabetes, and CVD, by focusing on mechanisms by which the physical
and fermentation properties of NDCs in the gastrointestinal (GI) system interfere with the
absorption of MD risk-associated metabolites, increase satiety, and improve gut health.
2. NDCs
NDCs are complex carbohydrates that resist hydrolysis by salivary and intestinal
digestive enzymes in the small intestine of humans owing to the configuration of their
osmotic bonds. NDCs, which are a heterogeneous group of carbohydrates with varying
chemical structures, consist primarily of carbohydrate polymers, such as resistant starch [
22
]
and non-starch polysaccharides that are components of plant cell walls, including cellulose,
psyllium fiber,
β
-glucan, hemicellulose, and pectin, as well as other polysaccharides and
oligosaccharides, such as gums, alginate, and inulin [
23
,
24
]. As shown in Table 1, these
NDCs are generally separated into water-soluble and insoluble NDCs [
23
,
25
,
26
]. Soluble
NDCs, including pectin, psyllium fiber,
β
-glucan, fructans, fructooligosaccharide (FOS),
galactooligosaccharide (GOS), gums, and hydrocolloids, are generally separated from oats,
fruits, vegetables, barley, seaweeds, or pulses [
23
,
27
,
28
], while insoluble NDCs, including
cellulose and some hemicellulose, are separated from whole grains, cereal brans, fruits, and
vegetables [
29
]. The solubility of NDCs is determined according to the length, type, location,
and binding type of monosaccharide units, which are generally joined by
β
-glycosidic
bonds [
25
], and is an important factor for determining their physical properties, such as
water retention, viscosity, and fecal bulking ability, as well as their fermentation properties
in the large intestine [
25
,
26
]. Many clinical and animal studies have suggested that these
properties are strongly associated with the health benefits of NDCs [21,23,24].
Appl. Sci. 2022,12, 3768 3 of 18
Table 1. Types of NDCs and their properties.
Type Structure Source Properties References
Soluble dietary fiber
Guar Gum
A linear chain of β1,4-linked mannose residues to
which galactose residues are 1,6-linked at every
second mannose
Seeds of the drought tolerant plant Gel-forming, thickening, and stabilization. [27]
Locust Bean Gum Galactomannan composed of galactose and mannose
units combined through glycosidic linkages Seeds of the carob tree Film-forming. [21]
Pectin
Chain of α-(1 4)-linked D-galacturonic acid units
interrupted by the insertion of (1 2)-linked
L-rhamnopyranosyl residues in adjacent or
alternate positions
Cell walls and intracellular tissues of
fruits and vegetables
Emulsifier, gelling agent, thickener,
stabilizer, and fat or sugar replacer in
low-calorie foods
[23]
Hydroxypropylmethylcellulose (HPMC) Propylene glycol ether of methylcellulose Film forming, stabilizing, and thickening. [21]
β-Glucan Mixed-linkage polysaccharide (1 3), (1 4)
β-D-glucan Cell walls of oats, barley, rye and wheat Altering foods structure, texture, and
viscosity [23]
Psyllium husk Arabinoxylan with (1 4) and (1 3)
xylopyranose backbones Seeds of Plantango ovata
Gel-forming, produce low-calorie, and high
fiber foods [28]
Arabinoxylan Diversely composed (1 4)-β-D-xylan polymer Wheat
Film-forming, balance of carbohydrate-rich
foods, improve the viscosity, texture,
sensory characteristics, and shelf-life of
food products
[24]
Alginate
Linear unbranched polysaccharides which contain
different amounts of (1 40)-linked β-D-mannuronic
acid and α-L-guluronic acid residues
Brown seaweeds Gelling, viscosifying, and stabilizing [21]
Inulin and inulin-type fructans A mixture of linear fructose polymers with different
chain length and a glucose molecule at each C2 end Chicory roots
Bulking agent in foods, improve the texture,
mouthfeel, taste, and replace sugar or fat. [21]
High amylose starch (resistant starch II) D-Glucose units linked by R-1,4/R-1,6 glucosidic bonds Raw starch (green banana and
raw potatoes)
Increase of food’s functional properties
does not change its sensory characteristics. [22]
Galactooligosaccharide (GOS) β
-Linked galactose moieties with galactose or glucose at
the reducing end. Soybeans and lactose from cow’s milk Improve the texture of foods and as a
bulking agent. [30]
Polydextrose A polysaccharide composed of randomly cross-linked
glucose units with all types of glycosidic bonding
Produced from the naturally occurring
components: glucose, sorbitol, and
citric acid
Bulking agent, stabilizer, thickener,
and humectant [21]
Appl. Sci. 2022,12, 3768 4 of 18
Table 1. Cont.
Type Structure Source Properties References
Resistant maltodextrin/dextrin (resistant
starch V)
Oligosaccharides of glucose molecules that are joined by
digestible linkages and non-digestible α-1,2 and
α-1,3 linkages
Corn, wheat, potato, and tapioca Increase the nutritional value of food [31]
Insoluble dietary fiber
Cellulose Linear homopolymer of β-(1 4) linked
β-D-glucose residues
Cell wall of plant (vegetables, fruits,
and cereals)
Increase the content of fiber in food,
thickening, gelling, and stabilizing [29]
Soluble/Insoluble dietary fiber
Mixed plant cell wall fibers Cellulose, hemicelluloses, and pectin Fruits, vegetables, grains, legumes,
pulses, nuts, and other plants Increase the viscosity or gel strength [21]
Non-dietary fiber NDCs
Resistant starch I Physically embedded starch Seeds or legumes and unprocessed
whole grains
Ingredients for creating fibre-rich food,
increase swelling, viscosity, and gel-
forming capacity
[22]
Resistant starch III Regenerated starch Starch-containing foods are cooked and
cooled (corn starches, pasta, stale bread)
Improves texture, strength, and crispness in
baked goods and extruded products such as
cereals and snack foods
[22]
Resistant starch IV Chemically modified starch Chemically modified starches food
(breads and cakes)
Improve taste and texture, increase
swelling, viscosity, and gel-
forming capacity
[22]
Appl. Sci. 2022,12, 3768 5 of 18
3. NDC Characteristics Related to Health Benefits
The main characteristics of NDCs related to health benefits in the human body are
water retention, fecal bulking, viscosity, and fermentation, and these characteristics mainly
differ according to their water solubility, as mentioned above. Soluble NDCs are generally
viscous and can ferment quickly in the intestine, whereas insoluble NDCs are non-viscous
and slowly fermentable. A high intake of soluble NDCs with high viscosity-forming proper-
ties reduces postprandial blood glucose and blood cholesterol levels because high viscosity
can interfere with the absorption of cholesterol and monosaccharides in the intestine [
32
].
