KR20200123009A - Composition for treating Sarcopenia including alginate oligosaccharide as an active ingredient - Google Patents

Abstract

The present invention relates to a composition for treating sarcopenia, containing alginic acid as an active component. More particularly, the present invention relates to: a composition for preventing or treating senile sarcopenia, containing, as an active component, low-molecular alginic acid (AOS), in which mannuronic acid and guluronic acid are mixed, having a high ratio of manneuronic acid, from among low-molecular alginic acids; and a method for preventing or treating senile sarcopenia by using the composition. According to the present invention, alginic acid enhances muscle mass and increases bone density without auxiliary exercise in an aging animal model (human age 80-year-old model) and, as a result, improves motor skills, thereby being usable as an agent for treating senile sarcopenia.

Description

Composition for treating sarcopenia including alginate oligosaccharide as an active ingredient}

The present invention relates to a composition for treating sarcopenia comprising alginic acid as an active ingredient, and more specifically, the present invention relates to a composition for treating sarcopenia containing alginic acid as an active ingredient, and more specifically, the present invention includes low molecular weight alginic acid (AOS, alginate oligosaccharide) as an active ingredient. It relates to a composition for preventing or treating and a method of preventing or treating sarcopenia by using the composition.

Muscopenia caused by degeneration of the spinal nerve, motor nerve or skeletal muscle fibers is one of the representative refractory diseases for which the cause of the disease has not been identified. According to studies so far, the motor nerve that induces the contraction of the skeletal muscle is degenerated so that the contraction of the skeletal muscle does not proceed, or the expression of the protein involved in the contraction of the muscle in the skeletal muscle is reduced (myopenia), or the protein is modified. It is known that normal skeletal muscle contraction does not proceed, and in the long term, the motor nerve or skeletal muscle is transformed into a fibrous tissue.

Among sarcopenia, sarcopenia is defined as a decrease in muscle mass associated with aging. It is increasingly recognized as having an important effect on the quality of life in old age, and in October 2016, the World Health Organization (WHO) newly issued a disease classification code and was formally classified as a new type of senile disease.

The prevalence of sacopenia is 13 to 24% in people under the age of 70, but the incidence increases to more than 50% in people over 80. Muscle weakness associated with muscle loss is known to be associated with increased risk of fractures such as fatigue, decreased work performance, and femur fractures (J Gerontal A Biol Sci Med Sci. 2009 May; 64(5):509-609 ). Patients suffering from sarcopenia have difficulties in their daily life, such as lowering the skeletal muscle index and lowering their grip strength and walking speed. While body composition, muscle mass is clearly lost, body fat tends to increase.

As a method of slowing the progression of such sarcopenia, a method of suppressing muscle atrophy caused by degeneration or progressive mutation of muscle cells, which is a type of sarcopenia, is mainly used. For example, WO 2007/088123 discloses a therapeutic agent for muscular dystrophy comprising a nitroxy derivative as an active ingredient, and WO 2006/081997 discloses a therapeutic agent for muscular atrophy comprising atlaric acid or a derivative thereof as an active ingredient. However, these therapeutic agents containing the compound as an active ingredient act not only on skeletal muscles in which muscular dystrophy has occurred, but also visceral muscles or myocardium that are not related to muscular dystrophy, and thus, various side effects such as small and large can be induced, and thus have not been used for practical treatment. . These hormone preparations do not have any side effects, but the side effects are significantly reduced compared to the compound preparations, and the development of similar hormone preparations is accelerating because of the nature of the hormone preparations and being bio-friendly. In addition to the above, nutritional approaches and exercise training methods are being studied as treatments for sarcopenia. Treatment using protein compounds such as appetite stimulants and testosterone has been proposed, but the therapeutic effect is not satisfactory. Exercise training method is difficult to see as an appropriate alternative because it is often not easy to even try exercise for the elderly with sarcopenia.

It is estimated that about 500,000 species of marine organisms, which account for 80% of the species on the planet, are inhabited, but less than 1% of them are being developed as useful biological resources, which has a very high development potential. Alginic acid, a representative seaweed polysaccharide as a functional material derived from seaweed, is contained 15-35% in brown algae such as kelp and seaweed, and β-D-mannuronic acid (M) and α- Two types of uronic acid, α-L-guluronic acid (G), are characterized as polyuronides with 1 and 4 glycoside bonds in various ratios. Oligosaccharides derived from alginic acid can be divided into mannuro-oligosaccharides (MOS), guluro-oligosaccharides (GOS), and mixed oligosaccharides of gluronic acid (AOS) according to the constituent sugars. It can be classified according to the double bond.

