Application of desulfurization vibrio in screening of medicines or functional foods for preventing and treating sarcopenia

Abstract

The invention provides application of desulfurization vibrio in screening of drugs or functional food for preventing and treating sarcopenia. According to the application disclosed by the invention, a main intestinal flora desulfurization vibrio capable of promoting amyotrophy is firstly found, and the desulfurization vibrio can be used as a main target for screening sarcopenia and can be used for screening medicines or functional foods for preventing and treating sarcopenia. Sinopenia susceptible people are screened through abundance of desulfurization vibrio in excrement, and early discovery and targeted early intervention can be carried out; aiming at the mechanism that desulfurization vibrio in intestinal tracts promotes occurrence and development of sarcopenia, drugs or functional food for treating sarcopenia can be further screened, and then substances / new therapy for preventing and treating sarcopenia are developed.

Description

Technical Field

[0001] This invention belongs to the fields of biomedicine and functional food, specifically involving the application of desulfovibrio in screening drugs or functional foods for the prevention and treatment of sarcopenia. Background Technology

[0002] Sarcopenia, also known as muscle wasting disease, is an age-related disorder characterized by a gradual decline in skeletal muscle mass and its systemic functional decline. With the accelerating aging of the population, the incidence of sarcopenia is steadily increasing, currently affecting 10%-16% of the elderly worldwide, and is projected to surge to 500 million cases by 2050. Sarcopenia leads to adverse outcomes such as weakness, falls, fractures, and the need for long-term care, and is closely associated with various chronic diseases and cachexia, making it a pressing public health issue. The main pathogenic factors of sarcopenia include environmental factors, genetic factors, inflammation, weakened neurological function, and age-related hormonal changes, but the specific mechanisms remain unclear. An assessment of the effects of genetic variations on gait speed, lean body mass, and grip strength found that single nucleotide polymorphisms are associated with synaptic function and neural maintenance, skeletal muscle fiber structure and function, and muscle metabolism; another cross-sectional study found that a higher level of physical activity and shorter sedentary time reduces the likelihood of developing sarcopenia.

[0003] In recent years, the important role of gut microbiota in the development of sarcopenia in the elderly has become a research hotspot. Gut microorganisms produce short-chain fatty acids and tryptophan metabolites, which play a significant regulatory role in sarcopenia. However, the specific mechanisms by which gut microbiota influence the development of sarcopenia remain inconclusive. Tryptophan is an essential amino acid that plays a crucial role in regulating muscle protein synthesis. Symbiotic microorganisms in the human gut can break down some tryptophan into indole metabolites, affecting tryptophan metabolism. 5-hydroxytryptamine (5-HT) can promote the secretion of pituitary growth hormone and induce the production of liver-derived IGF-1, ultimately contributing to muscle growth. Low tryptophan levels can inhibit the transmission of the growth hormone-IGF-1 signaling pathway, thereby reducing muscle mass and leading to muscle atrophy. Additionally, kynurenine can increase muscle lipid peroxidation and ROS production, causing sarcopenia through skeletal muscle atrophy. Improving the gut microbiota structure helps in the synthesis of 5-HT and inhibits the accumulation of kynurenine, thereby increasing muscle mass and inhibiting the occurrence of sarcopenia. Summary of the Invention

[0004] To address the aforementioned problems, this invention provides the application of *Desulfovibrio* in screening drugs or functional foods for the prevention and treatment of sarcopenia. This invention first identifies *Desulfovibrio*, a major gut microbiota that promotes muscle atrophy, as a primary target for sarcopenia screening, which can be used to screen drugs or functional foods for the prevention and treatment of sarcopenia. Screening for sarcopenia-susceptible populations by analyzing the abundance of *Desulfovibrio* in feces allows for early detection and targeted intervention. Furthermore, by understanding the mechanism by which *Desulfovibrio* in the gut promotes the development and progression of sarcopenia, further screening for drugs or functional foods to treat sarcopenia can be conducted, thereby developing substances / new therapies for the prevention and treatment of sarcopenia, which has significant clinical implications.

[0005] The technical solution of this invention is: Desulfurization Vibrio ( Desulfovibrionales The application of this as a new detection target in the preparation of pre-sarcopenia screening reagents.

[0006] This invention also provides a method for detecting desulfurization vibrio ( ) Desulfovibrionales The application of reagents in the preparation of pre-sarcopenia screening reagents.

