CN112480047B

CN112480047B - Compound with blood glucose reducing and lipid regulating effects, preparation and application thereof

Info

Publication number: CN112480047B
Application number: CN202011380761.6A
Authority: CN
Inventors: 杨莹; 李政; 耿新倩; 杨克; 李奕平; 周太成
Original assignee: YUNNAN SECOND PEOPLE'S HOSPITAL; Guangdong Pharmaceutical University; Ruinjin Hospital Affiliated to Shanghai Jiaotong University School of Medicine Co Ltd
Current assignee: YUNNAN SECOND PEOPLE'S HOSPITAL; Guangdong Pharmaceutical University; Ruinjin Hospital Affiliated to Shanghai Jiaotong University School of Medicine Co Ltd
Priority date: 2020-12-01
Filing date: 2020-12-01
Publication date: 2023-06-02
Anticipated expiration: 2040-12-01
Also published as: CN112480047A

Abstract

The invention discloses a compound with the functions of reducing blood sugar and regulating lipid, a preparation and application thereof, wherein the compound with the functions of reducing blood sugar and regulating lipid is a compound with a structure shown in a formula I and a formula II and a pharmaceutically acceptable salt, and the structures shown in the formula I and the formula II are as follows:

Description

Compound with blood glucose reducing and lipid regulating effects, preparation and application thereof

Technical Field

The invention belongs to the technical field of medicines, and further belongs to the technical field of medicines for treating glycolipid metabolic diseases, in particular to a compound with the functions of reducing blood glucose and regulating lipid, a preparation and application thereof.

Background

Metabolic syndrome is a common disease characterized by abnormal glucose and lipid metabolism, accompanied by elevated low density lipoprotein and lowered high density lipoprotein cholesterol, and common diseases are obesity, diabetes, hyperlipidemia, atherosclerosis, fatty liver and the like, wherein diabetes patients are also frequently complicated with diseases such as hyperlipidemia, cardiovascular diseases, diabetic nephropathy, diabetic neuropathy and the like. According to the world health organization publications, more than 2.2 hundred million people suffer from diabetes mellitus worldwide at present, wherein China becomes the most world of diabetes mellitus patients, more than 9200 ten thousand diabetes mellitus patients, and the current diabetes mellitus incidence rate of China is still in the rising period, and the current diabetes mellitus pre-patients in China are estimated to be about 1.5 hundred million. The continuously expanding diabetic population has brought great economic and medical burden to society. The world health organization indicates that if no effective measures are taken to cope with the development of diabetes, it is expected that in the next 10 years, only heart disease, stroke and diabetes will bring about economic losses of at least 5500 billion dollars to China. Thus, metabolic syndrome typified by diabetes has become a serious disease threatening the health of humans. Metabolic syndrome can be treated by dietary regulation and exercise, and when these fail to relieve symptoms, medication is required. In the aspect of the drug treatment of metabolic syndrome, the existing blood sugar-reducing drugs or lipid-lowering drugs used clinically have single action and have different ideal actions for improving various pathological indexes of metabolic syndrome, so that the research on drugs for improving metabolic syndrome in multiple fields is ongoing so as to bring safer and more effective novel drugs for metabolic syndrome patients.

Disclosure of Invention

The first object of the present invention is to provide a compound having a hypoglycemic and lipid-regulating effect; a second object is to provide a preparation of the compound having the hypoglycemic and lipid-regulating effects; a third object is to provide the use of the compound having the hypoglycemic and lipid-regulating effects.

The first object of the invention is realized in that the compound with the functions of reducing blood sugar and regulating lipid is a compound with a structure shown in a formula I and a formula II and a pharmaceutically acceptable salt, and the structures shown in the formula I and the formula II are specifically as follows:

。

the second aim of the invention is realized by adding pharmaceutically acceptable auxiliary materials into the compound with the functions of reducing blood sugar and regulating lipid to prepare tablets, capsules, powder, pills or injections.

The third object of the present invention is thus achieved, the use of said compounds having a hypoglycemic and lipid-regulating effect for the preparation of dual agonists of FFA 1/PPARdelta.