Marine-derived polysaccharides have been used in human life for a long time, and studies on physiological activities such as anti-cancer, antioxidant, antihypertensive, and antibacterial substances derived from marine organisms have been actively conducted worldwide. Alginic acid aid produced worldwide is about 100,000 tons, of which about 30% is used as food additives, but if it is developed as a high-value pharmaceutical ingredient, its value can be doubled. In the case of alginic acid-derived oligosaccharides, biological activities such as promotion of root growth of higher plants, growth promotion of Bifidobacterium sp., anti-inflammatory, antioxidant, and antibacterial activities are reported according to structural characteristics. As it is made, the application field is spreading widely.

Under this background, the present inventors have made intensive research efforts to develop an agent that can effectively treat sarcopenia or slow its progression, as a result of which manneuronic acid-gluronic acid mixed oligosaccharide (AOS), which is a kind of seaweed oligosaccharide, has declined. It has been confirmed that muscle sensitization can be effectively improved by recovering skeletal muscle and bone density and increasing muscle mass without exercise in aging mice, which are difficult to exercise, and came to the present invention.

One object of the present invention is to provide a composition for preventing or treating sarcopenia.

Another object of the present invention is to provide a method for preventing or treating sarcopenia using the composition.

Another object of the present invention is to provide a food composition for improving muscle function or for improving motor function, using the composition as an active ingredient.

In order to achieve the above object, the present invention provides a pharmaceutical composition for improving, preventing or treating sarcopenia containing alginic acid as an active ingredient.

Specifically, the alginic acid may be a low molecular weight alginic acid.

The low-molecular alginic acid may be characterized in that it is a mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid, and more specifically, unsaturated manneuronic acid oligosaccharide at a non-reducing terminal containing 60% or more and 40% or less of gluronic acid. It can be characterized by being.

In addition, the index component of the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid may be characterized in that penta-mannuronic acid sodium salt.

In an embodiment of the present invention, a food composition for improving, preventing or treating sarcopenia containing alginic acid as an active ingredient may be provided.

Specifically, the alginic acid may be a low molecular weight alginic acid.

The low-molecular alginic acid may be characterized in that it is a mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid, and more specifically, unsaturated manneuronic acid oligosaccharide at a non-reducing terminal containing 60% or more and 40% or less of gluronic acid. It can be characterized by being.

In addition, the index component of the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid may be characterized in that penta-mannuronic acid sodium salt.

Another embodiment of the present invention can provide a method for improving, preventing or treating sarcopenia using alginic acid as an active ingredient.

Specifically, the alginic acid may be a low molecular weight alginic acid.

The low-molecular alginic acid may be characterized in that it is a mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid, and more specifically, unsaturated manneuronic acid oligosaccharide at a non-reducing terminal containing 60% or more and 40% or less of gluronic acid. It can be characterized by being.

In addition, the index component of the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid may be characterized in that penta-mannuronic acid sodium salt.

In the present invention, alginic acid means alginic acid (molecular formula (C6H8O6)n), also called seaweed acid. Alginic acid can be extracted from seaweed such as kelp. Alginate is generally known to have a molecular weight of 32-400kDa, which has a wide range of molecular weights. The form is a fibrous or granular powder, which is usually marketed in the form of'sodium alginate' or'potassium alginate'.

In the present invention, alginic acid specifically means extracted from seaweed and dried after hydrolysis. In addition, it is used in a sense encompassing low-molecular alginic acid and more specifically mixed low-molecular alginic acid (AOS).

In the present invention, the term "low molecular weight alginic acid" refers to a product obtained by enzymatic decomposition of alginic acid, which is composed of a mixture of substances having a lower molecular weight than alginic acid. More specifically, in the present invention, low-molecular alginic acid is prepared by hydrolyzing sodium alginate extracted from natural seaweed as a raw material, and β-1,4 glycosidic bonds by mixing glutonic acid (G), mannuronic acid (M) or the two It is a cliccan connected by.

