Anti-diabetic mechanism of dietary polysaccharides based on their

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Anti-diabetic mechanism of dietary polysaccharides based on their gastrointestinal functions Jie-Lun Hu, Shao-Ping Nie, and Ming-Yong Xie J. Agric. Food Chem., Just Accepted Manuscript • DOI: 10.1021/acs.jafc.7b05410 • Publication Date (Web): 19 Apr 2018 Downloaded from http://pubs.acs.org on April 19, 2018

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Journal of Agricultural and Food Chemistry

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Anti-diabetic mechanism of dietary polysaccharides based

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on their gastrointestinal functions

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Jie-Lun Hu, Shao-Ping Nie*, Ming-Yong Xie

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State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China

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*Correspondence authors:

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Professor Shao-Ping Nie, Ph D

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Tel & Fax: +86-791-88304452

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Email: [email protected]

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ACS Paragon Plus Environment


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ABSTRACT

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Diabetes mellitus takes the worldwide concerns and obviously influences

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humans’ quality of life. Dietary polysaccharides were mainly from natural sources,

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namely plants, fungi, algae, etc. They were resistant to human digestion and

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absorption with complete or partial fermentation in the large bowel and have shown

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anti-diabetic ability. In this review, a literature search was conducted to provide

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information on anti-diabetic mechanism of dietary polysaccharides, based on the

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whole gastrointestinal process, which was a new angle of view for understanding their

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anti-diabetic mechanism. Further researches could take efforts on the mechanisms of

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the polysaccharide action through host-microbiota interactions targeting diabetes.

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Keywords: Dietary

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polysaccharides, Diabetes,

Gastrointestine,

mechanism

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Anti-diabetic

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INTRODUCTION

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Diabetes mellitus (DM) is an impaired carbohydrate, fat and protein metabolic

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syndrome induced by insufficient insulin secretion or decreased tissue sensitivity to

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insulin.1 DM is attracting global attention, which has severely affected the quality of

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life of human and is related to several severe complications.2 According to the

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statistics of the International Diabetes Federation, about 0.45 billion people develop

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DM in 2016, which is 14 times higher than the number of DM in 1980 and is expected

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to increase to 0.6 billion in 2030.3 DM can be classified into three types. Type 1 DM

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(T1DM), Type 2 DM (T2DM), and gestational DM (GDM). T2DM is focused in this

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review, which accounts for about 90% of all DM cases, while the remaining 10% are

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mainly T1DM and GDM.

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It has been realized that the optimal selection of food and dietary factors play key

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roles in preventing early T2DM and reducing the risk of lifelong T2DM.4 In terms of

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food and dietary factors, the polysaccharide shows protective effect on T2DM. The

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dietary polysaccharide mainly derives from natural foods, namely, plant, fungus and

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alga,5,6 which show anti-digestion and anti-absorption capacity for the completely or

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partly fermented human small intestine. In addition, they can protect against DM. This

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review aims to provide information regarding the mechanism of dietary

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polysaccharide against DM during the entire gastrointestinal process, so as to provide

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a brand new viewpoint for the anti-DM mechanism of dietary polysaccharide.

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Dietary polysaccharides

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Dietary polysaccharides are defined as the polysaccharides from natural edible

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sources, which are close to our daily life. They were mainly from various sources,

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such as grain, plants, fruits, vegetables, fungi, algae, etc. They are constituted by

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monosaccharide unit and connected through the glucosidic bond, which can provide

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monosaccharide or oligosaccharide at the time of hydrolysis.7 The monosaccharide in

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the polysaccharide has the general composition of (CH2O)n, where n is 3 or greater.8

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Examples of these monosaccharides are glucose, fructose, rhamnose, xylose,

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galactose, mannose and arabinose.

