Application of Eubacterium rectum in preparation of medicine for treating type 2 diabetes mellitus

Abstract

The invention discloses application of Eubacterium rectum in preparation of medicines for treating type 2 diabetes mellitus, and belongs to the technical field of microbial medicines. The strain can promote synthesis of short-chain fatty acid (SCFAs), enhance secretion of glucagon-like peptide-1 (GLP-1) and effectively improve glucose and lipid metabolism disorder and related physiological indexes. Experiments prove that the strain can significantly reduce the fasting blood glucose level, improve the impaired state of glucose tolerance, enhance the insulin secretion ability, regulate abnormal blood lipid metabolism and improve the liver function. The Eubacterium rectum provided by the invention can be widely applied to the development of functional foods, dietary supplements or pharmaceutical preparations, and is suitable for early-stage intervention of diabetes and adjuvant therapy of complications.

Description

Technical Field

[0001] The present invention relates to the technical field of microbial medicine, and in particular to application of Eubacterium rectum in preparing medicine for treating type 2 diabetes. Background Art

[0002] Type 2 diabetes is a highly prevalent metabolic disease worldwide. Its pathological characteristics are mainly manifested in insufficient insulin secretion and lipid metabolism disorders caused by the progressive decline of pancreatic β-cell function. Current clinical treatments mainly include oral hypoglycemic drugs (such as metformin, SGLT-2 inhibitors) and insulin injections, but long-term use may lead to gastrointestinal side effects, risk of hypoglycemia, and liver and kidney burden, and cannot repair the insulin secretion function from the root. In addition, existing drugs mostly target a single pathological link (such as blood sugar regulation) and lack a comprehensive improvement effect on the accompanying lipid metabolism disorders, liver damage, and intestinal barrier dysfunction. In recent years, intestinal flora imbalance has been proven to be closely related to the occurrence and development of type 2 diabetes.

[0003] Studies have shown that specific probiotics can intervene in the progression of diabetes by regulating host metabolism and repairing the intestinal barrier. For example, Bifidobacterium and Parabacteroides have been reported to have potential hypoglycemic effects, but their effects are significantly strain-specific, and the mechanisms of their coordinated regulation of glucose and lipid metabolism and liver protection remain unclear.

[0004] Eubacterium rectale, a core intestinal commensal bacteria, plays a crucial role in maintaining intestinal homeostasis. However, existing research on Eubacterium rectale has primarily focused on its ability to produce short-chain fatty acids and its association with intestinal inflammation. Its potential for directly regulating blood glucose homeostasis, improving liver metabolic function, and multidimensionally intervening in type 2 diabetes has yet to be systematically explored. Furthermore, existing strain libraries lack Eubacterium rectale strains with clear hypoglycemic properties, liver protection, and lipid metabolism regulation. Summary of the Invention

[0005] The present invention aims to provide the use of Eubacterium rectum in the preparation of a medicament for treating type 2 diabetes, thereby addressing the aforementioned problems of the prior art. The disclosed use of Eubacterium rectum in blood sugar regulation and lipid metabolism intervention can address the limitations of existing probiotic therapies and promote their practical application in functional foods, probiotic preparations, and adjunctive diabetes treatments, providing technical support for precision microbial intervention.

[0006] To achieve the above object, the present invention provides the following solutions:

[0007] One of the technical solutions of the present invention is the use of Eubacterium rectale in the preparation of medicine for treating type 2 diabetes.

[0008] The second technical solution of the present invention is a drug for treating type 2 diabetes, comprising Eubacterium rectale.

[0009] The third technical solution of the present invention is a functional food or dietary supplement, comprising the rectal Eubacterium.

[0010] Based on the above technical solution, the present invention has the following technical effects:

[0011] The present invention provides Eubacterium rectale or its preparations, which regulate blood glucose homeostasis through multi-target synergistic effects, including directly promoting insulin secretion, repairing glucose and lipid metabolism disorders, enhancing intestinal short-chain fatty acid production, and activating the GLP-1 signaling pathway. Due to the characteristics of this human commensal strain, the preparations are free of the toxic side effects of chemical drugs. Furthermore, the preparations are adaptable to a variety of dosage forms, providing a safe and effective microbial therapy for the prevention and treatment of diabetes and possessing broad application prospects. BRIEF DESCRIPTION OF THE DRAWINGS

[0012] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the following briefly introduces the drawings required for use in the embodiments. Obviously, the drawings described below are only some embodiments of the present invention. For ordinary technicians in this field, other drawings can be obtained based on these drawings without paying any creative work.

