Application of Sdccag3 gene in preparation of weight-reducing medicine for regulating glucose and lipid metabolism

Abstract

The invention relates to an application of an Sdccag3 gene in preparation of a weight-reducing medicine for regulating glucose and lipid metabolism. The Sdccag3 gene is used as an action target to be applied to preparation or screening of the weight-reducing medicine for regulating glucose and lipid metabolism, and the nucleotide sequence of the Sdccag3 gene is as shown in SEQ ID No. 1. According to the application disclosed by the invention, the specific overexpressed Sdccag3 in adipose tissues in a mouse body can obviously inhibit the increase of the blood fat level, and the overexpressed Sdccag3 can also obviously improve the poor glucose tolerance, improve the insulin sensitivity, reduce the levels of serum triglyceride, cholesterol and low-density lipoprotein cholesterol of an obese mouse, improve the poor glucose tolerance and improve the insulin sensitivity. The insulin sensitivity is improved, obesity-related glycolipid metabolism is effectively regulated and controlled, the effect of reducing blood lipid and blood sugar is achieved, and the compound can be used for preparing weight-losing drugs for reducing blood lipid and blood sugar.

Description

Technical Field

[0001] The present invention relates to the application of the Sdccag3 gene in the preparation of weight loss drugs for regulating glycolipid metabolism, and belongs to the fields of molecular biology and biotechnology. Background Art

[0002] Obesity is a chronic metabolic disease, mainly characterized by excessive accumulation of body fat and overweight. Severe obesity often occurs simultaneously with diseases such as dyslipidemia, non-alcoholic fatty liver, hypertension, coronary heart disease, impaired glucose tolerance or diabetes. In addition, obesity can lead to the occurrence and development of oral periodontitis by affecting the levels of inflammatory factors and inducing oxidative stress, and can also directly attack the alveolar bone, promote the generation of osteoclasts in bone tissue, resulting in bone loss and endangering oral health. The chronic metabolic diseases caused by obesity have led to an increasingly huge social medical expenditure and become a major burden on public health. However, the treatment methods and means for treating or alleviating the metabolic disorders caused by obesity are still very limited.

[0003] Obesity is the result of an imbalance between energy intake and consumption in the body. Excess energy is stored as fat in body adipose tissue. When the storage capacity of the tissue is overwhelmed, endocrine dysfunction occurs in adipose tissue, resulting in metabolic disorders, a decline in adipose tissue function, leading to ectopic fat accumulation and lipotoxic metabolic stress in other metabolically sensitive organs such as muscle, liver and heart, thereby promoting inflammation and metabolic dysfunction in the liver, skeletal muscle and heart, continuous elevation of blood glucose and lipid levels, and promoting insulin resistance. Severe obesity often occurs simultaneously with diseases such as dyslipidemia, type 2 diabetes and non-alcoholic fat, and increases the risk of cardiovascular disease. Due to complex metabolic changes occurring in multiple tissues, the pharmacological treatment of obesity and related metabolic disorder diseases will be more challenging.

[0004] Obesity is closely related to lipid metabolism disorders, which directly or indirectly lead to adverse metabolic outcomes. Elevated total cholesterol (CHO), triglyceride (TG) and low-density lipoprotein cholesterol (LDLC) are used to measure metabolic health status and disease risk. Numerous studies have shown that the blood cholesterol and triglyceride levels of obese patients are higher than those of normal body weight individuals, and the body mass index (BMI) is positively correlated with total cholesterol, triglyceride and low-density lipoprotein cholesterol. At the same time, among the metabolic disorders related to obesity, insulin resistance and glucose tolerance are of clinical significance because they are closely related to various diseases such as type 2 diabetes, hypertension, dyslipidemia, coagulation and fibrinolysis disorders, and these diseases are all independent risk factors for cardiovascular diseases (heart attack, stroke and peripheral artery disease). At the same time, elevated serum free fatty acid levels are an important cause of obesity-related insulin resistance. Therefore, finding factors that can stabilize the lipid metabolism homeostasis is of great significance for the control and treatment of obesity.