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T2DM

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T2DM is previously defined as insulin-independent DM, which takes up a

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majority of DM cases.9 A majority of T2DM patients are obese from the middle age,

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typically over 40 years. An individual can be diagnosed with T2DM at the fasting

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blood glucose (FBG) of ≥ 7.0 mmol/L (126 mg/dl) or 2 h oral glucose tolerance test of

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≥ 11.1mmol/L (200 mg/dl).10

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Polysaccharide targeting mechanism in diabetes

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Details about the anti-DM mechanism of polysaccharide during the

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gastrointestinal process are discussed below. Dietary polysaccharide can alleviate DM

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through the mechanisms of action of gastrointestinal viscosity, gastrointestinal satiety,

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large intestinal fermentation and gastrointestinal anti-inflammation. 4


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Targeting diabetes by gastrointestinal viscosity effect

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The effect of polysaccharide on regulating hyperglycemia mainly depends on its

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source, composition and preparation. Additionally, polysaccharide possesses a series

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of physiological effects based on its physiochemical properties, including the upper

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gastrointestinal tract viscosity.11 Meanwhile, the effect of polysaccharide on glucose

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control is mainly achieved through altering its small intestinal transit time (SBTT),

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preventing the carbohydrate from digestive enzyme suppression, and restraining these

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enzymes.12

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Inhibiting α-amylase and α-glucosidase activities

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There are two potential factors inhibiting the activity of polysaccharide on

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α-amylase. Firstly, it is found that there may be some groups or components (such as

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free carboxyl groups, tannin and phytic acid) for suppressing amylase in

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polysaccharide, which results in the direct effect of reducing α-amylase activity.

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Secondly, polysaccharide can be absorbed onto the starch, thus preventing the

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hydrolysis of starch by α-amylase.13

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Hyperglycemia is the most important clinical symptom of T2DM, which is also

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abnormal raised in fasting blood glucose and postprandial blood glucose. Therefore,

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control over postprandial hyperglycemia is the main treatment for the management of

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T2DM. All the digestible carbohydrates in mammals can be generally digested into

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fructose and glucose, and only monosaccharide can be easily absorbed into the blood 5



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in the small intestine.14 There are numerous active carbohydrates in the human body,

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among which, small intestinal glucosidase and pancreatic α-amylase are the two most

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important enzymes. α-amylase is the enzyme disintegrating the long-chain

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carbohydrate. The α-glucosidase in intestinal brush border is essential for digesting

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the oligosaccharide into monosaccharide. Consequently, restraining the α-glucosidase

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and α-amylase activities can remarkably inhibit the conversion of glucose into the

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blood glucose and decrease the postprandial blood glucose increase, which can thus

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serve as an effective pathway for controlling the level of blood glucose in T2DM

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patients.15 As is reported, multiple polysaccharides show inhibitory effect on

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α-amylase and α-glucosidase. Dietary polysaccharides inhibiting α-amylase and

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α-glucosidase from other natural sources are listed in Table 1.

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Inhibiting glucose absorption efficacy and postprandial glycemia

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Polysaccharide can reduce the uptake of postprandial blood glucose through

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delaying food digestion and absorption. Different clinical studies have emphasized the

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important role of soluble fiber viscosity in reducing postprandial blood glucose, which

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have also verified that polysaccharide has enhanced effect on postprandial blood

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glucose with the increase in viscosity. The diffusion rate of glucose can be inhibited

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through polysaccharide viscosity.16 In addition, some research also indicates that

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polysaccharide can bind with and adsorb glucose, thus maintaining low glucose

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concentration in the small intestine.17

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Targeting diabetes by gastrointestinal satiety effect

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Consumption of polysaccharide foods may add to the satiety and reduce hunger

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due to its huge volume and relatively low energy density, which will thus lead to

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decreased energy intake. Meanwhile, polysaccharide can also affect the secretion of

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intestinal hormones or peptides, such as cholecystokinin and glucagon-like peptide 1

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(GLP-1), which may serve as the satiety factors or change the glucose homeostasis.18

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Additionally, secrete of GLP-1 can be stimulated by soluble fiber fermentation in

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large intestine. These intestinal hormones contribute to satiety. In addition,

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polysaccharide-rich foods can also enhance the satiety through long-term chewing,

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which will affect the amount and velocity of food intake. Meanwhile, they can

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promote the production of saliva and gastric acid through enhancing gastric

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distension.19

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Targeting diabetes by large bowel fermentation

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Microbiota alteration

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The mammalian intestine is populated by billions of bacteria which mainly

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belong to the species of phyla Firmicutes and Bacteroidetes. Colonic microbes may