In the present invention, an alginic acid oligosaccharide having a ratio of 60% or more of unsaturated mannuronic acid at a molecular weight of 30 kDa or less decomposed by alginic acid lyase using AOS alginic acid as a substrate. to be. The low molecular weight alginic acid (AOS) mixed with mannuronate-gluronic acid of the present invention is 175 for 1 sugar, 351 for 2 sugars, 527 for 3 sugars, 704 for 4 sugars, 880 for 5 sugars, 1056 for 6 sugars, In the case of 7 sugar, it has a Z-average molecular weight (m/z) of 1232, and can be expressed as an example of the structural formula below.

In the present invention, the substance M5 refers to Penta-mannuronic acid sodium salt as an indicator component of alginate oligosaccharide, and can be expressed as an example of the structural formula below.

In the present specification, the term "non-reducing" refers to an anomer [a hemiacetal of a monosaccharide (formation of a ring between C-1 and C-5) and a hemicetal (ring formation between C-2 and C-5) in the structure of an oligosaccharide. A phenomenon in which diastereomers are formed in which the positions of a hydrogen atom attached to a carbon and a hydroxyl group are changed in a cyclization reaction that generates )) It refers to a property that does not have carbon.

In this specification, the term "unsaturated" refers to a form in which the carbon chain of a hydrogen atom is unsaturated, and "saturated form" refers to a form in which the carbon chain of a hydrogen atom is saturated.

The unsaturated low-molecular alginic acid at the non-reducing terminal of the present invention refers to all low-molecular alginic acids in the form of unsaturated carbon chains of hydrogen atoms that do not have the anomeric carbon of manneuronic acid or gluconic acid at the terminal.

In the present invention, as a result of ingesting low-molecular alginic acid (AOS) for 16 weeks in elderly mice, it was confirmed that muscular dystrophy was alleviated by improving exercise capacity, increasing muscle mass, and improving bone density.

According to an embodiment of the present invention, as a result of feeding low-molecular alginate (AOS) mixed with gluronic acid mannuronate to aging mice as an animal model, weight is increased, the size of skeletal muscle is increased, and grip strength is restored, compared to the control group, It was confirmed that bone minerals increased.

From this, the present inventors confirmed that the low molecular weight alginic acid (AOS) can be used for the prevention and treatment of sarcopenia. In particular, the increase in muscle mass and bone minerals in aging mice, which are difficult to exercise, compared to the exercise group, confirms that the substance of the present invention is suitable for the treatment of senile sarcopenia.

The term sarcopenia of the present invention includes sarcopenia, which is an age-related sarcopenia, in a state in which muscles are reduced and thus it is difficult to function properly.

The composition of the present invention may be prepared in the form of a pharmaceutical composition for the prevention or treatment of muscular dystrophy or sarcopenia disease, further comprising an appropriate carrier, excipient, or diluent commonly used in the manufacture of pharmaceutical compositions. Specifically, the pharmaceutical compositions are formulated in the form of powders, granules, tablets, capsules, suspensions, emulsions, syrups, aerosols, and other oral formulations, external preparations, suppositories, and sterile injectable solutions, respectively, according to conventional methods. I can. In the present invention, the carriers, excipients and diluents that may be included in the pharmaceutical composition include lactose, dextrose, sucrose, sorbitol, mannitol, xylitol, erythritol, maltitol, starch, acacia rubber, alginate, gelatin, calcium phosphate. , Calcium silicate, cellulose, methyl cellulose, microcrystalline cellulose, polyvinyl pyrrolidone, water, methylhydroxybenzoate, propyl hydroxybenzoate, talc, magnesium stearate, and mineral oil. In the case of formulation, it is prepared by using diluents or excipients such as commonly used fillers, extenders, binders, wetting agents, disintegrants, and surfactants. Solid preparations for oral administration include tablets, pills, powders, granules, capsules, and the like, and these solid preparations include at least one excipient, such as starch, calcium carbonate, in the extract and its fractions, It is prepared by mixing sucrose, lactose, or gelatin. In addition, in addition to simple excipients, lubricants such as magnesium stearate and talc may also be used. Liquid preparations for oral use include suspensions, liquid solutions, emulsions, syrups, etc. In addition to water and liquid paraffin, which are commonly used simple diluents, various excipients such as wetting agents, sweetening agents, fragrances, and preservatives may be included. . Preparations for parenteral administration include sterile aqueous solutions, non-aqueous solutions, suspensions, emulsions, lyophilized preparations, and suppositories. As the non-aqueous solvent and suspending agent, propylene glycol, polyethylene glycol, vegetable oil such as olive oil, and injectable ester such as ethyl oleate may be used. As a base for suppositories, witepsol, macrogol, tween 61, cacao butter, laurin, glycerogelatin, and the like may be used.