Moreover, some in vitro studies have suggested that soluble NDCs could decrease gastric
and pancreatic lipase activities because of the reduction of lipid emulsion caused by the
high viscosity of these soluble NDCs, resulting in a decrease in lipid absorption, small
bowel motility, and intestinal miscibility and an increase in the thickness of the unsettled
water layer, which might delay the final stage of lipid assimilation [
32
]. In addition to
soluble NDCs, a high intake of insoluble NDCs provides a fecal bulking effect linked to
various intestinal functions, including promoting regular bowel movement and increasing
fecal volume [
33
]. Although differences in the effects of soluble and insoluble NDCs on
gut microbiota are not clear, these properties are strongly related to changes in the gut
microbiota population [
34
]. The many functions of gut microbiota include contributing to
changing the bile acid pool in the gut, especially secondary bile acids, such as deoxycholic
acid and lithocholic acid, which are associated with a number of physiological functions,
including inflammation, CVDs, the immune system, and colon cancer [
35
]. Moreover,
during fermentation, the population of healthy gut microbiota increases, and by-products
such as SCFAs, including acetate, butyrate, and propionate, are produced [
36
]. SCFAs
play important physiological roles associated with various health benefits [
37
] throughout
the body as well as in the large intestine, including reducing the risk of coronary heart
disease, diabetes, CVD, and some cancers, and improving the immune system [
35
,
38
].
Accumulating evidence suggests that the population and diversity of gut microbiota as-
sociated with the production of secondary bile acids and/or SCFAs significantly change
according to the type, source, dose, and duration of NDC intake [
37
,
39
]. A piglet model
study showed that insoluble fibers such as cellulose and soluble fibers such as inulin
increased the relative abundance of Bacteroidetes,Phascolarctobacterium, and Coprococcus,
and Actinobacteria,Proteobacteria, and Blautia, respectively, which are the main bacteria that
produce SCFAs [40].
4. NDCs and SCFAs
During the last few decades, scientific evidence of the health benefits of NDC con-
sumption has accumulated. In particular, the relationship between gut health and NDCs is
well-demonstrated. The mechanisms by which NDCs modulate host health through the
gut microbiota are summarized in Figure 1. NDCs are fermented by the gut microbiota
and SCFAs; primarily, acetic acid, butyric acid, and propionic acid associated with var-
ious physiological functions in the human body [
41
] are produced during fermentation.
SCFAs produced from NDCs stimulate the secretion of satiety hormones, glucagon-like
peptide (GLP-1) and peptide tyrosine tyrosine (PYY) [
42
], through the activation of G
protein-coupled receptors (GPRs), GPR41 and GPR43, of the enteroendocrine L-cells in the
intestine, especially in the ileum and colon [
41
]. Both hormones influence the hypothalamus
to promote satiety. PYY acts on the arcuate nucleus in the hypothalamus, leading to the
suppression of neuropeptide Y neurons to promote satiety, activate proopiomelanocortin
neurons, reduce intestinal transit time from the mouth to the cecum, and decrease the
gastric emptying rate [
5
,
43
]. Moreover, GLP-1 stimulates the hypothalamus by binding
to the GLP-1 receptor, improving insulin sensitivity, and promoting glucose tolerance by
acting on pancreatic
β
-cells [
6
,
7
]. Furthermore, SCFAs can be converted into glucose via
intestinal gluconeogenesis (IGN), which activates adipocytes to produce leptin, thereby
improving satiety and preventing obesity [
8
]. Additionally, an increase in IGN by SCFAs
Appl. Sci. 2022,12, 3768 6 of 18
inhibits hepatic gluconeogenesis, resulting in increased glucose tolerance. For example,
butyrate activates IGN gene expression through a cAMP-dependent mechanism, whereas
propionate, an IGN substrate, stimulates IGN via a gut-brain neural circuit [
44
]. Along
with the direct effects of SCFAs, SCFAs shift the intestinal environment by decreasing pH,
preventing overgrowth of pH-sensitive pathogenic bacteria [
45
,
46
] and protease activity
associated with the production of harmful metabolites, such as ammonia, a potentially
carcinogenic product of protein fermentation [
47
,
48
]. Moreover, SCFAs are involved in
the intestinal defense system against pathogens and toxic compounds [
49
]. The primary
physical intestinal barriers that protect the gut from pathogen infection or toxic compounds
are mucin secreted from goblet cells and tight junctions (TJs) between mucosal epithelial
cells [
9
]. SCFAs improve gut barrier function by modulating the expression of mucin and TJ
proteins [
50
]. SCFA signaling through GPRs stimulates L-cells to secrete GLP-2, leading to
an increase in expression of TJ proteins, including zonula occludens-1 (ZO-1) and Claudin-3,
consequently reducing LPS translocation, inhibiting endotoxemia-induced inflammation,
and improving gut permeability [
51
]. Similarly, SCFAs increase goblet cell mucin secretion,
resulting in a reduction in LPS translocation through the epithelium. SCFAs also exert
immunomodulatory effects by regulating antimicrobial peptide (AMP) synthesis, Treg
expansion, and myeloid cell function, leading to reduced inflammation. Consequently, the
overall effect of NDC-induced SCFA production was associated with improvement in MD,
including obesity, T2D, and CVD [39].