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influence body weight, pro-inflammatory reaction, insulin resistance, and regulate gut

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hormones to promote beneficial effects on T2DM. The number of beneficial bacteria

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in patients with T2DM was lower than healthy individuals.20 Polysaccharides could

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play an important role in dyspepsia, and have anti-hyperlipidemic, hpyerglycemic

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effects when fermented by gut bacteria. The human gut microbiota plays a 7



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fundamental role in diseases such as diabetes. Rising researches showed that

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individuals with T2DM exhibited evidence of gut dysbiosis. Researchers observed

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significantly improved level of four Lactobacillus species and obviously lower levels

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of five Clostridium species in patients with T2DM than normal subjects.21 There were

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obviously decreased levels of Clostridium coccoides group, Atopobium cluster and

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Prevotella, and a significantly increased level of Lactobacillus in the feces of T2DM

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patients in comparison with healthy people. A decreased ratio of the major phyla

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Firmicutes/Bacteroidetes and changes in several bacterial species were associated

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with the development of T2DM in Chinese patients.22 Polysaccharides were reported

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to have the ability to affect these bacterial species and thus further influence the state

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of the diabetes. The possible mechanisms by which the polysaccharides are involved

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in the development of diabetes included energy metabolism, inflammation, innate

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immune system, and the bowel function of the intestinal barrier in microbiota. The

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endotoxin lipopolysaccharide (LPS) from intestinal Gram-negative bacteria may lead

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to inflammation and insulin resistance by stimulation of Toll-like receptor 4 (TLR4).23

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Diabetic animals feeding with the plant polysaccharides intervention could

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increase levels of gut Firmicutes and decreased levels of Bacteroidetes and alleviated

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diabetes. It was reported that the polysaccharide from Ganoderma lucidum reduced

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Firmicutes/Bacteroidetes ratio in high fat diet fed mice. It was also recently shown

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that a low Bacteroidetes-to-Firmicutes ratio was correlated with weight loss. 24 In

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addition, Faecalibacterium, a butyrate-producing bacterial group which could be

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enhanced by polysaccharide intake, showed anti-inflammatory and antidiabetic effects 8


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partly through reducing colonic cytokine synthesis and increasing anti-inflammatory

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cytokine secretion. Diabetic patients had lower abundance of Faecalibacterium

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compared with non-diabetic patients, suggesting a negative correlation with

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inflammatory cytokines C-reactive protein and IL-6. Another study also showed that

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the gut of T2DM patients was characterized by a reduction of Faecalibacterium

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compared with that of healthy people.25 Three other genera, Prevotella, Clostridium

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and Ruminococcus which were also reported to confer beneficial effects to diabetes,

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were increased after polysaccharide supplementation. Prevotella is a mucin degrading

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bacterium and associated with low-grade inflammation. Ruminococcus is the

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predominant acetogens in the enrichments of acetic acid. In addition, high abundance

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of Lachnospira may induce significant increases in fasting blood glucose levels and

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decreases in plasma insulin levels and HOMA-β values. Helicobacter infection has

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been defined as a predisposing factor to T2DM development. Importantly, they are

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Gram-negative bacteria. Other studies suggested that lipopolysaccharides (LPS) from

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intestinal Gram-negative bacteria into the bloodstream may lead to metabolic

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inflammation in diabetic mice due to stimulation of TLR4-mediated inflammation.

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Polysaccharide was also reported to induce the microbiota to reduce the production of

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intestinal Gram-negative bacteria and the gut hormones such as GLP-1, peptide YY,

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and cholecystokinin which regulate appetite and energy balance.26 Table 2 provides

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some examples of different dietary polysaccharides which could attenuate diabetes by

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monitoring microbiota.