[0007] As a preferred embodiment of the present invention, the order Desulfovibrio includes common desulfovibrio ( Desulfovibrio vulgaris ), desulfurization vibrio (Desulfovibriodesulfuricans ) and Pigra desulfurization vibrio ( Desulfovibriopigra ).

[0008] As a further preferred embodiment of the present invention, the detection of desulfurized Vibrio ( Desulfovibrionales The reagents include those for detecting desulfovibrio (Bacteroides). Desulfovibrionales PCR primers for bacteria and reagents for determining their metabolite hydrogen sulfide.

[0009] Desulfovibrioles ( Desulfovibrionales Its application as a target for sarcopenia treatment in screening sarcopenia treatment drugs or health foods.

[0010] The specific mechanism by which desulfovibrio promotes the development of sarcopenia was discovered through the following method: The main function of desulfovibrio is to reduce the substrate to H2S. H2S increases blood kynurenine levels and reduces 5-hydroxytryptamine synthesis by regulating tryptophan metabolism.

[0011] Furthermore, the present invention also provides a method for screening individuals susceptible to sarcopenia: quantitative PCR is used to detect the abundance level of Desulfovibrio in the feces of the individuals to be tested, and the results are compared with those of a control group without sarcopenia. Individuals with a higher relative abundance of Desulfovibrio than the control group without sarcopenia are considered susceptible to sarcopenia. Furthermore, individuals with higher levels of Desulfovibrio metabolite H2S, higher levels of kynurenine than the control group without sarcopenia, and lower levels of indolepropionic acid than the control group without sarcopenia are also considered susceptible.

[0012] Furthermore, the present invention also provides the application of substances that specifically inhibit desulfovibrio bacteria in the preparation of drugs or functional foods for the prevention and treatment of sarcopenia.

[0013] The sarcopenia mentioned above is usually sarcopenia in the elderly.

[0014] The beneficial effects of this invention are as follows: 1) This invention provides a new target for early screening of sarcopenia by screening susceptible individuals for sarcopenia through the abundance of desulfovibrio in feces, enabling early detection and targeted early intervention.

[0015] 2) This invention provides a new target for the treatment of sarcopenia, targeting the mechanism by which desulfovibrio in the gut promotes the occurrence and development of sarcopenia. This can further screen drugs or functional foods for the treatment of sarcopenia and develop new therapies for sarcopenia.

[0016] 3) This invention detected H2S levels in mouse serum, finding that the H2S levels in high-abundance *Desulfovibrio* mice (OS-4W) and low-abundance mice (OS-1W) were significantly higher than those in mice without *Desulfovibrio* abundance. Detection of blood tryptophan metabolites revealed that blood tryptophan and 5-HT levels in mice transplanted with low-abundance (OS-1W) and high-abundance *Desulfovibrio* (OS-4W) were significantly lower than those in mice transplanted without *Desulfovibrio* (NS-1W, NS-4W), while blood kynurenine and kynurenine / tryptophan levels were significantly higher. Decreased serotonin levels inhibited IGF-1 production in muscle tissue, and kynurenine, by increasing muscle lipid peroxidation and ROS production, led to skeletal muscle atrophy, ultimately causing sarcopenia. The results suggest that intestinal *Desulfovibrio* promotes muscle atrophy by increasing serum H2S levels and enhancing the effect of kynurenine, ultimately leading to increased ROS. Attached Figure Description