Appl. Sci. 2022, 12, x FOR PEER REVIEW 6 of 20
which activates adipocytes to produce leptin, thereby improving satiety and preventing
obesity [8]. Additionally, an increase in IGN by SCFAs inhibits hepatic gluconeogenesis,
resulting in increased glucose tolerance. For example, butyrate activates IGN gene
expression through a cAMP-dependent mechanism, whereas propionate, an IGN
substrate, stimulates IGN via a gut-brain neural circuit [44]. Along with the direct effects
of SCFAs, SCFAs shift the intestinal environment by decreasing pH, preventing
overgrowth of pH-sensitive pathogenic bacteria [45,46] and protease activity associated
with the production of harmful metabolites, such as ammonia, a potentially carcinogenic
product of protein fermentation [47,48]. Moreover, SCFAs are involved in the intestinal
defense system against pathogens and toxic compounds [49]. The primary physical
intestinal barriers that protect the gut from pathogen infection or toxic compounds are
mucin secreted from goblet cells and tight junctions (TJs) between mucosal epithelial cells
[9]. SCFAs improve gut barrier function by modulating the expression of mucin and TJ
proteins [50]. SCFA signaling through GPRs stimulates L-cells to secrete GLP-2, leading
to an increase in expression of TJ proteins, including zonula occludens-1 (ZO-1) and
Claudin-3, consequently reducing LPS translocation, inhibiting endotoxemia-induced
inflammation, and improving gut permeability [51]. Similarly, SCFAs increase goblet cell
mucin secretion, resulting in a reduction in LPS translocation through the epithelium.
SCFAs also exert immunomodulatory effects by regulating antimicrobial peptide (AMP)
synthesis, Treg expansion, and myeloid cell function, leading to reduced inflammation.
Consequently, the overall effect of NDC-induced SCFA production was associated with
improvement in MD, including obesity, T2D, and CVD [39].
Figure 1. Effect of non-digestible carbohydrates (NDCs) on metabolic diseases (MD) through
short-chain fatty acids (SCFA) produced by gut fermentation. AMP, antimicrobial peptides; CVD,
cardiovascular disease; GLP, glucagon-like peptide; IGN, intestinal gluconeogenesis; LPS,
lipopolysaccharides; PYY, peptide tyrosine tyrosine; SCFAs, short-chain fatty acids; T2D, type 2
diabetes; Tregs, regulatory T-cells; Zo-1, Zonula occludens.
Figure 1.
Effect of non-digestible carbohydrates (NDCs) on metabolic diseases (MD) through short-
chain fatty acids (SCFA) produced by gut fermentation. AMP, antimicrobial peptides; CVD, cardiovas-
cular disease; GLP, glucagon-like peptide; IGN, intestinal gluconeogenesis; LPS, lipopolysaccharides;
PYY, peptide tyrosine tyrosine; SCFAs, short-chain fatty acids; T2D, type 2 diabetes; Tregs, regulatory
T-cells; Zo-1, Zonula occludens.
Appl. Sci. 2022,12, 3768 7 of 18
5. NDCs and MDs
5.1. Obesity
Obesity, defined as a state of excess adiposity, is one of the most important risk factors
for MD [
52
]. Obesity is related to the balance between energy intake and expenditure;
thus, reducing energy intake and increasing energy expenditure are ways to control obesity.
Energy intake is particularly associated with eating habits. Among various foods, a high
intake of NDCs has a strong correlation with a reduction in obesity [53].
Intake of NDCs interferes with the absorption of energy sources, including glucose
and lipids, and with the accessibility of digestion enzymes to substrates in the intestine
because of the viscous and fecal bulking properties of NDCs, although SCFAs produced
from NDCs by gut microbiota are used as an energy source. Additionally, both properties
can increase the gastric emptying time, resulting in an increase in satiety [
54
]. SCFAs can
also stimulate satiety through the activation of satiety hormones, such as PYY and GLP-1,
and energy-balancing hormones, such as leptin [
55
]. Consequently, energy intake can be
reduced by the intake of NDCs, whereas the breakdown of stored energy sources, such
as fat in the body, can be increased through energy production metabolism, including
β
-oxidation and the citric acid cycle, resulting in a reduction in obesity [
56
]. Therefore,
intake of NDCs can reduce obesity and related disorders.
The anti-obesity effects of pectin,
β
-glucan, psyllium, FOS, GOS, and non-fiber NDCs
have been investigated (Table 2). Animal studies showed that fruit pectin intake showed
anti-obesity effects by regulating the circulation of energy balancing hormones such as
adiponectin, leptin, and ghrelin [
57
59
]. In particular, high-esterified pectin, a major com-
ponent of soluble dietary fiber present in vegetables and fruits, was more effective in sup-
pressing obesity than low-esterified pectin [
60
]. Intake of 2% barley
β
-glucan for
12 weeks
or 10% FOS for 6 weeks also reduced body weight gain and fat mass in HFD-induced obese
mice and increased secretion of gut hormones, PYY and GLP-1 in the plasma [
61
]. More-
over, mice fed with non-fiber soluble NDCs, such as malto-oligosaccharides (MOS
6 g/kg
for 11 weeks), chitin oligosaccharides (COS 200 mg/kg for 21 weeks), and bovine-milk
oligosaccharides (BMO, 6% BMO diet for 6 weeks) showed a reduction in BW, improved
lipid profile, and increased glucose tolerance [
62
64
]. However, some studies have shown
that the anti-obesity effect of NDCs differs according to their type and source. Mice fed
with 10% (w/w) insoluble cereal fiber for 45 weeks had lower weight gain and improved
insulin sensitivity compared with those fed with soluble guar fiber [
65
]. In a human study,
the anti-obesity effects of pectin were also reported [
66
] as similar to the results of animal
studies [
57
59
]. Psyllium husk has also been shown to have anti-obesity effects in obese
humans [
67
], but there was no significant difference in almost all anthropometric measures
in NAFLD patients consuming psyllium husk at 10 g/day for 12 weeks, except for the
reduction in body weight and BMI [
68
]. FOS and GOS showed decreased hunger, desire
to eat, energy intake, body weight, waist circumference, waist-to-height index, sagittal
abdominal diameter, body fat, and serum TG levels in obese adults and children [
69
72
].