[0005] Serologically defined colon cancer antigen 3 (Sdccag3) is a protein with a size of 45 kd and a coiled-coil domain. It has been found to have biological functions such as protein transport, mitosis, ciliogenesis, and promotion of osteogenesis. However, the functional role of Sdccag3 in obesity-related metabolic disorders has not been reported, especially the function of Sdccag3 in regulating glucose and lipid metabolism disorders caused by obesity has not been studied. Summary of the Invention

[0006] In view of the deficiencies of the prior art, the present invention provides the application of the Sdccag3 gene in the preparation of drugs for regulating obesity-related glucose and lipid metabolism. By establishing an adipose tissue-specific overexpression vector of Sdccag3, the present invention verifies that it can regulate the relevant serum biochemical indexes and glucose homeostasis caused by obesity in mice, and this gene can be used as a drug target for regulating obesity-related glucose and lipid metabolism to prepare lipid-lowering and hypoglycemic drugs.

[0007] The technical solution of the present invention is as follows:

[0008] The application of the Sdccag3 gene in the preparation of weight-loss drugs for regulating glucose and lipid metabolism, wherein the nucleotide sequence of the Sdccag3 gene is as shown in SEQ ID No.1.

[0009] Preferably according to the present invention, the application of the Sdccag3 gene in the preparation of weight-loss drugs for regulating glucose and lipid metabolism includes the following two aspects:

[0010] (1) Using the Sdccag3 gene as a target for the preparation of weight-loss drugs for regulating glucose and lipid metabolism;

[0011] (2) Using the Sdccag3 gene as a target for the screening of weight-loss drugs for regulating glucose and lipid metabolism.

[0012] Preferably according to the present invention, the weight-loss drug is a lipid-lowering and hypoglycemic drug for regulating obesity-related glucose and lipid metabolism.

[0013] Preferably according to the present invention, the application of the Sdccag3 gene as a target for the preparation of weight-loss drugs for regulating glucose and lipid metabolism means: using the Sdccag3 gene as a target of a drug or preparation to increase the expression level of the Sdccag3 gene in adipose tissue to develop weight-loss drugs or preparations for regulating glucose and lipid metabolism.

[0014] Preferably according to the present invention, the application of the Sdccag3 gene as a target in the screening of weight loss drugs for regulating glycolipid metabolism means that the Sdccag3 gene is used as the target of a drug or preparation, and the drug or preparation is screened to find a drug or preparation that can promote the expression of the Sdccag3 gene in adipose tissue as an alternative weight loss drug or preparation for regulating glycolipid metabolism.

[0015] Preferably according to the present invention, the weight loss drugs for regulating glycolipid metabolism include but are not limited to: nucleic acid molecules, carbohydrates, lipids, small molecule chemical drugs, antibody drugs, polypeptides, proteins or viruses.

[0016] More preferably, the weight loss drug for regulating glycolipid metabolism is an adeno-associated virus vector with specific overexpression of Sdccag3 in adipose tissue, and its active ingredient contains the nucleotide sequence shown in SEQ ID No.1. Specifically, it is prepared after co-transfecting host cells with a recombinant expression plasmid and a packaging system. By overexpressing the Sdccag3 gene, it can inhibit the increase in blood lipid levels, reduce the levels of serum triglyceride, cholesterol and low-density lipoprotein cholesterol in obese mice, reduce blood glucose, serum free fatty acid and serum insulin levels, and promote glucose tolerance and insulin sensitivity.

[0017] Preferably according to the present invention, the weight loss drug for regulating glycolipid metabolism also contains a pharmaceutically acceptable excipient.

[0018] More preferably, the excipient is one or more of glucose, sucrose, sorbitol, mannose, starch, microcrystalline cellulose, polyvinylpyrrolidone, cellulose, and water.

[0019] Preferably according to the present invention, the weight loss drug for regulating glycolipid metabolism is a tablet, pill, powder or injection.