The application of the compound with the functions of reducing blood glucose and regulating lipid in preparing the medicine for preventing and/or treating abnormal glucose metabolism and/or abnormal lipid metabolism diseases.

The auraptene is a simple coumarin derivative, mainly exists in fruits of plants in Rutaceae and Umbelliferae, has quite high content in pericarps of citrus fruits such as lemon, grapefruit and orange, has various pharmacological activities including anti-inflammatory, antioxidant and lipid metabolism regulating aspects, and has certain prevention and treatment effects on diabetes, fatty liver, cardiovascular system and some degenerative diseases. However, the coumarin structural fragment of aurapten is easy to metabolize in vivo, so that the pharmacokinetic property is poor, and the patent medicine has certain limitation. The inventor conducts repeated structure-activity relation research for the defects of the auraptene, finally, the compound I and the optimal enantiomer II thereof are preferably obtained, and the compound I and the optimal enantiomer II have dual agonistic activity of free fatty acid receptor 1 (FFA 1) and peroxisome proliferator-activated receptor delta (PPAR delta). FFA1 is mainly expressed in pancreas and intestine, and activation of FFA1 in intestine can promote GLP-1 secretion, while activation of FFA1 in pancreas can promote insulin secretion. Pparδ is mainly distributed in fat, skeletal muscle, heart and liver, and mainly regulates glycolipid metabolism, improves inflammatory reaction, insulin resistance and the like. The FFA 1/PPARdelta dual agonist has a synergistic mechanism for simultaneously promoting insulin secretion and improving insulin resistance, and has remarkable advantages for treating metabolic syndromes such as diabetes.

Aiming at the patent drug defect of natural product auraptene, the inventor researches and prefers FFA 1/PPARdelta dual agonist for many years, which can simultaneously play pharmacological actions of promoting insulin secretion and improving insulin resistance, thereby having excellent in vivo hypoglycemic lipid-regulating activity. Therefore, the compound and the pharmaceutically acceptable salt thereof can be potentially used for treating or preventing related metabolic syndromes such as diabetes, hyperlipidemia, fatty liver and the like, and have wide development prospect.

Detailed Description

The invention is further illustrated, but is not limited in any way, by the following examples, and any alterations or substitutions based on the teachings of the invention are within the scope of the invention.

The compound with the functions of reducing blood glucose and regulating lipid is a compound with a structure shown in a formula I and a formula II and a pharmaceutically acceptable salt, and the structures shown in the formula I and the formula II are specifically as follows:

。

the pharmaceutically acceptable salt is potassium salt, sodium salt or organic acid alkali salt containing alkaline groups.

The preparation of the compound with the effects of reducing blood sugar and regulating lipid is prepared by adding pharmaceutically acceptable auxiliary materials into the compound with the effects of reducing blood sugar and regulating lipid, and preparing into tablets, capsules, powder, pills or injection.

The application of the compound with the function of reducing blood sugar and regulating lipid is the application of the compound with the function of reducing blood sugar and regulating lipid in preparing FFA 1/PPARdelta dual agonist.

The application of the compound with the function of reducing blood glucose and regulating lipid is the application of the compound with the function of reducing blood glucose and regulating lipid in preparing medicines for preventing and/or treating abnormal glucose metabolism and/or abnormal lipid metabolism diseases.

The compound with the functions of reducing blood sugar and regulating lipid is applied to the preparation of medicaments for preventing and/or treating diabetes, diabetic nephropathy, obesity, hyperlipidemia, atherosclerosis and fatty liver.

The invention is further illustrated by the following examples:

example 1

(6-hydroxy-1-benzofuran-3-yl) acetic acid methyl ester

Ethyl 4-chloroacetoacetate (4.25 ml, 31.43 mmol) was dissolved in 20 ml concentrated sulfuric acid at 0 ℃, the resulting pale yellow viscous solution was cooled to about-5 ℃ in an ice bath, resorcinol (3.15 g, 28.57 mmol) was added in portions, the internal temperature was controlled to be lower than 0 ℃, the addition was completed, stirring was carried out at room temperature for 2h, the reaction solution was poured into 50ml ice water, a white solid was precipitated, the filter cake was washed with water (5 ml ×2) by suction filtration, and the off-white solid was obtained by drying, 5.6 g, and the crude yield was 82.3%.