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SCFA production of polysaccharide

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Polysaccharide has been shown to improve insulin sensitivity in hepatic as well

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as peripheral tissues in diabetic persons. This may include replacement of some easily

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digested carbohydrate with the polysaccharide, which is broken down in the digestive

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tract to SCFAs. The absorbed SCFAs may also have forthright effect on mechanisms

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associated with insulin sensitivity, by either substituting gluconeogenic response or

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enhancing glucose uptake by adipose tissue and muscle. The long-term reduction in

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postprandial

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supplementation, was thought to improve insulin sensitivity via the combined actions

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of decreasing diurnal insulin excursions, lowering postprandial counter regulatory

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hormone excretion and reducing gastric inhibitory polypeptide secretion.

level

of

carbohydrate

absorption

caused

by

polysaccharide

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Recently, a potential relationship between SCFAs and T2DM pathophysiology

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has been clearly suggested. In particular, propionic and butyric acids were shown to

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reduce low-grade inflammation, regulate cell proliferation and differentiation, and

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induce hormone release. Butyrate producing intestinal bacteria seems to play an

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important role in blood glucose regulation and lipid metabolism, as shown by fecal

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transplantation studies. These beneficial effects of SCFAs were not only related to

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their property as histone deacetylase inhibitors, but also associated with their

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activation

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Polysaccharides from various resources, such as Plantago asiataca L. seeds,

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Cyclocarya paliurus leaves, Ganoderma atrum, Dendrobium officinale and others

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have been confirmed to improve production of SCFAs, which were beneficial to the

of

the

transmembrane

cognate

G

10


protein-coupled

receptors.

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diabetics. For example, butyrate prevented and inhibited colon carcinogenesis,

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protected against oxidative stress of mucosal, decreased inflammation and enhanced

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colonic defense barrier in diabetes.27

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Concomitant with the improvement of SCFAs, dyslipidemia was significantly

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improved by polysaccharide treatment compared with untreated T2DM rats, and

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polysaccharide dose-dependently reduced FBG level and insulin resistance in T2DM

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rats. The butyrate stimulated enteroendocrine cells to increase concentration of serum

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GLP-1, and thus butyrate affected insulin sensitivity by stimulating the secretion of

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GLP-1.28 The improvement of insulin sensitivity in recipients was also found to relate

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with the increased butyrate-producing microbiota due to polysaccharide intake. In

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addition, the SCFAs production of polysaccharide beneficially affected lipid

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metabolism through acetate decreasing free fatty acids (FFA) levels, while propionate

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and butyrate reduce total cholesterol and triglyceride levels. The consequences of

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elevated free fatty acids levels include hepatic and peripheral insulin resistance,

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impaired pancreatic β-cell function and induction of apoptosis.

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Targeting diabetes by anti-gastrointestinal inflammation

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Polysaccharide targeting inflammation in diabetes

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The gut tract owns the highest immune activity of the body maintaining

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homeostasis with microbiota, and also responded to the inflammation by a network of

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innate and adaptive immunity. Studies have confirmed that an inflammatory process

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contributed to the dysfunction of islet β-cells and insulin resistance in T2DM. In 11



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preclinical studies, anti-inflammatory drugs, such as IL-1 and receptor antagonists,

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reduced hyperglycaemia, improved insulin sensitivity, and reduced inflammatory

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infiltrates and fibrosis in the islets, suggesting alleviated β-cell dysfunction and

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improved survival.29 The β-cell apoptosis is directly linked to the expression of Bax

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and Bcl-2. Significantly decreased Bcl-2 expression and evaluated Bax expression

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were observed in the pancreas of the diabetic rats in a previous report. After

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polysaccharide supplementation, these changes were effectively reversed and

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accompanied by an elevated ratio of the Bcl-2/Bax.

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During inflammation, a response is also enhanced by epithelial and innate

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immune cells through ligation of different receptors by polysaccharide intake in

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diabetes. The recognition of microbial particles particularly metabolites could take

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place in the environment of innate NOD-like receptors, toll-like receptors, G

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protein-coupled receptors (GPCRs), and others.

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SCFA production of polysaccharide targeting inflammation in diabetes

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T2DM is characterized by low-grade inflammation with increased levels of

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cytokines, such as interleukin (IL)-6, IL-1, or tumor necrosis factor-alpha (TNF-α).