To further explain the differences in the impact of NDCs on obesity according to the type
and source of NDCs, other mechanisms, such as population and diversity of gut microbiota
and their metabolites, including secondary bile acids, except for SCFAs, may be needed
because many studies suggest that gut microbiota and secondary bile acids affected by
high intake of NDCs are strongly related to obesity [39].
5.2. CVD
Many clinical trials have found that a high intake of NDCs reduces the risk of
CVD [20,73,74]
, which is the most common cause of mortality worldwide [
4
]. Accord-
ing to a systematic review and meta-analysis of 22 cohort studies, the association between
CVD risk and NDC intake was dose-dependent (risk ratio 0.91 per 7 g/day). Moreover,
Marc et al. (2017) reviewed 31 meta-analyses and confirmed that NDC intake significantly
reduced the relative risk (RR) of CVD mortality (RR = 0.77–0.83), the incidence of CVD (RR
= 0.72–0.91), coronary heart disease (RR = 0.76–0.93), and stroke (RR = 0.83–0.93), which is
Appl. Sci. 2022,12, 3768 8 of 18
particularly noticeable with water-soluble, gel-forming NDCs, such as
β
-glucan and psyl-
lium [
20
]. In particular, NDCs such as
β
-glucan and FOS have been shown to lower blood
cholesterol because their viscous properties interfere with the absorption of cholesterol and
bile acids in the intestine and reduce lipase activity [
75
]. Decreased reabsorption of bile
acid leads to increased hepatic conversion of cholesterol into bile acid; as a result, more
cholesterol stored in the body is used to produce bile acid [
76
]. NDCs also enhance diges-
tive regularity by promoting rapid gastric emptying, decreasing intestinal transit time, and
increasing fecal bulk [
75
]. Moreover, SCFAs suppress endotoxemia-induced inflammation
by increasing tight junction gene expression, which reduces LPS translocation [77,78].
Rats fed a 32% FOS diet for 12 weeks showed significantly increased hypertrophy
of cardiomyocytes through subcellular changes in cardiac metabolism and contractility,
which could affect myocardial function and alter the risk of CVD [
79
]. In humans, intake of
barley or oat
β
-glucan at 3–5 g/day for 3–5 weeks improves blood lipid profile and reduces
CVD risk factors such as body mass index, waist circumference, blood pressure, LDL,
and triglyceride levels [
80
82
]. Moreover, patients with non-diabetic CVD who consumed
12 g/day of FOS for 3 months had lower circulating levels of IL-6, a pro-inflammatory
cytokine, and preserved endothelial function [
83
]. Non-dietary fiber NDCs, such as some
types of resistant starch (RS), such as RS IV, have also been reported to have a preventive
effect on CVD. Participants with several MD comorbidities who consumed a diet containing
30% RS4 for 4 weeks [
84
] and elderly patients with type 2 diabetes with a diet containing
53.7% fructose-free RS IV for 6 weeks [
85
] had improved dyslipidemia and cardiovascular
risk biomarkers, including monocyte chemotactic protein-1 and soluble E-selectin.
However, not all trials provide similar results. A cohort study of 31,036 women
from the UK for 14.3 years reported that increased total NDC intake may not provide
cardiovascular benefit in terms of mortality, but it may help to reduce the risk of fatal
stroke in those without CVD risk factors such as hypertension and angina. A systematic
review of 23 randomized controlled trials with 1513 participants also showed that there is
no evidence of the effects of NDCs on CVD clinical events because the majority of studies
were short-term, had a risk of bias, and insufficient information [
86
]. In addition, young
healthy adults with an intake of extracted oat and barley
β
-glucans of 3.3 g/day for 3 weeks
had no effect on cholesterol metabolism [
87
]. These results showed that the effects of NDC
intake on the reduction of CVD risk are dependent on the type and source of fiber, doses,
health condition, and sex of the participant, as well as the size and duration of the trial. To
further understand the relationship between intake of NDCs and the reduction of CVD
risk, studies focusing on the effect of NDCs on gut health and the biological networking of
NDCS-related gut metabolites and other tissues are needed, although some studies have
shown that gut microbiota profiles are affected by NDCs, and the metabolites they produce
differ according to NDC type [39].
5.3. Diabetes
The relationship between NDC intake and type 2 diabetes mellitus (T2DM) has been
clinically investigated for decades. Many recent meta-analyses and clinical studies have
shown that a high intake of NDCs, especially dietary fiber, for >1 month lowered the risk
of developing T2DM and might have therapeutic effects in patients with T2DM [
88
,
89
],
although some studies have shown no significant effects of dietary fiber on T2DM [
90
]. Ran-
domized studies of 15 studies from 1980 to 2010 suggested that an increasing dietary fiber
diet reduced fasting blood glucose and glycosylated hemoglobin (HbA1C) levels in patients
with T2DM [
91
,
92
]. Similar results were reported in a meta-analysis of
28 randomized
controlled trials (n= 1394) on T2DM patients with a viscous fiber diet at a median dose
of approximately 13.1 g/day [
93
]. However, the effect of NDCs on the risk reduction of
T2DM depends on the type and intake of NDCs.