[0017] Figure 1 PCA analysis of gut microbiota based on 16sRNA microbiota sequencing data showed significant differences in gut microbiota composition between elderly individuals with sarcopenia and controls without sarcopenia. NS: controls without sarcopenia, S: individuals with sarcopenia. Figure 2 LefSe analysis of 16sRNA microbiota sequencing data revealed characteristic differences in gut microbiota between elderly individuals with sarcopenia and controls without sarcopenia (Figure A is the LEfSe multilevel species tree; Figure B is the LDA discriminant bar chart), where NS represents controls without sarcopenia and S represents individuals with sarcopenia. Figure 3Figure A shows the abundance level and structural composition of Desulfovibrioles in the feces of elderly sarcopenic muscular dystrophy patients and non-sarcopenic muscular dystrophy control patients; Figure B shows the structural composition of Desulfovibrioles strains in the feces of elderly sarcopenic muscular dystrophy patients and non-sarcopenic muscular dystrophy control patients; NS: non-sarcopenic muscular dystrophy control patients, S: sarcopenic muscular dystrophy patients. Figure 4 This study investigated the effects of fecal transplantation from elderly individuals with sarcopenia on muscle mass and function in mice. Figure A shows a comparison of the gastrocnemius, quadriceps, soleus, extensor digitorum longus, and tibialis anterior muscles after fecal transplantation from elderly individuals with sarcopenia to normal mice. Figure B shows the weight of each skeletal muscle. Figure C shows the gastrocnemius muscle index. Figure D shows the changes in grip strength before and after transplantation. Figure E shows the changes in gait speed before and after transplantation. In the figures, NS represents the control group without sarcopenia, and S represents the sarcopenic group. Figure 5 16SRNA microbiota sequencing revealed the abundance levels of Desulfovibrioles in the gut microbiota after receiving fecal transplantation from different sources, where NS: control group without sarcopenia, and S: sarcopenia group. Figure 6 This study investigated the effects of fecal transplantation of different abundance levels of *Desulfovibrio* into normal mice on sarcopenia development. Figure A shows the composition of the intestinal flora in mice after fecal transplantation; Figure B shows the abundance level of *Desulfovibrio*; Figure C shows the grip strength of normal mice after fecal transplantation carrying different abundance levels of *Desulfovibrio*; Figure D shows gait speed; and Figure E shows the muscle mass of the quadriceps, gastrocnemius, soleus, tibialis anterior, and extensor digitorum longus muscles. FMT1, FMT2, FMT3, and FMT4 represent weeks 1, 2, 3, and 4 after transplantation, respectively. NS-1W: Fecal transplanted from mice with sarcopenia-free control groups for one week, then transplanted into normal mice; NS-1W: Fecal transplanted from mice with sarcopenia-free control groups for four weeks, then transplanted into normal mice; OS-1W: Fecal transplanted from mice with sarcopenia groups for one week, then transplanted into normal mice; OS-4W: Fecal transplanted from mice with sarcopenia groups for four weeks, then transplanted into normal mice. Figure 7 The effect of fecal transplantation with different abundance levels of Desulfovibrio on tryptophan metabolism was investigated. A represents tryptophan, B represents kynurenine, C represents 5-hydroxytryptamine (5-HT), D represents 5-HIAA level, and E represents the change in kynurenine / tryptophan ratio. Figure 8 The effect of different abundance levels of Desulfovibrio on serum hydrogen sulfide levels after fecal transplantation. Detailed Implementation

[0018] The following embodiments are used in this invention, but do not limit the scope of the invention. Unless otherwise stated, the technical means used in the embodiments are conventional means familiar to those skilled in the art, and the raw materials used are commercially available commodities.

[0019] Example 1 Fecal samples were collected from 36 elderly individuals with sarcopenia (S) and 36 controls without sarcopenia (NS). 16S rRNA sequencing analysis of the fecal microbiota composition showed significant differences in microbiota expression profiles between the two groups. PCA dimensionality reduction analysis revealed that the gut microbiota structure of the elderly individuals with sarcopenia and the controls without sarcopenia was distributed in different regions, with significant differences. Figure 1 LefSE analysis showed that the two groups of bacteria exhibited different levels of enrichment. Figure 2 Species-level analysis also showed significant differences in gut microbiota structure between the two groups, mainly manifested in a significantly higher level of Desulfovibrio strains in the elderly sarcopenia group than in the control group without sarcopenia. Figure 3 A), and it can effectively distinguish between elderly individuals with sarcopenia and control individuals without sarcopenia, indicating that the order Desulfovibrioles ( Desulfovibrionales (This is related to the development of sarcopenia.) The main desulfurizing strains include *Vibrio vulnificus* (common desulfurizing bacteria). Desulfovibriovulgaris ), desulfurization vibrio ( Desulfovibriodesulfuricans ), and Pigra desulfurization vibrio ( Desulfovibriopigra See also Figure 3 B.

[0020] Example 2: This study, based on human fecal transplantation into normal mice, found that mice with fecal microbiota transplanted from elderly sarcopenic individuals showed decreased weight, decreased muscle index, decreased grip strength, and decreased gait speed in the gastrocnemius, quadriceps, soleus, extensor digitorum longus, and tibialis anterior muscles.