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These inflammatory molecules are up-regulated in insulin-target tissues, including the

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liver, adipose tissue, and muscles, thus contributing to insulin resistance. It has been

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reported that alterations in the SCFA production resulting from polysaccharide intake

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could promote an anti-inflammatory state of the adipose tissue that is associated with

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T2DM and subsequent insulin resistance.30 The up-regulation of TLR4 mRNA levels 12


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induced by high-fat diet in the liver of diabetes was shown to be counteracted by

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butyrate resulting from polysaccharide intake. High-fat diet was associated with the

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up-regulation of TNF-α and phosphorylation of NF-κB in the ileum, confirming that

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fat intake might increase mediators of intestinal permeability and inflammation. The

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polysaccharides can partly counteract these harmful effects through production of

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SCFAs, particularly propionic and butyric acids that could have anti-inflammatory

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effects in the body. The anti-inflammatory effects of SCFAs production of

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polysaccharide

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pro-inflammatory mediators, such as TNF-α and IL-6, and induction of

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anti-inflammatory cytokines. The regulation of blood glucose concentrations may

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involve several positive effects exerted by SCFA production of polysaccharide

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occurring at different levels (Figure 1): (1) inhibition of inflammatory state that

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decreased insulin resistance, (2) up-regulation of GLP-1 secretion that stimulates

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insulin release, and (3) enhancement of beta-cell function that results from

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improvement of glucose homeostasis.

are

probably

due

to

a

balance

between

suppression

of

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Therefore, the use of polysaccharide in the food of diabetic patients could be a

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promising and important way in controlling T2DM, because the dietary

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polysaccharides could attenuate diabetes by the mechanisms of gastrointestinal

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viscosity, gastrointestinal satiety, large bowel fermentation, and gastrointestinal

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anti-inflammation effects (Figure 2). However, there is still a lot to learn about the

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anti-diabetic mechanisms of the polysaccharides. The future challenge is to gain a

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better understanding of the relationship between the polysaccharide-induced 13



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microbiota change and the related anti-diabetic effects on host. Thus, the interactions

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between microbiota and the host could play an important role at an anti-diabetic level.

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Whether members of the microbiota and their other metabolites (lipids, peptides,

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amino acids, vitamins, and nucleic acids) could promote anti-inflammatory effects in

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diabetes also need further investigation. This presents a good opportunity for

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scientists to evaluate the anti-diabetic roles of dietary polysaccharides and produce

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high potential anti-diabetic dietary polysaccharides. Due to the significant effects of

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polysaccharide on gastrointestinal process, further researches focus on the

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mechanisms of the polysaccharide through host-microbiota interactions targeting the

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diabetes should have priority and will be important for further understanding the

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anti-diabetic mechanisms of the polysaccharides.

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COMPETING INTERESTS

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The authors declare that they have no competing interests.

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ACKNOWLEDGEMENTS

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The financial support from the National Key R&D Program of China (2017YFD0400

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203), Outstanding Science and Technology Innovation Team Project in Jiangxi

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Province (20165BCB19001), the Project of Academic Leaders of the Major

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Disciplines in Jiangxi Province (20162BCB22008), Collaborative Project in

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Agriculture and Food Field between China and Canada (2017ZJGH0102001),

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Research Project of State Key Laboratory of Food Science and Technology 14


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(SKLF-ZZA-201611) and National Natural Science Foundation of China (31501483

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and 31770861) is gratefully acknowledged.

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Jennifer, C.; Johannes, G.; Frank, R.; Gribble, F. M. Short-chain fatty acids stimulate

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glucagon-like peptide-1 secretion via the G-protein–coupled receptor FFAR2.

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Diabetes 2012, 61, 364-371.

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23. Hu, J. L.; Nie, S. P.; Li, C.; Xie, M. Y. Invitro fermentation of polysaccharide

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from the seeds of Plantago asiatica L. by human fecal microbiota. Food Hydrocolloid.

389

2013, 33, 384-392.

390

24. Zhang, G.; Nie, S.; Huang, X.; Hu, J.; Cui, S. W.; Xie, M. Y.; Phillips, G. O.

391

Study on Dendrobium officinale O-acetyl-glucomannan (Dendronan®): Part VII.

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Improving effects on colonic health of mice. J. Agric. Food Chem. 2016, 64,

393

2485-2491.