In particular, soluble fibers with viscous and/or gel-forming properties, such as psyl-
lium,
β
-glucan, and pectin, have been associated with lower postprandial glucose and
blood cholesterol levels because the increased viscosity of intestinal contents by soluble
Appl. Sci. 2022,12, 3768 9 of 18
fiber can delay gastric emptying, reduce the accessibility of digested enzymes, including
amylase and lipase, and slow the intestinal absorption of nutrients, such as monocarbohy-
drates and cholesterol [
94
]. Delayed gastric emptying in the stomach can enhance satiety
and consequently lower energy intake, resulting in an increase in fat oxidation, eventually
leading to a decrease in body weight [
95
]. In this mechanism, various hormonal responses
associated with satiety and insulin sensitivity, which are relevant factors contributing to
diabetes, can be affected by viscous soluble fibers. Moreover, soluble fibers can be easily fer-
mented in the gut, resulting in the production of various metabolites, especially SCFAs, and
changes in the gut microbiome [
39
,
96
]. SCFAs can be absorbed via
GPR41/43 metabolism
in the gut and used as an energy source [
41
]. Absorbed SCFAs can increase satiety, decrease
fat accumulation, and increase glucose tolerance via modification of lipid metabolism and
insulin sensitivity, and consequently, can decrease the risk of T2DM [
6
,
95
]. In addition
to the high production of SCFAs, the population of the healthy gut microbiome can be
increased by the intake of soluble fibers, which can improve inflammation and the immune
system associated with many diseases, including T2DM [39].
Unlike soluble fibers, insoluble fibers with non-viscous properties are mostly poorly
fermented in the gut and thus produce fewer SCFAs than soluble fibers [
92
]. However,
accumulated insoluble fibers in the gut decrease gut transit time and increase fecal bulk
because of their water-holding and swelling capacities [
96
]. Decreased gut transit time
and increased fecal bulk due to insoluble fibers interfere with the absorption of glucose
and cholesterol, resulting in the reduction of blood glucose and cholesterol levels [
94
,
97
].
Moreover, similar to soluble fibers, insoluble fibers can modify the population of the gut
microbiome, reduce inflammation, increase insulin sensitivity, and consequently, reduce the
risk of T2DM [
94
,
97
]. However, the difference between the effects of soluble and insoluble
fibers on T2DM is not clear, and the mechanism is currently unclear, although there is an
accumulation of scientific evidence on soluble fibers.
Many studies have suggested that soluble NDCs are more effective in reducing the
risk of T2DM than insoluble NDCs, but recent studies have shown contrasting results.
Prospective cohort studies have shown that a high dietary fiber diet (>25 g/day in women
and >38 g/day in men) reduces the risk of developing T2DM by 20–30%. In particular, a
high intake of whole grains and insoluble cereal fibers improved diabetes risk, but soluble
fiber did not [
98
]. Other cohort studies have shown that cereal fiber intake has a strong
inverse association with the risk of T2DM (relative risk (RR) = 0.75; 95% confidence interval
(CI) 0.65–0.86), whereas only a very weak association was observed for fruit soluble/viscous
fiber (RR = 0.95; 95% CI 0.87–1.03) unlike other soluble fibers, such as psyllium and ß-
glucans, although many studies clearly indicated that soluble fibers, including fruit fiber,
reduce glycemic response [94,99].
In addition to the type of NDC, the amount and feed period of NDC intake are also
associated with a reduction in the risk of developing T2DM. A randomized, crossover
study of 13 patients with T2DM showed that the intake of a high-fiber diet (50 g/day; 25 g
of soluble fiber and 25 g of insoluble fiber) for 6 weeks lowered plasma glucose, insulin,
and cholesterol levels by 6–12%, compared with the diet recommended by the American
Diabetes Association (24 g/day; 8 g of soluble fiber and 16 g of insoluble fiber) [
100
]. Cereal
fibers, especially
β
-glucans in oats, barley, psyllium and rye, have been shown to lower
glycemia in healthy people, but only when the daily dose of
β
-glucans is at least 4 g [
94
]. A
soluble fiber diet of 10 g and 20 g/day for one month reduced the risk of developing T2DM
and may have therapeutic effects, as per a study conducted on 117 patients with T2DM
aged between 40 and 70 years. In particular, soluble fibers such as pectin, GOS, HPMC, and
hemicellulose were also shown to improve T2D [
101
106
] Fasting blood glucose, insulin
resistance, TG, and connected (C)-peptide levels in patients with T2DM were lowered by
the soluble dietary fiber diet for the short-term intervention period. However, there were
no significant differences in these effects between the 10 g/day and 20 g/day groups [
107
].
Appl. Sci. 2022,12, 3768 10 of 18
Table 2. The effect of NDCs on metabolic diseases.
Types Model Dosage
(g/day or %)
Duration
(weeks) Related Disease Physiological Effects References
Soluble dietary fiber
Guar Gum Human 15 96 L/M Serum LDL-C and TC with
cardiometabolic problems [108]
Pectin
- Pectin Human 650 or 1300 12 Ob
Fasting BG, TG, cholesterols, AIP,
HOMR-IR, insulin level, BW, body mass,
leptin, and ghrelin. Adiponectin
[66]
- Pectin (soybean) Human (Man) 10 g 3 h IR Plasma glucose, insulin, and iAUC [101]
- Pectin (citrus peel) Mice 2% 8 Ob Body and fat weight gain, dyslipidemea,
hyperglycemia, and insulin resistance [58]
Rat (DB) 0.25–2 (g/kg/day) 4 T2D
Improve glucose tolerance, hepaticglycogen
content, BG, and blood lipid level. pAkt
and GSK3βexpression
[87]
- High-esterified pectin
(HEP, apple) Rat/Mice 2–10% 6–8 Ob/NAFLD
Improve/restored adioistatic/adipokine
sensitivity. Prevented the development of
NAFLD, browning of adipose tissue
[57,59]
Hydroxypropylmethylcellulose
(HPMC) Rat (ZDF) 4–8% 6 DB/Ob
BG, urinary excretion of glucose, ketone
bodies, epididymal fat pad, liver lipid, liver
weight, adipose, and plasma cholesterol
[102,103]
β-glucan
- Oat β-glucan Human 3–3.5 4 CVD LDL-c, TC, TC: HDL, non-HDL-c, and
Framingham CVD risk [81,82]
- Barley β-glucan Human 3 or 5 5 CVD
Change in microbiota profile: Bacteroides,
Prevotella, and Dorea composition correlated
with shifts of CVD risk factors: BMI, waist
circumference, blood pressure, and TG levels
[80]
Mice (HFD) 2–5% 12 Ob Weight gain and fat mass (2%), secretion
of PYY and GLP-1 (5%) [55]
- Yeast β-glucan Mice (HFD) 0.4 (g/kg/day) 10 MD IL-6 and IL-1βin plasma, HDL-c and
BG, TC, LDL-c + VLDL-c, TG [109]
Appl. Sci. 2022,12, 3768 11 of 18
Table 2. Cont.