[0021] 1. Human fecal matter was transplanted into mice (C57BL / 6 breed, 8 weeks old, purchased from Vital River Pharmaceuticals, Beijing) to observe its effects on muscle mass and function. (1) Preparation of pseudo-germ-free mice: Mice were given amphotericin B (1 mg / kg) every 12 hours for 3 days to prevent fungal infection. For the next 14 days, mice were given a mixed antibiotic (Abx) containing vancomycin (50 mg / kg), neomycin (100 mg / kg), metronidazole (100 mg / kg), and amphotericin B (1 mg / kg) by gavage every 12 hours. During this period, mice were given water containing ampicillin (1 g / L).

[0022] (2) Human-derived fecal microbiota transplantation: Five individuals were randomly selected from 36 elderly individuals with sarcopenia and 36 controls without sarcopenia. Fresh feces were collected and thoroughly mixed using a vortex mixer. The fecal suspension was filtered through gauze to remove food residue. It was then filtered layer by layer using molecular sieves of different diameters to remove small particles. The fecal microbiota filtrate was centrifuged at 2500 rpm / min for 5 minutes, and the supernatant was discarded. Sterile physiological saline was added to the centrifuge tube after discarding the supernatant to the original suspension volume and shaken well. The mixture was then centrifuged at 4000 rpm / min for 5 minutes, and washed three times. Glycerol was added at a ratio of 10:1 and shaken well. The bacterial suspension was stored at -80℃ for later use. The prepared bacterial suspension was administered to pseudo-germ-free mice by gavage at a dose of 200 μL per mouse for 4 weeks to complete the microbiota transplantation.

[0023] (3) Sequencing of 16S RNA from colonic contents: Genomic DNA was extracted using an environmental sample DNA extraction kit (OMEGA). DNA concentration and integrity were measured using NanoDrop 200 and 1% agarose gel electrophoresis, respectively. The V3-V4 regions of bacterial 16S rRNA were amplified using an ABIGeneAmp 9700 real-time fluorescence PCR system with upstream primer 338F (5′-ACTCCTACGGGAGGCAGCAG-3′) and downstream primer 806 (5′-GGACTACHVGGGTWTCTAAT-3′), and quantified using a Quantus fluorometer (Promega, USA). The sequencing library was generated by TruSeq™ DNA SamplePrep Ki (Illumina, San Diego, California, USA), and sequencing and data analysis were performed using the Illumina PE300 platform.

[0024] (4) Measurement of mouse muscle mass: Mice were euthanized after the last fecal microbiota transplantation. The quadriceps femoris, gastrocnemius, soleus, tibialis anterior, and extensor digitorum longus muscles were isolated and weighed under 4°C ice bath conditions. The gastrocnemius muscle is the muscle most affected by aging, and the gastrocnemius index was further evaluated and expressed as gastrocnemius muscle / body weight.

[0025] (5) Mouse muscle function assessment: Mouse grip strength and gait speed. Grip strength was measured using a grip strength meter. After the mouse's forelimbs gripped the lever, the mouse's tail was grasped, and the tail was pulled horizontally with uniform force until both forelimbs released. The grip strength value was recorded in g. The measurement was repeated three times for each mouse at 5-minute intervals, and the maximum value was taken as the final grip strength. Gait speed was measured using an open field test. Each mouse was placed in the center of a 50cm×50cm×25cm chamber and allowed to explore freely for 30 seconds before the formal experiment began for 5 minutes. The mouse's movement trajectory was recorded using an ANY-maze (Stoelting, Kiel, WI, USA), and the average gait speed (m / s) was calculated based on the total distance (m) and time.

[0026] In human fecal transplantation experiments, compared with mice receiving feces from non-sarcopenic control groups, mice receiving feces from aged sarcopenic individuals showed decreased weights in the gastrocnemius, quadriceps, soleus, extensor digitorum longus, and tibialis anterior muscles. Figure 4 A, B), decreased muscle mass ( Figure 4 C) Decreased grip strength ( Figure 4 D), the mice's walking speed slowed down ( Figure 4 E). 16SRNA microbiota sequencing showed differential changes in desulfovibrio in the gut microbiota after receiving fecal transplants from different sources. The order Desulfovibrio (…) was higher in fecal transplants from mice with sarcopenia. Desulfovibrionales The abundance of *Desulfovibrio* species was high, and the bacteria were transplanted from feces of control individuals without sarcopenia. Desulfovibrionales The abundance of *Desulfovibrio* was low, and changes in the abundance of *Desulfovibrio* were associated with alterations in mouse muscle mass and function. Figure 5 ).