The crude product (2 g, 9.50 mmol) was taken in a 200 ml single neck flask, 1N NaOH solution (100 ml) was added, the solution turned to a strong yellow immediately, the solution was put in an oil bath and heated to reflux 2h, the reaction was completed, cooled to room temperature, the pH of the obtained solution was adjusted to 2-3 with concentrated sulfuric acid, the obtained solution was extracted with ethyl acetate (30 ml X4), the organic phases were combined, washed with saturated brine (20 ml X2), dried over anhydrous sodium sulfate, filtered, the solvent was distilled off under reduced pressure to obtain a tan columnar crystal 1.3 g, and the crude product yield was 71.2%. The crude product (1 g, 5.20 mmol) was suspended in 10 ml methanol, 0.5 ml concentrated sulfuric acid was added dropwise, the mixture was then heated to reflux for about 4h, the methanol was distilled off under reduced pressure after the reaction was completed, the residual liquid was poured into 30 ml water, extracted with ethyl acetate (20 ml ×3), the organic phases were combined, washed with saturated sodium bicarbonate solution (15 ml ×2) respectively, saturated brine (15 ml ×2) was washed, dried over anhydrous sodium sulfate, filtered, the solvent was distilled off under reduced pressure to obtain a tan oil, and the column chromatography (petroleum ether/ethyl acetate, 80:20, v/v) was purified to obtain a pale yellow solid of 0.75 g, yield 70%.

¹ H NMR (300 MHz, DMSO-d ₆ ) δ: 9.54 (s, 1H, ArOH), 7.69 (s, 1H, ArH), 7.33 (d, J = 8.41 Hz, 1H, ArH), 6.87 (d, J = 1.89 Hz, 1H, ArH), 6.75, 6.72 (dd, J = 2.01, 8.40 Hz, 1H, ArH), 3.71 (s, 2H, ArCH ₂ CO), 3.63 (s, 3H, -OCH ₃ ).

Example 2

(6-hydroxy-2, 3-dihydro-1-benzofuran-3-yl) acetic acid methyl ester

Raw material ester (2 g, 9.7 mmol) is dissolved in methanol, catalytic amount of palladium carbon 0.2 g is added, hydrogen is replaced for three times, hydrogen is introduced and stirred at room temperature for 24h, diatomite is used as a pad for filtering after the reaction is finished, filter cake is washed, and the filtrate is decompressed and distilled to remove solvent to obtain off-white powdery solid 1.93 g, and the yield is 95.5%.

¹ H NMR (300 MHz, CDCl ₃ ) δ: 6.97 (d, J = 8.71 Hz, 1H, ArH), 6.31–6.34 (m, 2H, ArH), 4.82 (brs, 1H, ArOH), 4.75 (t, J = 9.10 Hz, 1H, -OCH ₂ ), 4.26, 4.24 (dd, J =5.72, 9.10 Hz, 1H, -OCH ₂ ), 3.74–3.84 (m, 1H, ArCH), 3.72 (s, 3H, -OCH ₃ ), 2.74, 2.69 (dd, J = 5.72, 16.41 Hz, 1H, -COCH ₂ ), 2.55, 2.50 (dd, J = 9.11, 16.41 Hz, 1H, -COCH ₂ ).

Example 3

(E) -2- (6- (((3, 7-dimethyloctyl-2, 6-dien-1-yl) oxy) -2, 3-dihydrobenzofuran-3-yl) acetic acid (I)