[0020] Technical features and beneficial effects of the present invention:

[0021] 1. The present invention first verified the effects of Sdccag3 overexpression on the body weight, fat size and distribution of obese mice, and found that overexpression of Sdccag3 did not significantly improve the body weight, fat size and distribution of obese mice. Then, it verified the effects of the adeno-associated virus vector with specific overexpression of Sdccag3 in adipose tissue on the blood lipid metabolism level, glucose tolerance and insulin sensitivity of mice, and found that overexpression of Sdccag3 could significantly inhibit the increase in blood lipid levels induced by obesity in mice, and overexpression of Sdccag3 could also significantly improve glucose intolerance and increase insulin sensitivity, thus providing a theoretical basis for preparing or screening drugs or preparations that promote the expression of the Sdccag3 gene as alternative lipid-lowering and hypoglycemic drugs or preparations for regulating obesity-related glycolipid metabolism.

[0022] 2. By injecting the Sdccag3 adipose tissue-specific overexpression adeno-associated virus vector and the control adeno-associated virus vector, the present invention discovers that specific overexpression of Sdccag3 in adipose tissue in mice can significantly inhibit the increase in blood lipid levels, reduce the levels of serum triglyceride, cholesterol, and low-density lipoprotein cholesterol in obese mice, improve glucose intolerance, enhance insulin sensitivity, effectively regulate obesity-related glycolipid metabolism, achieve the effects of lipid-lowering and blood sugar-lowering, and can be used for the preparation of weight-loss drugs for lipid-lowering and blood sugar-lowering.

[0023] 3. The present invention uses the Sdccag3 gene as the action target to prepare or screen lipid-lowering and blood sugar-lowering drugs for regulating obesity-related glycolipid metabolism. The drug screening is mainly for unknown drugs. The drugs are applied to the target gene, and lipid-lowering and blood sugar-lowering drugs for regulating obesity-related glycolipid metabolism are screened according to whether the drug can promote the expression of the target gene; the drug preparation is mainly based on the target gene, and lipid-lowering and blood sugar-lowering drugs for regulating obesity-related glycolipid metabolism are prepared or constructed specifically to promote the expression of the target gene; the screened or prepared drugs are of great significance in regulating obesity phenotype-related glycolipid metabolism and lipid-lowering and blood sugar-lowering. BRIEF DESCRIPTION OF THE DRAWINGS

[0024] Figure 1 It is a schematic diagram of the comparison results of the body shapes of mice after specific overexpression of Sdccag3 in mouse adipose tissue using the Sdccag3 overexpression adeno-associated virus vector.

[0025] Figure 2 It is a schematic diagram of the results of the change in body weight gain of mice after specific overexpression of Sdccag3 in mouse adipose tissue using the Sdccag3 overexpression adeno-associated virus vector.

[0026] Figure 3 It is a schematic diagram of the results of the Micro-CT scan reconstruction of the abdominal fat of mice after specific overexpression of Sdccag3 in mouse adipose tissue using the Sdccag3 overexpression adenovirus vector.

[0027] Figure 4 It is a schematic diagram of the comparison results of the epididymal adipose tissue of mice after specific overexpression of Sdccag3 in mouse adipose tissue using the Sdccag3 overexpression adenovirus vector.

[0028] Figure 5 It is a schematic diagram of the results of the weight of the epididymal adipose tissue of mice after specific overexpression of Sdccag3 in mouse adipose tissue using the Sdccag3 overexpression adenovirus vector.

[0029] Figure 6 It is a schematic diagram of the results of the ratio of the epididymal adipose tissue to the body weight of mice after specific overexpression of Sdccag3 in mouse adipose tissue using the Sdccag3 overexpression adenovirus vector.