[0027] Example 3: Effects of fecal transplantation of different abundance levels of *Desulfovibrio* on muscle mass and function in normal mice Feces containing different abundance levels of *Vibrio desulfurans*, obtained from feces of NS (transplanted from control populations without sarcopenia) and OS (transplanted from feces of elderly sarcopenia patients), were transplanted into normal mice to observe their effects on muscle mass and function.

[0028] (1) Fecal transplantation: Feces from NS and OS mice at 1 week and 4 weeks of age were transplanted into normal mice, respectively. 10g of fresh feces was collected in a sterile 50mL centrifuge tube and mixed thoroughly with 20mL of sterile saline. After centrifugation at 2000 rpm / min for 15 min, the supernatant was transferred to a new sterile tube. After centrifugation at 8000 rpm / min for 5 min, the supernatant was discarded, and sterile saline was added to the sterile tube to repeatedly mix and centrifuge the bacterial cells. The centrifuged bacterial cells were then mixed with sterile saline (bacterial content 10). 9The prepared bacterial suspension was administered to pseudo-germ-free mice by gavage at a rate of 200 μL per mouse for 4 weeks to complete the microbial transplantation.

[0029] (2) Sequencing of 16S RNA from colonic contents: Genomic DNA was extracted using an environmental sample DNA extraction kit (OMEGA). DNA concentration and integrity were measured using NanoDrop 200 and 1% agarose gel electrophoresis, respectively. The V3-V4 regions of bacterial 16S rRNA were amplified using an ABIGeneAmp 9700 real-time fluorescence PCR system with upstream primer 338F (5′-ACTCCTACGGGAGGCAGCAG-3′) and downstream primer 806 (5′-GGACTACHVGGGTWTCTAAT-3′). Quantification was performed using a Quantus fluorometer (Promega, USA). The sequencing library was generated using TruSeq™ DNA SamplePrep Ki (Illumina, San Diego, California, USA), and sequencing and data analysis were performed using Illumina's PE300 platform.

[0030] (3) Measurement of mouse muscle mass: Mice were euthanized after the last fecal microbiota transplantation. The quadriceps femoris, gastrocnemius, soleus, tibialis anterior, and extensor digitorum longus muscles were isolated and weighed under 4°C ice bath conditions. The gastrocnemius muscle is the muscle most affected by aging, and the gastrocnemius index was further evaluated and expressed as gastrocnemius muscle / body weight.

[0031] (4) Mouse muscle function assessment: mouse grip strength and gait speed. Grip strength was measured using a grip strength meter. After the mouse's forelimbs gripped the lever, the mouse's tail was grasped, and the tail was pulled horizontally with uniform force until both forelimbs released. The grip strength value was recorded in g. The measurement was repeated three times for each mouse at 5-minute intervals, and the maximum value was taken as the final grip strength. Gait speed was measured using an open field test. Each mouse was placed in the center of a 50cm×50cm×25cm chamber and allowed to explore freely for 30 seconds before the formal experiment began for 5 minutes. The mouse's movement trajectory was recorded using an ANY-maze (Stoelting, Kiel, WI, USA), and the average gait speed (m / s) was calculated based on the total distance (m) and time.

[0032] After fecal microbiota transplantation, the results showed that the intestinal flora structure of mice changed significantly. Compared with mice inoculated with feces from NS mice, the abundance level of *Desulfovibrio* was significantly increased in mice inoculated with feces from OS-1W and OS-4W mice, and the abundance level of *Desulfovibrio* in OS-4W mice was also significantly higher than that in OS-1W mice. Figure 6 A, B). Additionally, the muscle mass of the quadriceps femoris, gastrocnemius, soleus, tibialis anterior, and extensor digitorum longus muscles was significantly decreased in OS-1W and OS-4W mice. Figure 6 E), pace ( Figure 6 D) and significantly reduced grip strength ( Figure 6 C).

[0033] Example 4: Effects of fecal transplantation with different abundance levels of *Desulfovibrio* on tryptophan metabolism Fecal samples containing different abundance levels of *Desulfovibrio*, obtained from feces of NS (transplanted from feces of controls without sarcopenia) and OS (transplanted from feces of elderly sarcopenia patients), were transplanted into normal mice (see Example 3). Four weeks after transplantation, the mice were sacrificed, and blood was collected. Serum levels of tryptophan, serotonin (5-HT), 5-HIAA, kynurenine, and the kynurenine / tryptophan ratio were detected using an ELISA kit.