[0013] Figure 1 Figure 3. Changes in blood glucose during the intervention with Eubacterium rectale in type 2 diabetic mice, as well as fasting blood glucose and serum insulin concentrations at the end of the fourth week of the experiment. A represents the trend of fasting blood glucose during the intervention period, B represents the fasting blood glucose values at the end of the intervention, and C represents the serum insulin levels after the intervention.

[0014] Figure 2 These are the oral glucose tolerance test curve and the area under the glucose tolerance test curve during the final week of Eubacterium rectale intervention in type 2 diabetic mice. A represents the oral glucose tolerance test curve, and B represents the area under the glucose tolerance test curve.

[0015] Figure 3 Figure 3. Changes in blood lipids and liver function after Eubacterium rectale intervention. A represents total cholesterol, B represents total triglycerides, C represents aspartate aminotransferase, and D represents alanine aminotransferase.

[0016] Figure 4 The short-chain fatty acid content in cecal contents after Eubacterium rectale intervention, where A is acetic acid, B is propionic acid, C is butyric acid, and D is total short-chain fatty acids.

[0017] Figure 5Figure 5: Serum glucagon-like peptide-1 (GLP-1) levels and GLP-1-related gene (Gcg, Ngn3, Pcsk1) mRNA expression levels after Eubacterium rectale intervention. A represents the glucagon-like peptide-1 (GLP-1) level, B represents the mRNA expression level of Gcg, C represents the mRNA expression level of Ngn3, and D represents the mRNA expression level of Pcsk1. DETAILED DESCRIPTION

[0018] Various exemplary embodiments of the present invention will now be described in detail. This detailed description should not be considered as limiting the present invention, but rather as a more detailed description of certain aspects, features, and embodiments of the present invention.

[0019] It should be understood that the terms described herein are intended only to describe particular embodiments and are not intended to limit the present invention. In addition, for numerical ranges herein, it should be understood that each intermediate value between the upper and lower limits of the range is also specifically disclosed. Each smaller range between any intermediate value within a stated value or stated range and any other stated value or intermediate value within the stated range is also encompassed by the present invention. The upper and lower limits of these smaller ranges may be independently included or excluded within the scope.

[0020] Unless otherwise indicated, all technical and scientific terms used herein have the same meaning as commonly understood by those skilled in the art. Although only preferred methods and materials are described herein, any methods and materials similar or equivalent to those described herein may also be used in the practice or testing of the present invention. All documents mentioned in this specification are incorporated by reference to disclose and describe the methods and / or materials associated with the documents. In the event of any conflict with any incorporated document, the contents of this specification shall prevail.

[0021] It will be apparent to those skilled in the art that various modifications and variations may be made to the specific embodiments of the present invention without departing from the scope or spirit of the invention. Other embodiments will be apparent to those skilled in the art from the present invention. The present description and examples are intended to be illustrative only.

[0022] The words “include,” “including,” “have,” “contain,” etc. used in this document are open-ended terms, meaning including but not limited to.

[0023] Unless otherwise specified, the technical solutions described in the present invention are all conventional solutions in the field, and the reagents or raw materials used, unless otherwise specified, are purchased from commercial channels or have been disclosed.

[0024] The embodiment of the present invention provides the use of Eubacterium rectale in the preparation of a medicine for treating type 2 diabetes.

[0025] In some specific embodiments, the Eubacterium rectale is derived from the Japan Culture Collection of Microorganisms with the accession number JCM17463.

[0026] In some specific embodiments, the drug is used for the prevention or adjuvant treatment of lowering blood sugar levels, alleviating type 2 diabetes and its related metabolic disorders.

[0027] An embodiment of the present invention further provides a medicine for treating type 2 diabetes, comprising Eubacterium rectale.