[0030] Figure 7 Schematic diagram of the results of the content of serum triglyceride (TG) in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0031] Figure 8 Schematic diagram of the results of the content of serum total cholesterol (CHO) in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0032] Figure 9 Schematic diagram of the results of the content of serum low-density lipoprotein cholesterol (LDLC) in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0033] Figure 10 Schematic diagram of the results of serum free fatty acids (FFA) in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0034] Figure 11 Schematic diagram of the results of fasting serum insulin in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0035] Figure 12 Schematic diagram of the results of fasting blood glucose in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0036] Figure 13 Schematic diagram of the results of the glucose tolerance test in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3.

[0037] Figure 14 Schematic diagram of the results of the insulin tolerance test in mice after specific overexpression of Sdccag3 in adipose tissue using an adenovirus vector overexpressing Sdccag3. Detailed implementation manners

[0038] The present invention will be further described below in conjunction with embodiments. The embodiments are only used to illustrate the present invention and do not limit the protection scope of the present invention.

[0039] For the drugs and reagents involved in the embodiments, unless otherwise specified, they are all ordinary commercially available products; for the experimental operations involved in the embodiments, unless otherwise specified, they are all carried out according to the conventional operations in the art.

[0040] In the embodiments of the present invention, the Sdccag3 adipose tissue-specific overexpression adeno-associated virus vector used is rAAV9-FABP4p-MCS-SDCCAG3-SV40, and its active ingredient contains the nucleotide sequence shown in SEQ ID No. 1, which is available for sale from Shanghai GeneChem Co., Ltd. The adeno-associated virus empty vector as a control is also available for sale from Shanghai GeneChem Co., Ltd.

[0041] Example 1. Establishment of animal model

[0042] Thirty-two 4-week-old male C57BL / 6J mice were randomly divided into 4 groups. The Sdccag3 adipose tissue-specific overexpression adeno-associated virus vector (rAAV9-FABP4p-MCS-SDCCAG3-SV40) was dissolved on ice, diluted with sterile normal saline, and the abdominal injection site of the mice was disinfected with iodophor. The adipose tissue of the mice in the first and second groups was infected by intraperitoneal injection. At the same time, the adeno-associated virus empty vector was injected into the mice in the third and fourth groups as a control group. After injection, the mice were fed and observed for 2 weeks, and then the mice in the first and third groups were fed with normal feed, denoted as NCD-AAV-SDCCAG3 and NCD-AAV-NC mice, and the mice in the second and fourth groups were fed with high-fat feed, denoted as HFD-AAV-SDCCAG3 and HFD-AAV-NC mice. All mice in the experiment were raised in sterilized standard cages with a 12-hour light-dark cycle, provided with free drinking water and corresponding standard diets. After 16 weeks of feeding, normal mouse models (NCD-AAV-SDCCAG3 and NCD-AAV-NC) and high-fat mouse models (HFD-AAV-SDCCAG3 and HFD-AAV-NC) were obtained.

[0043] Take the NCD-AAV-NC, NCD-AAV-SDCCAG3, HFD-AAV-NC, and HFD-AAV-SDCCAG3 mice after 16 weeks of feeding above, take pictures and weigh them after anesthesia, and the results Figures 1 - 2 are shown as follows.

[0044] As Figures 1 - 2 can be seen, there were no significant differences in the body size and weight between the normal mouse models (NCD-AAV-SDCCAG3 and NCD-AAV-NC) and the high-fat mouse models (HFD-AAV-SDCCAG3 and HFD-AAV-NC). It shows that overexpression of Sdccag3 did not change the body weight development of mice under normal and high-fat diets. That is, overexpression of Sdccag3 was not able to affect the body weight development of mice induced by high-fat diet.

[0045] Example 2. Micro-CT scanning and reconstruction of mice

[0046] Abdominal fat Micro-CT scans were reconstructed for the NCD-AAV-SDCCAG3, NCD-AAV-NC mice and HFD-AAV-SDCCAG3, HFD-AAV-NC mice constructed in Example 1, and the analysis results are as Figure 3 shown.