[0034] The results are as follows Figure 7 As shown, the blood tryptophan and 5-HT levels in mice transplanted with low-abundance (OS-1W) and high-abundance *Vibrio desulfurization* (OS-4W) were significantly lower than those in mice transplanted without *Vibrio desulfurization* (NS-1W, NS-4W), while the blood kynurenine and kynurenine / tryptophan ratios were significantly higher in mice transplanted without *Vibrio desulfurization*.

[0035] Example 5: Studying the target sites of intestinal desulfovibrio and elucidating the mechanism by which desulfovibrio promotes sarcopenia. (1) Detection of H2S content in serum using chemiluminescence immunoassay 1) Preparation of NaHS standard: Weigh 0.0224 g NaHS and add 1 mL of double-distilled water to obtain a 400 mM NaHS solution. Dilute with double-distilled water to 200 μM, 100 μM, 50 μM, 25 μM, 12.5 μM, 5 μM, 2.5 μM, and 0 μM to obtain the standard.

[0036] 2) Prepare a mixed solution of 1% zinc acetate and 12% NaOH; 3) Take 50 μL of serum and 50 μL of different concentrations of NaHS standard, mix them with 200 μL of freshly prepared zinc acetate and NaOH mixture, and incubate at 37°C for 10 minutes.

[0037] 4) After incubation, add 200 μL of 20 mM NND (N,N-dimethyl-p-phenylenediamine), 200 μL of 30 mM FeCl3, and 300 μL of double-distilled water to the reaction mixture in sequence. Mix well and react in the dark for 10 minutes. After the reaction is complete, centrifuge at 14000g for 5 minutes.

[0038] 5) Detect the absorbance value at 670nm using an ELISA reader.

[0039] 6) Plot a standard curve and calculate the H2S concentration in mouse serum samples.

[0040] The main function of *Vibrio desulfurans* is to reduce substrates to H2S. H2S regulates tryptophan metabolism, increasing blood kynurenine levels and decreasing serotonin synthesis. Results showed that the serum H2S content in mice with high *Vibrio desulfurans* abundance (OS-4W) and low abundance mice (OS-1W) was significantly higher than that in mice without *Vibrio desulfurans* abundance. Figure 8 ).

Claims

1. Desulfovibrioles ( Desulfovibrionales The application of this as a new detection target in the preparation of pre-sarcopenia screening reagents.

2. The application as described in claim 1, characterized in that, The order Desulfovibrio includes common desulfovibrio ( Desulfovibrio vulgaris ), desulfurization vibrio ( Desulfovibriodesulfuricans ) and Pigra desulfurization vibrio ( Desulfovibriopigra ).

3. The application as described in claim 1, characterized in that, The sarcopenia mentioned refers to sarcopenia in the elderly.

4. Detection of desulfurized Vibrio ( ) Desulfovibrionales The application of reagents in the preparation of pre-sarcopenia screening reagents.

5. The application as described in claim 4, characterized in that, The reagents for detecting desulfovibrio include PCR primers for detecting desulfovibrio bacteria and reagents for measuring their metabolite hydrogen sulfide.

6. The application of Desulfovibrio as a target for sarcopenia treatment in the screening of sarcopenia treatment drugs or health foods.

7. The application as described in claim 6, characterized in that, The order Desulfovibrio includes common desulfovibrio ( Desulfovibrio vulgaris ), desulfurization vibrio ( Desulfovibriodesulfuricans ) and Pigra desulfurization vibrio ( Desulfovibriopigra ).

8. The application as described in claim 6, characterized in that, The sarcopenia mentioned refers to sarcopenia in the elderly.

9. A method for screening individuals susceptible to sarcopenia, characterized in that, Quantitative PCR was used to detect the abundance level of Desulfovibrio in the feces of the subjects and compared with that of a control group without sarcopenia. The subjects with a higher relative abundance of Desulfovibrio than the control group without sarcopenia were identified as susceptible to sarcopenia. The susceptible subjects were also identified by the content of Desulfovibrio metabolite H2S, higher kynurenine content and lower indolepropionic acid content than the control group without sarcopenia.

10. Application of substances that specifically inhibit desulfovibrio bacteria in the preparation of drugs or functional foods for the prevention and treatment of sarcopenia.

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