Types Model Dosage
(g/day or %)
Duration
(weeks) Related Disease Physiological Effects References
Psyllium husk Human 5 52 Ob BW [67]
Human (T2D) 20 12 T2D BW, blood glucose, blood lipid, HbA1c,
cholesterol, and TG [88]
Human
Human (NAFLD)
9–10
10
8–10
12
T2D/NAFLD
NAFLD
Waist circumference, oxidized lipoproteins,
calorie and carbohydrate intake, ALT, weight,
and body fat
BW, BMI
[68,110,
111]
Inulin and inulin-type fructans
- Fructans (75% FOS) Human (Ob) 8 12 Ob Hunger, desire to eat, and energy intake [69]
- FOS /FOS + probiotics Human (T2D) 0.1–10 6–8 Ob/CVD
BW, waist circumference, serum TG, fat
mass, fasting BG, HbA1c, LCL-c, TC/HDL-c
and LDL-c/HDL-c
[70,71,
112]
- Fructooligosaccharide (FOS) Human (CVD) 12 12 CVD IL-6 level, total p-cresyl sulfate (PCS) [83]
Rat 32% 12 CVD Hypertrophic of cardiomyocytes [79]
Rat 10% 6 Ob Energy intake, BW, fat mass, plasma
glucose, and GIP. PYY [61]
Mice 0.38 5 Ob Cecal content pH ad BW. Cecal SCFAs [113]
High amylose starch (resistant
starch II)
- High-amylose corn starch Human (T2D) 6.8 or 25 8 T2D No significant different in fasting BG,
fasting insulin level [90]
Human (women) 0–30 4–6 h IR
No significant different in fasting BG and
insulin, the post-prandial glucose and
insulin AUCs
[114,115]
Galactooligosaccharide (GOS) Human 5–18 2–3 Ob
Colonic permeability, food intake,
lipopolysaccharides, CRP, and BMI.
antioxidative enzymes
[72,116]
Mice 0.083–0.83 6 Ob/DB BG, TC, TG, LDL-C, and liver lipid
deposition. HDL-c, SCFAs [104,105]
Appl. Sci. 2022,12, 3768 12 of 18
Table 2. Cont.
Types Model Dosage
(g/day or %)
Duration
(weeks) Related Disease Physiological Effects References
Polydextrose Human (men) 12 15–75 min Ob Energy intake in low protein group but not
high protein group [117]
Insoluble dietary fiber
Cellulose Rat 10% 24 G/M TG [118]
Soluble/Insoluble dietary fiber
Mixed plant cell wall fibers (corn
starchhemicellulose) Human 10 g/day 48 T2D Improve insulin release, peripheral insulin
sensitivity, and blood glucose control [106]
Non-dietary fiber NDCs
Resistance starch III Mice 23% 4 T2D Improve glucose and lipids profile (TC, TG,
LDL, HDL) [119]
Resistance starch IV Human 30%/53.7% 12/6 CVD/T2D
Improve dyslipidemia and body composition.
HbA1c, improve glycaemic control and
cardiovascular risk without altering lipid
metabolism
[84,85]
Maltooligosaccharides (MOS) Mice 6 g/kg 11 Ob/DB BW gain, adipose size, serum TC, TG, and
insulin resistance [62]
Chitosan oligosaccharides (COS) Mice 200 mg/kg 21 MD BG, TG, lipopolysaccharides, and
adipose inflammation [63]
Bovine-milk oligosaccharides
(BMO) Mice 6% 6 Ob
glucose tolerance, insulin secretion and
HDL-C. BW, LBP, hepatic steatosis, gut
permeability, total fat, mass, and adipocyte
cell size
[64]
AIP, atherogenic index of plasma; AXOS, arabinoxylan oligosaccharides; BG, blood glucose; BW, body weight; BMI, body mass index, CVD, cardiovascular disease; DB, diabetes;
DM, methyl-esterification
; G/M, glucose metabolism; GIP, gastric inhibitory polypeptide; GOS, galactooligosaccharide; HDL-c, high-density lipoprotein cholesterol; HEP, high-esterified
pectin; HFD, high fat diet; HMAP, highly methoxylated apple pectin; HOMA-IR, homeostasis model assessment insulin resistant; iAUC, incremental area under the curve; IR: insulin
resistant; LBP, binding protein; L/M, lipid metabolism; LDL-c, low-density lipoprotein cholesterol; MD: metabolic disease; NAFLD, non-alcoholic fatty-liver disease; Ob, obesity;
PYY, peptide YY; T2D, type 2 diabetes; TC, total cholesterol; TG, triglycerides; XOS, xylooligosaccharide; ZDF, Zucker Diabetic Fatty.