[0047] The specific process is as follows: Micro-computed tomography (micro CT) was performed using a Quantum GX2 Live animal Imaging System (PerkinElmer, Japan). The abdomen and lower limbs of c57 were scanned at a resolution of 72 microns to obtain DICOM files. The obtained DICOM files were analyzed using Mimics Research 21.0. The abdomen and lower limb regions of c57 were selected to analyze the distribution of visceral fat and subcutaneous fat. The CT value of adipose tissue was -187 to -22 HU. Taking the abdominal cavity margin as the boundary, the adipose tissue within the abdominal cavity was visceral fat, represented in orange, and the adipose tissue outside the abdominal cavity was subcutaneous fat, represented in green. It was separated through Split Mask to obtain the distribution of visceral fat and subcutaneous fat in the sagittal plane (anatomical landmark reference: os penis), coronal plane (anatomical landmark reference: bladder and testis), and horizontal plane (anatomical landmark reference: external oblique abdominal muscle).

[0048] It can be Figure 3 seen that there was no significant difference in the abdominal fat distribution between the normal mouse models (NCD-AAV-SDCCAG3 and NCD-AAV-NC) and the high-fat mouse models (HFD-AAV-SDCCAG3 and HFD-AAV-NC). This indicates that overexpression of Sdccag3 did not change the abdominal fat distribution in mice under normal and high-fat diets. That is, overexpression of Sdccag3 was not able to affect the abdominal fat distribution induced by high-fat diet in mice.

[0049] Example 3. Sampling of epididymal adipose tissue

[0050] The NCD-AAV-SDCCAG3, NCD-AAV-NC mice and HFD-AAV-SDCCAG3, HFD-AAV-NC mice constructed in Example 1 were sacrificed by cervical dislocation. The testes of the mice were found in the lower abdomen, lifted with forceps, and the white fat attached to them was epididymal fat. It was dissected along the vas deferens to the end of the testis and then cut off. After each sample was taken out, it was rinsed thoroughly with sterile PBS solution and the water was blotted dry with absorbent paper.

[0051] The above-mentioned epididymal adipose tissue was weighed and photographed, and the results are as Figures 4 - 6 shown.

[0052] It can be Figures 4 - 6It can be seen that there are no significant differences in the size, weight of epididymal adipose tissue and the ratio of epididymal adipose tissue to body weight between the normal mouse models (NCD-AAV-SDCCAG3 and NCD-AAV-NC) and the high-fat mouse models (HFD-AAV-SDCCAG3 and HFD-AAV-NC). This indicates that overexpression of Sdccag3 does not change the size, weight of epididymal adipose tissue and the ratio of epididymal adipose tissue to body weight in mice under normal and high-fat diets. That is, overexpression of Sdccag3 fails to affect the adipose tissue growth induced by high-fat diet in mice.

[0053] Example 4: Collection of mouse serum and biochemical analysis

[0054] The NCD-AAV-SDCCAG3, NCD-AAV-NC mice and HFD-AAV-SDCCAG3, HFD-AAV-NC mice constructed in Example 1 were sacrificed by cervical dislocation. Before blood coagulation, blood was collected from the medial canthal venous plexus using a capillary glass tube with an inner diameter of 0.3 mm. After the blood samples were left standing overnight at 4 °C, they were centrifuged at 4000 r / min for 15 min, and the upper-layer serum was separated and placed in a newly collected tube. After being aliquoted, it was stored at -80 °C.

[0055] The above serum samples were taken for biochemical analysis and determination. Serum triglyceride, cholesterol, and low-density lipoprotein cholesterol were measured using commercial kits (S03030; S03040; S03027; S03042; S03025; S03029, Rayto, China) and an automatic biochemical analyzer (Chemray 800, Rayto, China). Serum free fatty acids were measured using a free fatty acid content detection kit (BC0590, Solarbio, China), and serum insulin was measured using a mouse insulin elisa kit (sekm-0141, Solarbio, China) according to the commercial instructions. The results are as Figures 7 - 11 shown.