The pharmaceutical composition of the present invention may be administered in a pharmaceutically effective amount, and the term "pharmaceutically effective amount" of the present invention is used to treat or prevent a disease at a reasonable benefit/risk ratio applicable to medical treatment or prevention. It means a sufficient amount, and the effective dose level is the severity of the disease, the activity of the drug, the patient's age, weight, health, sex, the patient's sensitivity to the drug, the time of administration of the composition of the present invention used, the route of administration and the rate of excretion. The duration, factors including drugs used in combination or co-use with the composition of the present invention used, and other factors well known in the medical field. The pharmaceutical composition of the present invention may be administered alone or may be administered in combination with a known agent for treating muscular dystrophy or sarcopenia. It is important to take into account all of the above factors and administer an amount capable of obtaining the maximum effect in a minimum amount without side effects.

The route of administration of the pharmaceutical composition for the treatment of muscular atrophy or sarcopenia of the present invention may be administered through any general route as long as it can reach the target tissue. The pharmaceutical composition of the present invention is not particularly limited thereto, but may be administered through a route such as intraperitoneal administration, intravenous administration, intramuscular administration, subcutaneous administration, intradermal administration, oral administration, intranasal administration, rectal administration, etc. I can.

When the pharmaceutical composition for preventing or treating sarcopenia provided by the present invention is administered to an individual suffering from sarcopenia, the weight of the reduced body weight and skeletal muscle due to sarcopenia can be restored to a normal state without auxiliary exercise. It could be widely used in the development of treatments for hypothyroidism.

1 shows the analysis of the molecular weight of the substance to be tested.
Figure 2 shows the component ratio of manneuronic acid (M) and gluronic acid (G) in low molecular alginic acid.
3 shows the weight change record (A) of the experimental animals for 16 weeks and the final weight change amount (B) for each experimental group.
4 shows the change in food intake of experimental animals for 16 weeks (A) and the average food intake for each experimental group (B).
Figure 5 shows the change in water intake (A) of the experimental animals for 16 weeks and the average water intake by experimental group (B).
6 shows the change in muscle mass (A) and mineral content of the leg bones (B) of aging mouse legs for each experimental group.
Figure 7 shows the muscle mass and BMC improvement efficiency compared to the AOS intake.
8 shows the results of the rotarod test performed in the 14th week of the experiment.
9 shows changes in the expression of muscle atrophy marker genes as a result of treatment with M5 after induction of muscle atrophy in C2C12 cells.

Hereinafter, the present invention will be described in more detail through examples. However, these examples are for illustrative purposes only, and the scope of the present invention is not limited to these examples.

Example 1: Characterization of AOS material

The molecular weight of low-molecular alginic acid (AOS) mixed with manneuronic acid and gluronic acid, which is an active substance of the present invention, was analyzed by gel filtration chromatography analysis. Samples were prepared in a high-performance chromatography system (e2695 Separations Module, Waters, 0.6 mL/min) using a total of 4 columns, Ultrahydrogel 120, 250, 500, 1000 (1.8 × 300 nm), in 0.1M sodium phosphate buffer (pH7. 0) was used as the eluent for analysis. The calibration curve was prepared using polyethylene glycol (PEG), and the relative molecular weight was calculated by comparing the retention time of the standard and the sample. The molecular weight of sodium alginate, the starting material before decomposition, was analyzed by gel permeation chromatography analysis. Samples were prepared using Shodex SB-804 HQ and SB-802.5 HQ OHPak (Showa Denko, Japan) columns in a high-performance chromatography system (HPLC-YL9100, Young Lin instruments, 0.6 mL/min) in 0.1M sodium phosphate buffer (pH7. 0) was used as the eluent for analysis. The calibration curve was calculated by using Maltooligosaccharide and Pullulan Kit (P-82) to calculate the sizes of G2 to G7 monosaccharides and polysaccharides, respectively. Relative molecular weight was calculated by comparing the retention times of standards and samples.

As shown in FIG. 1, the weight average molecular weight (Mw) of sodium alginate, which is the starting material before decomposition, was measured as 484,039 Da as a result of GPC analysis. The decomposed sodium alginate showed three main peaks with a weight average molecular weight (Mw) of 30,962 Da, 841 Da and 222 Da, respectively, as a result of GPC analysis.