Appl. Sci. 2022,12, 3768 13 of 18
6. Conclusions
A high intake of NDCs, such as dietary fibers and resistant starch, is strongly associated
with a reduced risk of MD, including CVD and T2DM, because of their physical and
fermentation properties. In particular, the properties of NDCs, such as water retention,
fecal bulking, viscosity, and fermentation in the gut, are important for reducing the risk of
MD by decreasing blood glucose and lipid levels, increasing satiety and insulin sensitivity,
and modifying the gut microbiome. Moreover, SCFAs produced by certain gut bacteria
mainly contribute to reducing the risk of MD by controlling satiety hormones and energy
metabolism, decreasing inflammation, and enhancing the immune system. However, these
mechanisms are not sufficient to explain the differences in the impact of NDCs on MD
according to the type and source of the NDCs and the answers to many questions about
how NDCs suppress the development of MD still remain unclear. In particular, the study
on the structural property of NDCs, the effects of NDCs on the gut microbial ecosystem,
and the biological networking of gut metabolites produced by fermentation of NDCs
have been limited. In structural property, the structures of NDCs and their sizes after
partial digestion by the GI system are associated with various health benefits [
120
], but
the study on structural property on MD has been rarely conducted except for the degree
of esterification in pectin [
60
]. In the gut microbial ecosystem, although the microbial
profiles are significantly different according to individual NDC and the metabolites profiles
they produce are also different [
121
], the factors related to the fermentation property of
NDCs except for their physical property mentioned in this review and other metabolites
produced by fermentation except for SCFAs have been rarely investigated [
122
]. In the
biological networking of gut metabolites, various metabolites can be produced during
gut fermentation, but studies over the past decade have focused only on SCFAs [
120
].
Gut metabolites can transfer to the whole body, including the brain, liver, kidney, lung,
and skin, via blood and the central nervous system, and can affect many physiological
functions associated with the risk of MD through biological networking [
123
]. However,
the biological networking of other gut metabolites has been rarely investigated. Although
there remain gaps in understanding how NDCs reduce the risk of MD, this review showed
how NDCs regulate the incidence of MD by focusing on mechanisms by which the physical
and fermentation properties of NDCs in the GI system, and we believe that a better
understanding of the relationship between NDC intake and MD is imperative to improve
NDC intake guidelines for MD.
Author Contributions:
Conceptualization, H.-J.K.; writing—original draft preparation, S.C., Q.-A.N.,
and H.-J.K.; writing—review and editing, H.-J.K.; visualization, S.C.; supervision, H.-J.K. All authors
have read and agreed to the published version of the manuscript.
Funding:
This research was supported by the Research Program (E0210600-01) of the Korea Re-
search Food Institute (KFRI) and the Basic Science Research Program through the National Research
Foundation of Korea (NRF) funded by the Ministry of Education (2020R1I1A3072463).
Institutional Review Board Statement: Not applicable.
Informed Consent Statement: Not applicable.
Data Availability Statement:
The data presented in this study are available on request from the
corresponding author.
Conflicts of Interest: The authors declare no conflict of interest.
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... It has been well-established that oxidative stress caused by an overabundance of reactive oxygen species (ROS) that remains in the organism is the root of the pathogenesis of a number of disorders [1]. Oxidative stress can be triggered by various external and internal factors, including elevated blood glucose and insulin levels, which in turn lead to an increased risk of chronic non-communicable diseases, including obesity and type 2 diabetes [2,3]. Type 2 diabetes is now a serious problem in many countries around the world and represents 90% of all types of this disease, while being one of the five leading causes of death in the human population [4]. ...
... Starch-rich foods such as white bread, pasta, rice, cornflakes and other cereal-based products became the major contributors to the energy intake of the human daily diet and constitute a basis of nutrition for the world's population. In most of these foods, starch is rapidly digested and absorbed, which contributes to increased oxidative stress, high plasma glucose levels, increased insulin resistance and elevated hypertension [20], which consequently may favor weight gain and the development of type 2 diabetes, cardiovascular diseases and certain types of cancer, including colon tumors [3,21]. At the same time, for the better part of the global population, it is impossible to give up consuming too much of the starchy food products, which are available at any time at a decent price. ...
... This fraction is generally called resistant starch [20,24]. From a nutritional point of view, this RS has a favorable, stabilizing effect on blood glucose levels and has potential to be a part of management and treatment programs to control type 2 diabetes [3,20]. Among the different factors affecting starch digestibility, both internal (the amylose-to-amylopectin ratio, dietary fiber, fat, protein contents, starch-macromolecule interactions) and external ones can be specified (processing: cooking, parboiling, soaking, cooling or retrogradation) [20]. ...
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... Moreover, diet interventions including nondigestible carbohydrates (resistant starch and dietary fiber) have shown increased intestinal viscosity, fecal bulking, and production of SCFAs resulting in improved blood glucose, lipid, and insulin levels, reducing energy intake and promoting satiety. However, these effects are different depending on the type, source, dose, and duration of the intake [113,114]. ...
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Background: Patients with metabolic syndrome (MetS) have a higher risk of developing cardiovascular diseases (CVD). However, controversy exists about the impact of MetS on the prognosis of patients with CVD. Methods: Pubmed, Cochrane library, and EMBASE databases were searched. Cohort Studies and randomized controlled trials post hoc analyses that evaluated the impact of MetS on prognosis in patients (≥18 years) with CVD were included. Relative risk (RR), hazard rate (HR) and 95% confidence intervals (CIs) were calculated for each individual study by random-effect model. Subgroup analysis and meta-regression analysis was performed to explore the heterogeneity. Results: 55 studies with 16,2450 patients were included. Compared to patients without MetS, the MetS was associated with higher all-cause death [RR, 1.220, 95% CI (1.103 to 1.349), P, 0.000], CV death [RR, 1.360, 95% CI (1.152 to 1.606), P, 0.000], Myocardial Infarction [RR, 1.460, 95% CI (1.242 to 1.716), P, 0.000], stroke [RR, 1.435, 95% CI (1.131 to 1.820), P, 0.000]. Lower high-density lipoproteins (40/50) significantly increased the risk of all-cause death and CV death. Elevated fasting plasma glucose (FPG) (>100 mg/dl) was associated with an increased risk of all-cause death, while a higher body mass index (BMI>25 kg/m2) was related to a reduced risk of all-cause death. Conclusions: MetS increased the risk of cardiovascular-related adverse events among patients with CVD. For MetS components, there was an increased risk in people with low HDL-C and FPG>100 mg/dl. Positive measures should be implemented timely for patients with CVD after the diagnosis of MetS, strengthen the prevention and treatment of hyperglycemia and hyperlipidemia.