[0028] In some specific embodiments, the Eubacterium rectale is derived from the Japan Culture Collection of Microorganisms with the accession number JCM17463.

[0029] In some specific embodiments, the medicament further comprises a pharmaceutically acceptable carrier.

[0030] In some specific embodiments, the dosage form of the drug is a solid dosage form, a liquid dosage form, a cream dosage form or an emulsion dosage form.

[0031] In some specific embodiments, the medicament treats type 2 diabetes through at least one of the following mechanisms:

[0032] 1) Reduce fasting blood sugar, increase insulin secretion, and improve impaired glucose tolerance;

[0033] 2) Improve dyslipidemia;

[0034] 3) Alleviate liver damage;

[0035] 4) Increase the content of short-chain fatty acids;

[0036] 5) Upregulate the concentration of glucagon-like peptide-1 and the expression of glucagon-like peptide-1 related genes.

[0037] An embodiment of the present invention further provides a functional food or dietary supplement comprising the Eubacterium rectale.

[0038] The Eubacterium rectum strain provided by the present invention can promote the synthesis of short-chain fatty acids (SCFAs) and enhance the secretion of glucagon-like peptide-1 (GLP-1), effectively improving glucose and lipid metabolism disorders and related physiological indicators. Experiments have confirmed that this strain can significantly reduce fasting blood sugar levels, improve impaired glucose tolerance, enhance insulin secretion capacity, regulate abnormal blood lipid metabolism, and improve liver function indicators. The Eubacterium rectum provided by the present invention can be widely used in the development of functional foods, dietary supplements, or pharmaceutical preparations, and is suitable for prediabetes intervention and adjunctive treatment of complications.

[0039] This invention discloses a novel use of Eubacterium rectale in the preparation of blood sugar-regulating preparations. Addressing the technical issues of existing hypoglycemic drugs, which suffer from a single target and the safety risks associated with long-term use, this invention experimentally demonstrates that Eubacterium rectale can improve glucose and lipid metabolism disorders through a multi-pathway synergistic mechanism, providing a novel microbial therapy strategy for the prevention and treatment of type 2 diabetes and its complications.

[0040] The data were analyzed using SPSS 29.0 with one-way ANOVA and Tukey's HSD post hoc test. "*" indicates significant difference compared with the model group (*: p < 0.05; **: p < 0.01; ***: p < 0.001; ****: p < 0.0001).

[0041] The mice involved in the examples were purchased from Jiangsu Jicui Yaokang Experimental Animal Co., Ltd. and were raised at 25±2°C, constant humidity 50±5%, 12-h light / dark cycle, with free access to food and water. The experiment began after one week of adaptive feeding.

[0042] The insulin kit, glucagon-like peptide-1 kit (purchased from Crystal Chem, catalog numbers: 90080, 81508), blood glucose test strips and blood glucose meters involved in the examples were purchased from Roche; the total cholesterol (TC) kit (catalog number: A111-1), triglyceride TG kit (A110-1-1), aspartate aminotransferase (AST) kit, and alanine aminotransferase (ALT) kit involved were purchased from Nanjing Jiancheng Bioengineering Institute; the Trizol reagent (catalog number: 15596018) involved in the following examples was purchased from Thermo Fisher Scientific, USA; the reverse transcription kit (catalog number: RR047A) and real-time quantitative kit (catalog number: RR820A) involved in the examples were purchased from Baoriyi Biotechnology (Beijing) Co., Ltd.; the culture medium components involved in the examples were all purchased from Aladdin Biochemical Technology Co., Ltd.; the high-fat feed involved in the examples was purchased from Research Diets, USA (catalog number: D12492). The normal feed involved in the examples was purchased from Chengdu Biopark Technology Co., Ltd. (rat and mouse maintenance feed). The primers involved in the examples were all ordered from Shanghai Sangon Bioengineering Co., Ltd.