In order to analyze the composition of the M/G ratio in AOS, circular dichroism (CD) experiments were performed with a J-1500 spectrometer (JASCO, Tokyo, Japan). The absorbance of AOS dissolved in PBS solution (2.5mg/mL) was measured at 190-260nm at 25°C using a 1mm path cell. Specific conditions are bandwidth 1nm; Time constant, 1 second; The scanning speed is 200 nm/min. The three spectra corrected against the background were averaged by sample. The CD spectrum of the fermentation broth showed a peak at 201 nm and the lowest point at 214 nm. The M/G ratio was measured to be 1.97 based on the mdeg value, and AOS was confirmed to be composed of 66.29% mannuronic acid and 33.71% glutonic acid. The characteristic peak of unsaturated low molecular alginic acid (AOS) was observed from 234 nm (Fig. 2). This can be explained by the properties of unsaturated alginic acid decomposed with alginate lyase.

As a result of confirming the indicator substance of AOS, it was confirmed that it was Penta-mannuronic acid sodium salt, and this was named M5.

Example 2: Preparation of an aging animal model

17-month-old C57BL/6J female mice were purchased at the Korean Basic Science Research Institute's Aging Science Facility (Gwangju, Korea). Experimental animals were housed in groups in a room with controlled temperature and photoperiod (10 hours of dark conditions, 14 hours of light conditions (06:00-20:00)). Animals were allowed free intake of food and water. Body mass, food intake, and water consumption were measured on Monday between 09:00-11:00 hours. All animals were maintained and treated according to the guidelines of the National Institutes of Health for the care and use of laboratory animals with the approval of the Chonnam National University Institutional Animal Care and Use Committee.

Example 3: Comparison method between exercise group and AOS treatment group using aging mice

The effect on the in vivo efficacy of low-molecular alginic acid (AOS) mixed with manneuronic acid and gluconic acid was investigated. Before the start of the experiment, elderly (17 months) female mice were divided into 3 groups and maintained for 1 week for adaptation. At the start of the experiment, one group began taking AOS (200 ppm) dissolved in sterile water (sDW) as drinking water per day. The control group and the exercise group consumed only sterile water for 16 weeks. The athletic group had free access to voluntarily running wheels to carry out the activity. For the exercise group, the mice were placed in a larger (23.62 × 35.3 × 19.56 cm) cage containing a 12.7 cm diameter driving wheel (Automated Wheel Monitor, LaFayette Instruments, LaFayette, IN) and equipped with a mechanical counter on each activity wheel. The number of rotations in either direction was recorded when the mouse was moving or walking.

Example 4: Effect of AOS on the weight of aged mice

As shown in Figures 3-5, the exercise group and the AOS fed group consumed less food and water than the control group. In addition, the exercise group showed a weight loss for 16 weeks, but the AOS group showed an increase in body weight like the control group. This is due to an increase in bone density and muscle mass.

Example 5: Effect of AOS on body composition changes in aged mice

Body composition before and after 16 weeks of aging Mausu who ingested AOS using a full-body scanner (InAlyzer dual X-ray absorptiometry, Medikors, Gyeonggi, Korea) was measured by applying the dual energy X-ray absorption assay (DXA). Prior to measurement, mice were anesthetized with Alfaxan 80mg/kg-1 and Rompun 10mg/kg-1. InAlyzer software was used to measure the body composition parameters of the rats' body weight and bone mineral contents (BMC). The efficiency calculation method was expressed as a percentage after calculating the feed intake and water consumption coefficient. Feed intake and water consumption were adjusted for the lowest weight group to determine consumption by weight. The coefficients were calculated by dividing each standardized feed intake and water consumption by lean mass increase and bone mineral content increase.

As can be seen from Figure 6, the exercise group maintained the same level as the initial experiment, while the control group's lean mass and BMC steadily decreased over the course of 16 weeks. Even if the AOS group did not exercise, it may be determined that it exhibited the same effect as the exercise group. In particular, the BMC measured value showed that the AOS group increased the bone mineral content more than the exercise group.

As can be seen in Figure 7, the aging mice showed low muscle mass efficiency in all experimental groups in proportion to food intake and water consumption. However, the muscle mass efficiency was higher in the AOS group than in the exercise group, and the efficacy of BMC decreased in both the control group and the exercise group, but increased remarkably only in the AOS group.