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The consumption of recommended amount of dietary fiber is a challenge not only for most consumers but also for the food scientists to design fiber-enriched foods with acceptable eating quality, texture, color and flavor. The addition of psyllium husk (PS) significantly made the bread texture softer with increasing levels, producing the lowest compression force value (2.48 ± 0.37 N) at a 5% level. Addition of coarse wheat bran (at 10 and 20% levels) to white wheat flour (WWF) produced a significantly softer bread texture (4.65 ± 0.61 to 5.27 ± 0.32 N) compared with the harder texture with the fine wheat bran addition (5.04 ± 0.33 to 6.82 ± 0.57 N) for the control samples, respectively. When psyllium at 5% level was added to either the WWF or wholegrain wheat flour (WGF), it produced a significantly softer bread texture. Interestingly, the incorporation of diacetyl tartaric acid esters of mono- and diglyceride (DATEM) emulsifier (0.5%) in the WWF or WGF bread samples containing 5% psyllium did not significantly improve the textural properties of bread samples. When WWF + 5%PS (4.03 ± 0.12 N) buns were compared with WGF + 5%PS, the WGF +5%PS buns (7.37 ± 0.16 N) had a significantly harder texture. The results of compression force (N) and higher consumer acceptability values of these products clearly brought out the superior textural properties of wheat pan bread and buns made by this newer approach, than the common approach of using only the wholegrain wheat flour. Future studies on the effect of various wheat bran treatments, such as steaming or extrusion on the textural properties of pan bread and buns are recommended.
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Background High-molecular-weight (MW) oat β-glucan (OBG), consumed at 3–4 g/d, in solid foods reduces LDL cholesterol by a median of ∼6.5%. Objectives We evaluated the effect of a beverage providing 3 g/d high-MW OBG on reduction of LDL cholesterol (primary endpoint) when compared with placebo. Methods We performed a parallel-design, randomized clinical trial at a contract research organization; participants, caregivers, and outcome assessors were blinded to treatment allocation. Participants with LDL cholesterol between 3.0 and 5.0 mmol/L, inclusive [n = 538 screened, n = 260 ineligible, n = 23 lost, n = 48 withdrawn (product safety); n = 207 randomly assigned, n = 7 dropped out, n = 9 withdrawn (protocol violation); n = 191 analyzed; n = 72 (37.7%) male, mean ± SD age: 43.3 ± 14.3 y, BMI: 29.7 ± 5.2 kg/m2], were randomly assigned to consume, 3 times daily for 4 wk, 1 g OBG (n = 104, n = 96 analyzed) or rice powder (Control, n = 103, n = 95 analyzed) mixed into 250 mL water. Treatment effects were assessed as change from baseline and differences analyzed using a 2-sided t test via ANOVA with baseline characteristics as covariates. Results After 4 wk, change from baseline least-squares-mean LDL cholesterol on OBG (−0.195 mmol/L) was less than on Control (0.012 mmol/L) by mean: 0.207 mmol/L (95% CI: 0.318, 0.096 mmol/L; P = 0.0003); the following secondary endpoints were also reduced as follows: total cholesterol (TC) (0.226 mmol/L; 95% CI: 0.361, 0.091 mmol/L; P = 0.001), TC:HDL cholesterol ratio (0.147; 95% CI: 0.284, 0.010; P = 0.036), non-HDL cholesterol (0.194 mmol/L; 95% CI: 0.314, 0.073 mmol/L; P = 0.002), and Framingham cardiovascular disease (CVD) risk (0.474; 95% CI: 0.900, 0.049, P = 0.029). Changes in HDL cholesterol, triglycerides, glucose, and insulin did not differ between treatment groups (P > 0.05). Lipid treatment effects were not significantly modified by age, sex, BMI, or hypertension treatment. There were no major adverse events, but both treatments transiently increased gastrointestinal symptoms. Conclusions Consuming a beverage containing 1 g high-MW OBG 3 times daily for 4 wk significantly reduced LDL cholesterol by ∼6% and CVD risk by ∼8% in healthy adults with LDL cholesterol between 3 and 5 mmol/L. This trial was registered at clinicaltrials.gov as NCT03911427.
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Background Microbiota-derived uremic toxins have been associated with inflammation that could corroborate with endothelial dysfunction (ED) and increase cardiovascular risk in patients with chronic kidney disease (CKD). This trial aimed to evaluate the effect of the prebiotic fructooligosaccharide (FOS) on endothelial function and arterial stiffness in nondialysis CKD patients. Methods In a double-blind controlled trial, 46 nondiabetic CKD patients were randomized to receive 12 g/day of FOS or placebo (maltodextrin) for 3 months. Total p-cresyl sulfate (PCS) and indoxyl sulfate by high-performance liquid chromatography, urinary trimethylamine N-oxide by mass spectrometry, C-reactive protein, interleukin-6 (IL-6), serum nitric oxide and stroma-derived factor-1 alfa were measured at baseline and at the end of follow-up; endothelial function was assessed through flow-mediated dilatation (FMD) and arterial stiffness by pulse wave velocity (PWV). Results The mean (± standard deviation) age of the study participants was 57.6 ± 14.4 years, with an estimated glomerular filtration rate of 21.3 ± 7.3 mL/min/1.73 m2. During the follow-up, regarding the inflammatory markers and uremic toxins, there was a significant decrease in IL-6 levels (3.4 ± 2.1 pg/mL versus 2.6 ± 1.4 pg/mL; P = 0.04) and a trend toward PCS reduction (55.4 ± 38.1 mg/L versus 43.1 ± 32.4 mg/L, P = 0.07) only in the prebiotic group. Comparing both groups, there was no difference in FMD and PWV. In an exploratory analysis, including a less severe ED group of patients (FMD ≥2.2% at baseline), FMD remained stable in the prebiotic group, while it decreased in the placebo group (group effect P = 0.135; time effect P = 0.012; interaction P = 0.002). Conclusions The prebiotic FOS lowered circulating levels of IL-6 in CKD patients and preserved endothelial function only in those with less damaged endothelium. No effect of FOS in arterial stiffness was observed.