[0043] The culture medium involved in the embodiment is:

[0044] YCFA liquid medium (calculated per liter of medium): 10.0 g casein peptone, 2.5 g yeast extract, 2.0 g glucose, 2.0 g soluble starch, 2.0 g cellobiose, 0.45 g dipotassium hydrogen phosphate, 0.45 g potassium dihydrogen phosphate, 0.9 g sodium chloride, 4.0 g sodium bicarbonate, 0.9 g ammonium sulfate, 0.09 g magnesium sulfate, 0.09 g calcium chloride, 1.0 g L-cysteine hydrochloride, and 0.001 g resazurin. Mix thoroughly, adjust the pH to 6.5-7.2, sterilize at 115-121°C for 15-20 min, and after cooling, add 5 mg of filter-sterilized hemin and 10 μL of vitamin K to obtain the YCFA liquid medium.

[0045] Chocolate agar plate: 18.0 g of polyvalent peptone, 1.0 g of starch, 5.0 g of sodium chloride, and 15.0 g of agar were added to about 800 mL of distilled water, heated and stirred until completely dissolved, the volume was filled to 1000 mL and the pH was adjusted to 7.2-7.6, and the plate was sterilized by autoclaving at 121° C. for 15 min. After cooling to 50-55° C., 40 mL of defibrinated sheep blood was added under sterile conditions to obtain the chocolate agar plate.

[0046] The detection method involved in the embodiment of the present invention is as follows:

[0047] Method for detecting the content of short-chain fatty acids: Weigh 100 mg of mouse cecal contents, add 1 mL of normal saline, homogenize, centrifuge at 12000 g for 5 min at 4°C, take 500 μL of supernatant, add 0.2 mL of 50% (v / v) sulfuric acid and 400 μL of ether, vortex and let stand for 2 min, centrifuge at 13000 g for 2 min at 4°C, take the supernatant and pass it through a 0.22 μm filter membrane, and then measure it on a gas chromatograph (6890N).

[0048] RNA extraction and gene expression determination: Total RNA of colon tissue was extracted using Trizol reagent, and reverse transcription was performed on the total RNA of colon tissue using a reverse transcription kit. The cDNA obtained by reverse transcription was used as a template, and the PCR reaction system (20 μL) was prepared using the TB Green Premix Ex Taq II kit (TAKARA), namely 10 μL TB Green Premix Ex Taq II (Tli RNase H Plus), 6 μL dd H2O, 0.8 μL upstream primer, 0.8 μL downstream primer, 0.4 μL ROX Reference Dye II and 2 μL cDNA template. The primers are detailed in Table 1, where β-actin is the internal reference gene. Reaction conditions: 50°C for 2 min, 95°C for 30 s for initial denaturation; followed by 40 cycles of 95°C for 20 s, 60°C for 30 s, and 72°C for 30 s; extension at 72°C for 5 min to terminate the reaction. According to the Ct value of the target gene and the internal reference gene, 2 -△△Ct The relative expression of target genes was calculated by this method.

[0049] Table 1 Target genes and primer sequences

[0050]

[0051]

[0052] The strain Eubacterium rectale JCM17463 used in the present invention is from Japan Culture Collection of Microorganisms, with the accession number being JCM17463.

[0053] Example 1

[0054] Effects of Eubacterium rectale on fasting blood glucose, glycosylated serum protein and serum insulin in type 2 diabetic mice

[0055] 1.1 Preparation of Cryopreservatives of Eubacterium rectale:

[0056] (1) Culture method: Under a sterile anaerobic environment, streak Eubacterium rectale onto chocolate agar plates and culture under anaerobic conditions for 48 hours. Once a single colony is formed, pick a single colony and inoculate it into YCFA liquid medium. Subsequently, culture at 37°C anaerobically for 16-24 hours to allow the bacteria to grow to the stationary phase, at which point the OD value is 0.7-1.0, to prepare the seed solution.

[0057] (2) Preparation of protective agent: Dissolve 1 g / L cysteine hydrochloride and 200-300 g / L glycerol evenly in distilled water and sterilize at 115-121°C for 15-20 min.

[0058] (3) Preparation of cryopreservative: Centrifuge the Eubacterium rectum seed solution at 8000 rpm for 10 min. Collect the bacterial precipitate and wash it 1-2 times with sterile phosphate buffer (pH 7.2). Subsequently, resuspend the cells in a pre-prepared protective agent to obtain the Eubacterium rectum cryopreservative solution, which is then stored at -80°C until use.