Example 6: Effect of AOS on exercise capacity of aged mice

14 weeks after the start of the experiment, a rotarod test was performed using an accelerated rotarod (B.S. Technolab Inc., Korea). Aged mice (three per group) were placed on the rotarod through three times, and a 15-minute rest was taken between each trial. Rotarod acceleration was set to 4-20 rpm for 2 minutes and the time it took for the mouse to fall was recorded. The results were analyzed by averaging the time the mice fell in three tests.

As can be seen in Figure 8, both the exercise group and the AOS group showed significant results when compared to the control group. However, there was no significant difference between the exercise group and the AOS group. The exercise group and the AOS group were able to withstand the rotarod longer than the control group. The speed dropping from the machine dropped below 10 rpm in the control group, but it was confirmed that the exercise group and the AOS group were 15 rpm or more. It was confirmed that the AOS group had as good exercise ability as the exercise group.

Example 7: Analysis of effects at the cellular level

2C12 cells were cultured for 4 days in horse serum conditions to confirm the formation of myotubes. After that, the muscle atrophy situation was simulated by culturing the muscle atrophy-inducing culture condition (glucose-free DMEM media + dexamethasone (DEX) for an additional 2 days.) A synthetic analogue of glucocorticoid to reproduce the phenomenon of muscle atrophy induced by glucocorticoid. dexamethasone (DEX) was used.

Alginate Oligosaccharide (AOS) (1ug/mL) or Penta-mannuronic acid sodium salt, M5 (1ug/mL), one of the indicators of AOS, was treated with DEX (10uM) for 48 hours at the same time, and then the diameter of the myotube was measured or The gene expression of MuRF1 and atrogin-1, which are representative muscle atrophy marker genes, was confirmed by q-RT-PCR.

As a result of the analysis, it was confirmed that the expression of MuRF1 and atrogin1 was significantly reduced (p>0.01) compared to the DEX-only treatment group, demonstrating that alginic acid or alginic acid oligosaccharides were effective in preventing or treating senile muscle loss.

Claims (18)

A pharmaceutical composition for improving, preventing or treating sarcopenia containing alginic acid as an active ingredient. The pharmaceutical composition for improving, preventing or treating sarcopenia according to claim 1, wherein the alginic acid is a low-molecular alginic acid. The pharmaceutical composition for improving, preventing or treating sarcopenia according to claim 2, wherein the low-molecular alginic acid is a mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid. The method of claim 3, wherein the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid is a non-reducing terminal unsaturated manneuronic acid oligosaccharide containing 60% or more of manneuronic acid and 40% or less of glutonic acid. , Prophylactic or therapeutic pharmaceutical composition. The pharmaceutical for improving, preventing or treating sarcopenia according to claim 3, wherein the index component of the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid is penta-mannuronic acid sodium salt. Composition. The pharmaceutical composition for improving, preventing or treating sarcopenia according to claim 1, wherein the sarcopenia is senile sarcopenia. A food composition for improving, preventing or treating sarcopenia containing alginic acid as an active ingredient. The food composition for improving, preventing or treating sarcopenia according to claim 7, wherein the alginic acid is a low-molecular alginic acid. The food composition according to claim 8, wherein the low-molecular alginic acid is a mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid. The method of claim 9, wherein the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid is a non-reducing terminal unsaturated manneuronic acid oligosaccharide containing 60% or more of manneuronic acid and 40% or less of glutonic acid. , Food composition for prevention or treatment. The food for improving, preventing or treating sarcopenia according to claim 9, wherein the index component of the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid is penta-mannuronic acid sodium salt. Composition. The food composition for improving, preventing or treating sarcopenia according to claim 7, wherein the sarcopenia is senile sarcopenia. A method of improving, preventing or treating sarcopenia using alginic acid as an active ingredient. The method of claim 13, wherein the alginic acid is a low molecular weight alginic acid. 14. The method of claim 13, wherein the low-molecular alginic acid is a mixed low-molecular alginic acid (AOS) of manneuronic acid and gluronic acid. The method of claim 15, wherein the mixed low-molecular weight alginic acid (AOS) of manneuronic acid and gluconic acid is a non-reducing terminal unsaturated manneuronic acid oligosaccharide containing 60% or more of manneuronic acid and 40% or less of glutonic acid. How to improve, prevent or treat. The method of claim 15, wherein the index component of the mixed low-molecular alginic acid (AOS) of manneuronic acid and gluconic acid is penta-mannuronic acid sodium salt, which improves, prevents, or treats sarcopenia. Way The method of claim 13, wherein the sarcopenia is senile sarcopenia.

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