394

25. Wu, T.; Guo, Y.; Liu, R.; Wang, K.; Zhang, M. Black tea polyphenols and

395

polysaccharides improve body composition, increase fecal fatty acid, and regulate fat 18


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396

metabolism in high-fat diet-induced obese rats. Food Funct. 2016, 7, 2469-2478.

397

26. Goodpaster, B. H.; Katsiaras, A.; Kelley, D. E. Enhanced fat oxidation through

398

physical activity is associated with improvements in insulin sensitivity in obesity.

399

Diabetes 2003, 52, 2191-2197.

400

27. Wu, H. J.; Wu, E. The role of gut microbiota in immune homeostasis and

401

autoimmunity. Gut Microbes 2012, 3, 4-14.

402

28. Round, J. L. The gut microbiota shapes intestinal immune responses during health

403

and disease. Nat. Rev. Immunol. 2009, 9, 313-323.

404

29. Kaneto, H.; Obata, A.; Kimura, T.; Shimoda, M.; Okauchi, S.; Shimo, N.;

405

Matsuoka, T. A.; Kaku, K. Beneficial effects of SGLT2 inhibitors for preservation of

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pancreatic β-cell function and reduction of insulin resistance. J. Diabetes 2016, 9,

407

219-225.

408

30. Osborn, O.; Olefsky, J. M. The cellular and signaling networks linking the

409

immune system and metabolism in disease. Nat. Med. 2012, 18, 363-374.

410 411 412 413 414 415 416 417 19



418 419

FIGURE LEGENDS

420

Figure 1 SCFAs improve metabolic functions in T2DM. SCFAs were shown to affect

421

pancreatic beta-cell function by directly acting as Histone deacetylase (HDAC)

422

inhibitors (promoting β-cell development, proliferation, and differentiation) or by

423

indirectly increasing GLP-1 secretion from enteroendocrine L-cells (leading to insulin

424

release). Furthermore, SCFAs reduce the release of proinflammatory cytokines by

425

adipose tissue and weaken leukocyte activation. These anti-inflammatory effects

426

improve insulin resistance, tissue glucose uptake, and blood glucose levels.

427

Figure 2 Overview summarizing the mechanisms of dietary polysaccharides

428

attenuating diabetes based on the whole gastrointestinal process. SCFA, short-chain

429

fatty acid; FFA, free fatty acid.

430 431 432 433 434 435 436 437 438 439 20


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Table 1 Dietary polysaccharides inhibiting α-amylase and/or α-glucosidase. Dietary intake or Name

Sources

Mw

α-amylase

α-glucosidase

800 mg/kg BW

─

+

Structure related information IC 50

CFPA-3

Camellia oleifera

186,019 Da

Abel. fruit hull

GluA: GalA: Gal: Ara: Galactosamine = 0.80:0.06:0.22:1.14:4.16

Beta-glucan

Oat (Avena

Nm

Glc

IC50=10.95 mg/ml

─

+

378,824 Da

GluA: Gal: Xyl: Galactosamine =

IC50=11.8 mg/ml

─

+

IC50=15 mg/ml

─

+

Nm

+

+

sativa L.) CFPB

Camellia oleifera Abel. fruit hull

DTPS

Oolong tea

1.01:1.79:1.19:3.27 2640 kDa

L-rhamnose, D-fucose, L-arabinose, D-xylose, D-mannose, D-glucose and D-galacose in a molar ratio of 10.31:5.09:22.93:0.28:5.21:22.59: 33.59

EPS

Shaddock (Citrus paradise)

10 kDa

Rha, Ara, Gal, Glc, Xyl, Man, Ribib, GalA and GlcA in a molar ratio of 1.0:0.8:1.6:0.9:0.7:2.7: 0.9: 21



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0.4: 1.3 MFP-1

Mulberry fruit

Nm

IC50=7 µg/ml

─

+

IC50=9 µg/ml

─

+

Gal (86.4%) and Glc (13.6%)

IC50=550 µg/ml

─

+

Rha, Ara, Xyl, Man, Gal, Glc and

IC50=200 µg/ml

─

+

IC50=50 µg/ml

─

+

IC50=450 µg/ml

─

+

IC50=10 mg/ml

+

─

Ara (7.19%), Gal (6.33%), Glc (86.48%)