[0059] 1.2 Preparation of Eubacterium rectale

[0060] (1) Strain activation: The prepared Eubacterium rectale cryostock was streaked onto chocolate agar plates and cultured under anaerobic conditions for 48 h. After a single colony was formed, a single colony was picked and inoculated into YCFA liquid culture medium and cultured anaerobically at 37°C for 16-24 h until the stable phase (OD value 0.7-1.0) was reached.

[0061] (2) Preparation of inoculum: 100 μL of culture medium of different dilutions was spread on chocolate agar plates and colonies on the plates were counted to calculate the number of viable bacteria in the liquid culture medium. The bacteria were washed 1-2 times with sterile phosphate buffer (pH 7.2) and the concentration of the inoculum was adjusted to 1×10 9 CFU / mL, prepare bacterial agent.

[0062] 1.3 Experimental methods

[0063] Intervention treatment experimental process:

[0064] In this study, a high-fat diet combined with streptozotocin was used to induce a type 2 diabetes model in mice. After one week of adaptation, all mice were randomly assigned to a normal group, a model group, and a rectal Eubacterium group (n=6).

[0065] The mice in the normal group were given standard feed and free access to water during the modeling period. During the treatment period, they continued to be given normal feed and were gavaged with 0.2 mL of sterile phosphate buffer once a day.

[0066] The mice in the model group and the Eubacterium rectale group were fed a high-fat diet for 7 weeks and then fasted for 12 hours before being intraperitoneally injected with streptozotocin (70 mg / kg body weight) to induce type 2 diabetes, while the mice in the normal group were injected with an equal amount of citric acid buffer.

[0067] After 7 days, fasting blood glucose was measured, and mice with fasting blood glucose ≥11.1 mmol / L were identified as type 2 diabetes model mice. Subsequently, the diabetic model mice were randomly divided into two groups and received different treatments for 4 weeks: (1) model group: high-fat diet + 0.2 mL sterile phosphate buffer; (2) rectal Eubacterium group: high-fat diet + 0.2 mL rectal Eubacterium inoculum.

[0068] After four weeks of intervention, mice were anesthetized and sacrificed. Blood was collected from the eye sockets and centrifuged at 3000 rpm for 15 minutes to obtain serum. Serum, colonic, and cecal contents were stored at -80°C for subsequent analysis.

[0069] 1.4 Effects of Eubacterium rectale on fasting blood glucose and serum insulin in type 2 diabetic mice

[0070] Figure 1 Center A shows the changing trends in fasting blood glucose levels in each group of mice during the intervention period. While blood glucose levels in the normal group remained stable, those in the model group continued to rise, reaching 17.30±1.24 mmol / L at week 4. Blood glucose levels in the Eubacterium rectale group began to decrease after week 2, reaching 12.30±1.26 mmol / L at week 4.

[0071] Figure 1 Figure B shows the fasting blood glucose levels of mice in each group at the end of the intervention. The results showed that the fasting blood glucose levels of the model group were significantly higher than those of the normal group (p<0.0001). The blood glucose levels of mice in the model group were significantly lower after the Eubacterium rectum intervention than those in the model group (p<0.0001).

[0072] After intervention, the serum insulin levels of mice in each group were as follows Figure 1 As shown in middle C. The results showed that the serum insulin concentration of diabetic mice was significantly lower than that of normal mice (p<0.0001), and the serum insulin content of mice after intervention with Eubacterium rectum increased by 71.28% compared with that of the model group (p<0.001).

[0073] The above results indicate that Eubacterium rectum intervention can reduce the fasting blood glucose level and increase the serum insulin content in diabetic mice.

[0074] Example 2

[0075] The effect of Eubacterium rectale on glucose tolerance in type 2 diabetic mice was investigated as follows:

[0076] The specific experimental method was the same as in Example 1. Three days before the end of the intervention, the animals were fasted for 12 hours. Baseline blood glucose was measured at 0 min, followed by oral administration of 1.0 g / kg glucose. Blood was collected from the tail vein of the mice and measured using a Roche blood glucose meter at 30, 60, 90, and 120 min after oral administration. A blood glucose-time curve was plotted, and the area under the curve (AUC) for each group was calculated based on the blood glucose values at each time point.