[0056] From Figures 7 - 11It can be seen that there are no significant differences in serum triglyceride, cholesterol, low-density lipoprotein cholesterol, free fatty acid and insulin between the two groups of mice, namely NCD-AAV-NC and NCD-AAV-SDCCAG3. However, in the HFD-AAV-SDCCAG3 mice, the levels of serum triglyceride, cholesterol and low-density lipoprotein cholesterol are decreased, free fatty acid is reduced, and insulin level is decreased compared with those in the HFD-AAV-NC group. This indicates that overexpression of Sdccag3 fails to affect the levels of serum triglyceride, cholesterol, low-density lipoprotein cholesterol, free fatty acid and insulin in mice under normal diet, while it inhibits the increase in serum triglyceride, cholesterol and low-density lipoprotein cholesterol induced by high-fat diet, reduces free fatty acid, and decreases insulin level. That is, overexpression of Sdccag3 can effectively inhibit the increase in obesity-related serum biochemical indexes.

[0057] Example 5: Blood glucose detection in mice

[0058] The NCD-AAV-SDCCAG3, NCD-AAV-NC mice and HFD-AAV-SDCCAG3, HFD-AAV-NC mice constructed in Example 1 were fasted for 12 hours before the experiment while maintaining normal drinking water. The tail vein blood determination method was used. At the beginning of the experiment, the mice were placed in a fixator, the tail was fully exposed, the tip of the tail was wiped and disinfected with an alcohol cotton ball, the tip of the tail vein was pricked with a disposable microtip blood collector, one drop of blood was wiped off, and the second drop of blood was collected with a blood glucose test strip and then placed in a blood glucose meter for determination. The reading was recorded, and the results Figure 12 are shown as follows.

[0059] As Figure 12 can be seen, there is no significant difference in blood glucose level between the two groups of mice, namely NCD-AAV-NC and NCD-AAV-SDCCAG3. However, the blood glucose level in the HFD-AAV-SDCCAG3 mice is significantly decreased compared with that in the HFD-AAV-NC group. This indicates that overexpression of Sdccag3 fails to affect the blood glucose level in mice under normal diet, while the blood glucose level induced by high-fat diet is significantly decreased. That is, overexpression of Sdccag3 can effectively inhibit the increase in blood glucose level induced by high-fat diet.

[0060] Example 6: Glucose tolerance test in mice

[0061] The NCD-AAV-SDCCAG3, NCD-AAV-NC mice, HFD-AAV-SDCCAG3, and HFD-AAV-NC mice constructed in Example 1 were fasted for 16 hours before the experiment while maintaining normal water intake. At the start of the experiment, the weight of each mouse was first measured. Blood was collected from the tip of the mouse's tail vein using a blood glucose test strip and measured with a blood glucose meter, and the blood glucose value at 0 min was recorded. After the mice were allowed to acclimate for 30 min, a 20% glucose solution was prepared with physiological saline at a dosage of 2 g / kg, and the injection volume was 0.1 ml / g. The glucose solution was injected intraperitoneally, and the blood glucose levels were measured and recorded at 15 min, 30 min, 60 min, and 120 min after injection. The results are as Figure 13 shown.

[0062] It can be Figure 13 seen that there was no significant difference in glucose tolerance between the two groups of mice, NCD-AAV-NC and NCD-AAV-SDCCAG3. However, after intraperitoneal injection of glucose, the blood glucose level of the HFD-AAV-SDCCAG3 mice increased less significantly and returned to the basal level faster than that of the HFD-AAV-NC group. This indicates that overexpression of Sdccag3 did not affect the glucose tolerance of mice on a normal diet but tended to normalize the glucose tolerance of mice fed a high-fat diet. That is, overexpression of Sdccag3 can effectively improve glucose intolerance induced by a high-fat diet.