MFP-2

Mulberry fruit

Nm

Ara (36.01%), Gal (34.12%), Glc (29.87%)

PP-1

Pumpkin (Cucurbita

8.7 kDa

moschata) fruit PTPS-3

Puerch

tea

with

mild 631 kDa

fermenting for 3 years

Fuc in a molar ratio of 6.82:26.22: 0.35:13.83:39.34:10.23:3.21

PTPS-5

Puerch

tea

with

mild 1160 kDa

fermenting for 3 years

Rha, Ara, Xyl, Man, Gal, Glc and Fuc in a molar ratio of 15.98:20.84:

TFPS

Green tea flower

30.9 kDa

0.15:15.29:40.33:6.08:1.68 Rha, Ara, Gal, Glc, Xyl, Man, GalA and GlcA in a molar ratio of 4.95:11.57: 11.89: 4.26: 1.31: 1.98: 8.41: 1.00.

N-CSPS

Corn silk

105.2 kDa

Rha, Ara, Xyl, Man, Gal, glc in a

22


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molar ratio of 4.17:17.33:5.59:18.65: 19.11:35.14 S-CSPS

Corn silk

64.4 kDa

Rha, Ara, Xyl, Man, Gal, Glc in a

IC50=8 mg/ml

+

─

IC50=5 mg/ml

+

+

molar ratio of 8.83:15.77:7.92:12.39: 11.15:43.94 PLP

Plantago asiatica L. seeds.

1894 kDa

Rha, Ara, Xyl, Man, Glu and Gal with a molar ratio of 0.05:1.00:1.90: 0.05:0.06:0.10

Nm: not mentioned. BW: body weight. +: A significant difference (P < 0.05) or very significant difference (P < 0.01) with control group. −: No significant difference with control group or not detected.

23



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Table 2 Dietary polysaccharides attenuate diabetes by monitoring microbiota. Name

Sources

Mw

Structure related information

Dietary intake

Influenced bacterial species

MSP

Maydis stigma

80 kDa

Glu, Ara, Man, Gal and Xyl with a

400 mg/kg BW

Increased

molar proportion of

Lactobacillus

and

Bacteroides

5.73:0.50:0.10:0.06:0.05 PPSB

Physalis

alkekengi

var. 107 kDa

francheti

Rha, Ara, Man, Glu and Gal with a mass

50 mg/kg BW

percent of 12.01:60.36:2.95:

Increased Lactobacillus, Clostridium butyricum, and Bacteroides

9.93:9.78 PLP

MLPII

Plantago asiatica L. seeds.

Mulberry leaves

1894 kDa

Nm

Rha, Ara, Xyl, Man, Glu and Gal with a

100 mg/kg BW

Increased

Bacteroides

vulgatus,

molar ratio of 0.05:1.00:1.90:

Lactobacillus fermentum, Prevotella

0.05:0.06:0.10

loescheii and Bacteroides vulgates

Man, Rha, Glc, Xyl and Ara with a

150 mg/kg BW

molar proportion of

Increased

Lactobacillus

and

Bacteroides

8.73:1.04:6.53:2.13:1.00 beta glucan

Oat

Nm

Glu

3 g per day

Increased

Bacteroides-Prevotella

group L2

Lentinula edodes

26 kDa

Heteropolysaccharide, Glu (87.5%), Gal

40 mg/kg BW

(9.6%), Ara (2.8%) MDG-1

Roots of Ophiopogon

5000 Da

β-D-fructan, molar ratio of Fru and Glc 24


Increased

Helicobacteraceae

and

reduced S24-7 300 mg/kg BW

Decreased

the

ratio

of

Page 25 of 28


is approximately 35:1 GLP

Ganoderma lucidum

186,019 Da

GluA: GalA: Gal: Ara: Galactosamine = 0.80:0.06:0.22:1.14:4.16

Nm: not mentioned. BW: body weight.

25


Firmicutes/Bacteroidetes 200 mg/kg BW

Increased Enterococcus


Figure 1

26


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Figure 2

27



TOC Graphic

Table of Contents categories: Bioactive Constituents and Functions

28


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Anti-diabetic mechanism of dietary polysaccharides based on their

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