[0077] The oral glucose tolerance test (OGTT) is a classic method for assessing the body's ability to regulate blood sugar after a glucose load. It is primarily used to evaluate the body's ability to uptake, utilize, and clear glucose, and is an important indicator of impaired glucose tolerance and the early diagnosis of diabetes.

[0078] Figure 2 Center A shows the results of an oral glucose tolerance test. Blood glucose levels in the normal group decreased rapidly after a glucose load, while those in the model group remained elevated, indicating impaired glucose tolerance in diabetic mice. The blood glucose curve in the Eubacterium rectum intervention group was lower than that in the model group, but still higher than that in the normal group, indicating that Eubacterium rectum intervention can partially improve glucose tolerance. Figure 2 Figure B quantified the area under the curve (AUC) of the oral glucose tolerance test. The results showed that the AUC in the model group was significantly higher than that in the normal group (p < 0.0001), indicating impaired glucose tolerance. The AUC was significantly reduced after intervention with Eubacterium rectale (p < 0.0001).

[0079] The above results indicate that Eubacterium rectale intervention can significantly improve impaired glucose tolerance caused by diabetes.

[0080] Example 3

[0081] The effects of Eubacterium rectum on blood lipids and liver function in type 2 diabetic mice are as follows:

[0082] The specific experimental method is the same as that in Example 1. After the fourth week, the mice were anesthetized and killed. The serum was taken to measure the total cholesterol, total triglyceride, aspartate aminotransferase, and alanine aminotransferase levels. Figure 3 shown.

[0083] Figure 3 Results from the A and B assays showed that serum total cholesterol and total triglyceride levels in the model group were significantly higher than those in the normal group (p<0.0001), indicating significant lipid metabolism abnormalities in diabetic mice. Following treatment with Eubacterium rectale, total cholesterol and total triglyceride levels decreased significantly (p<0.001), suggesting that Eubacterium rectale intervention can improve lipid metabolism in diabetic mice.

[0084] Figure 3 CD reflects liver damage. In the model group, aspartate aminotransferase and alanine aminotransferase levels were significantly elevated (p < 0.0001), indicating liver damage in diabetic mice. Following treatment with Eubacterium rectum, both ALT and AST were significantly decreased (p < 0.0001), suggesting that Eubacterium rectum intervention may help alleviate diabetic-induced liver damage.

[0085] The above results indicate that Eubacterium rectum intervention can reduce blood lipid levels and improve liver function in diabetic mice, and it plays a certain role in regulating glucose and lipid metabolism and protecting liver function.

[0086] Example 4

[0087] The effect of Eubacterium rectum on the content of short-chain fatty acids in type 2 diabetic mice is as follows:

[0088] The specific experimental method is the same as that in Example 1. After the fourth week, the mice were anesthetized and killed. Cecal content samples were collected and the acetic acid, propionic acid and butyric acid contents were detected by GC technology. The experimental results are shown in Figure 2. Figure 4 shown.

[0089] Figure 4 AC showed that the levels of acetate, propionate, and butyrate in the model group were lower than those in the normal group, with butyrate decreasing from 21.00±2.24μmol / g (normal group) to 11.58±1.57μmol / g (p<0.0001). After treatment with Eubacterium rectale, acetate, propionate, and butyrate in the cecal contents of mice increased to 39.23±3.03, 18.30±1.89, and 22.39±1.38μmol / g, respectively, all significantly different from those in the model group (p<0.05, p<0.05, p<0.0001).

[0090] The total short-chain fatty acid content in the cecum of mice in each group was as follows Figure 4 As shown in middle D, the total short-chain fatty acid level of mice in the model group was significantly lower than that in the normal group (p<0.001), while after the intervention of Eubacterium rectale, the total SCFAs content was significantly increased (p<0.0001).