[0063] Example 7. Mouse insulin tolerance test

[0064] The NCD-AAV-SDCCAG3, NCD-AAV-NC mice, HFD-AAV-SDCCAG3, and HFD-AAV-NC mice constructed in Example 1 were fasted for 4 hours before the experiment while maintaining normal water intake. At the start of the experiment, the weight of each mouse was first measured. Blood was collected from the tip of the mouse's tail vein using a blood glucose test strip and measured with a blood glucose meter, and the blood glucose value at 0 min was recorded. After the mice were allowed to acclimate for 30 min, insulin was injected intraperitoneally at a dosage of 0.5 U / kg, and the blood glucose levels were measured and recorded at 15 min, 30 min, 60 min, and 120 min after injection. The results are as Figure 14 shown.

[0065] It can be Figure 14It can be seen that there is no significant difference in insulin sensitivity between the two groups of mice, namely NCD-AAV-NC and NCD-AAV-SDCCAG3. However, after intraperitoneal injection of insulin, the blood glucose level of HFD-AAV-SDCCAG3 mice decreased significantly and returned to the basal level more slowly compared with that of the HFD-AAV-NC group, indicating that they were significantly controlled by insulin. This shows that overexpression of Sdccag3 did not affect the insulin sensitivity of mice under normal diet, but weakened the insulin resistance of mice fed with high-fat diet. That is, overexpression of Sdccag3 can effectively improve the insulin sensitivity induced by high-fat diet.

[0066] The preferred embodiments of the present invention have been described in detail above. However, the present invention is not limited thereto. Within the scope of the technical concept of the present invention, various simple modifications can be made to the technical solutions of the present invention, including any other suitable combination of each technical feature. These simple modifications and combinations should also be regarded as the disclosed content of the present invention and fall within the protection scope of the present invention.

Claims

1. Use of the Sdccag3 gene in the preparation of a weight loss drug for regulating glycolipid metabolism, characterized in that, The nucleotide sequence of the Sdccag3 gene is shown in SEQ ID No.

1.

2. The application according to claim 1, characterized in that The application of the Sdccag3 gene in the preparation of weight loss drugs for regulating glycolipid metabolism includes the following two aspects: (1) Using the Sdccag3 gene as a target for the preparation of weight loss drugs for regulating glycolipid metabolism; (2) Using the Sdccag3 gene as a target for screening weight loss drugs for regulating glycolipid metabolism.

3. The application according to claim 2, characterized in that, Using the Sdccag3 gene as a target for the preparation of weight loss drugs for regulating glycolipid metabolism means: using the Sdccag3 gene as a target of a drug or preparation to increase the expression level of the Sdccag3 gene in adipose tissue, so as to develop weight loss drugs or preparations for regulating glycolipid metabolism.

4. The application according to claim 2, wherein Using the Sdccag3 gene as a target for screening weight loss drugs for regulating glycolipid metabolism means: using the Sdccag3 gene as a target of a drug or preparation to screen the drug or preparation, so as to find drugs or preparations that can promote the expression of the Sdccag3 gene in adipose tissue as alternative weight loss drugs or preparations for regulating glycolipid metabolism.

5. The application according to claim 1, characterized in that The weight loss drugs for regulating glycolipid metabolism include but are not limited to: nucleic acid molecules, carbohydrates, lipids, small molecule chemical drugs, antibody drugs, polypeptides, proteins or viruses.

6. The application according to claim 5, characterized in that, The weight loss drug for regulating glycolipid metabolism is an adipose tissue-specific overexpression adeno-associated virus vector of Sdccag3, and its active ingredient contains the nucleotide sequence shown in SEQ ID No.1, specifically prepared by co-transfecting host cells with a recombinant expression plasmid and a packaging system.

7. The application according to claim 1, characterized in that The weight loss drug for regulating glycolipid metabolism also contains a pharmaceutically acceptable excipient.

8. The application according to claim 1, characterized in that, The excipient is one or more of glucose, sucrose, sorbitol, mannose, starch, microcrystalline cellulose, polyvinylpyrrolidone, cellulose, water.

9. The application according to claim 8, wherein The weight loss drug for regulating glycolipid metabolism is in the form of tablets, pills, powders or injections.

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