[0091] The above results showed that the intervention of Eubacterium rectale effectively increased the content of acetate, propionate and butyrate in the cecal contents of diabetic mice and restored the level of total SCFAs, indicating that this strain has application potential in optimizing the production of short-chain fatty acids.

[0092] Example 5

[0093] The effects of Eubacterium rectum on serum glucagon-like peptide-1 (GLP-1) levels and GLP-1-related gene expression in type 2 diabetic mice were investigated as follows:

[0094] The specific experimental methods were the same as in Example 1. After the fourth week, mice were anesthetized and sacrificed, and serum was collected for GLP-1 content using an ELISA kit. Colonic tissue was rinsed with PBS, and one-third of the tissue was soaked in RNAwait solution overnight and frozen at -80°C for RNA extraction and qPCR analysis to measure the relative mRNA expression levels of Gcg, Pcsk1, and Ngn3.

[0095] GLP-1 is encoded by Gcg, and its maturation and processing are dependent on Pcsk1. Ngn3, involved in endocrine cell differentiation, is closely associated with GLP-1 production. Furthermore, as a key blood glucose-regulating hormone, GLP-1 promotes insulin secretion, inhibits glucagon release, and enhances glucose uptake in peripheral tissues, thereby lowering blood glucose. Therefore, GLP-1 secretion and the expression of its associated genes are crucial for maintaining glucose homeostasis.

[0096] The experimental results showed that the GLP-1 level in diabetic mice was significantly decreased (p<0.01), while it was significantly increased after intervention with Eubacterium rectum (p<0.001, Figure 5 Meanwhile, the mRNA expressions of Gcg, Pcsk1, and Ngn3 were significantly downregulated in the model group (p<0.0001), but significantly increased after the intervention of Eubacterium rectum (p<0.01, Figure 5 This suggests that Eubacterium rectum intervention may improve GLP-1 levels by affecting GLP-1 production and its processing.

[0097] The above results showed that the intervention of Eubacterium rectum increased the secretion level of GLP-1 and upregulated the expression of Gcg, Pcsk1 and Ngn3, indicating that it may enhance the GLP-1-mediated blood glucose regulation mechanism by regulating the GLP-1 production pathway, and has a potential role in maintaining glucose metabolism homeostasis.

[0098] Obviously, the above embodiments of the present invention are merely examples for the purpose of clearly illustrating the present invention and are not intended to limit the implementation methods of the present invention. A person skilled in the art will be able to make other variations or modifications based on the above description. It is not necessary and impossible to enumerate all implementation methods here. Any modifications, equivalent substitutions, and improvements made within the spirit and principles of the present invention shall be included within the scope of protection of the claims of the present invention.

Claims

1. Application of Eubacterium rectum in the preparation of medicines for treating type 2 diabetes.

2. The use according to claim 1, characterized in that The Eubacterium rectale is from Japan Culture Collection of Microorganisms, with the collection number being JCM17463.

3. The use according to claim 1 or 2, characterized in that The medicine is used for lowering blood sugar levels, alleviating type 2 diabetes and preventing or assisting in the treatment of related metabolic disorders.

4. A drug for treating type 2 diabetes, characterized in that: Including Eubacterium rectale.

5. The drug according to claim 4, characterized in that The Eubacterium rectale is from Japan Culture Collection of Microorganisms, with the collection number being JCM17463.

6. The drug according to claim 4, characterized in that The drug further includes a pharmaceutically acceptable carrier.

7. The drug according to claim 4, characterized in that The dosage form of the medicine is a solid dosage form, a liquid dosage form, a paste dosage form or an emulsion dosage form.

8. The drug according to claim 4, characterized in that The drug treats type 2 diabetes through at least one of the following mechanisms: 1) Reduce fasting blood sugar, increase insulin secretion, and improve impaired glucose tolerance; 2) Improve dyslipidemia; 3) Alleviate liver damage; 4) Increase the content of short-chain fatty acids; 5) Upregulate the concentration of glucagon-like peptide-1 and the expression of glucagon-like peptide-1 related genes.

9. A functional food or dietary supplement, characterized in that The method comprises the Eubacterium rectale described in claim 1 or 2.

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