Geraniol (1 g, 6.5 mmol) is added to a dichloromethane solution of 5 ml thionyl chloride cooled in advance in an ice bath in portions, stirred uniformly, then heated and refluxed for reaction 1 h, the reaction solution is distilled off under reduced pressure to remove the excess thionyl chloride, the obtained brown oil is dissolved in 20 ml THF, raw ester (1 equivalent), anhydrous potassium carbonate (3 equivalent) and catalytic amount KI are added, reaction 8h is heated to 60 ℃, filtration, distillation under reduced pressure to remove the solvent, the residue is dissolved in 30 ml water, extraction with ethyl acetate (20 ml ×3), the organic phases are combined, washing with saturated brine (15 ml ×2), drying with anhydrous sodium sulfate, filtration, distillation of the filtrate under reduced pressure to remove the solvent, the residue is purified by column chromatography (petroleum ether/ethyl acetate, 5:1, v/v) to obtain white solid, dissolved in 4 mL tetrahydrofuran, 6 mL methanol and 2 mL water, liOH (2 equivalent) are added, room temperature is reacted for 8h, tetrahydrofuran and methanol are distilled off under reduced pressure, 1N hydrochloric acid is added dropwise in ice water, PH is adjusted, the white solid is separated out, and white solid is obtained as a white solid filtered.

¹ H NMR (300 MHz, DMSO-d ₆ ) δ 7.11 (d, J = 8.0 Hz, 1H), 6.54 – 6.25 (m, 2H), 5.39 (t, J = 6.8 Hz 1H), 5.07 (t, J = 7.2 Hz, 1H), 4.48 (d, J = 6.4 Hz, 2H), 4.23 – 4.15 (m, 1H), 3.74 – 3.64 (m, 1H), 2.80 – 2.61 (m, 1H), 2.59 – 2.38 (m, 2H), 2.14 – 1.91 (m, 4H), 1.69 (s, 3H), 1.65 (s, 3H), 1.58 (s, 3H).¹³ C NMR (75 MHz, DMSO-d ₆ ) δ 173.77, 161.12, 159.72, 140.39, 131.51, 125.01, 124.25, 122.10, 120.28, 107.02, 96.94, 77.61, 64.96, 40.69, 39.85, 37.61, 26.24, 25.94, 18.02, 16.76. ESI-MS m/z: 329.1 [M-H] ^- .

Example 4

(S) - (6-hydroxy-2, 3-dihydro-1-benzofuran-3-yl) acetic acid methyl ester

Dissolving ester (9.32 g,48 mmol) in acetone (50 ml), heating and refluxing, slowly dripping acetone solution (2.91 g,24 mmol,15 ml) of R-phenethylamine into the solution, stopping heating after dripping, naturally cooling the obtained mixture to room temperature, stirring overnight, precipitating white precipitate, suction filtering, suspending the obtained filter cake in mixed solution of ethyl acetate (15 ml) and water (10 ml), dripping 1M diluted hydrochloric acid until pH of the mixed solution is less than 2, extracting the obtained mixed solution with ethyl acetate (20 ml ×3), mixing organic phases, washing with saturated saline solution (15 ml ×2), drying with anhydrous sodium sulfate, filtering, concentrating the filtrate under reduced pressure, dissolving the obtained residue in acetone (30 ml), heating and refluxing, dripping acetone solution (1.53 g,12.7 mmol,10 ml) of R-phenethylamine into the solution after dripping, stopping heating, naturally cooling the reaction solution to room temperature, stirring overnight, suction filtering, washing the obtained filter cake with a small amount of acetone (3 ml), recrystallizing the filter cake with acetone, dissolving the obtained white crystal in methanol (20 ml), dropwise adding 0.2 ml concentrated sulfuric acid, heating the reaction solution to 50 ℃ for 2h, cooling to room temperature after the reaction is finished, steaming under reduced pressure to remove excessive methanol, adding water (20 ml) into the residue, extracting with ethyl acetate (30 ml ×4), merging the organic phases, washing with saturated saline (20 ml ×2), drying with anhydrous sodium sulfate, filtering, steaming the filtrate under reduced pressure to remove the solvent to obtain a white solid suspension in 20 ml methanol, dropwise adding 0.2 ml concentrated sulfuric acid, after the dropwise adding, heating and refluxing to react about 4h, steaming under reduced pressure to remove methanol, pouring the residual liquid into 30 ml water, extraction with ethyl acetate (20 ml X3), combining the organic phases, washing with saturated aqueous sodium bicarbonate (15 ml X2), washing with saturated brine (15 ml X2), drying over anhydrous sodium sulfate, filtering, distilling off the solvent under reduced pressure to give a pale yellow solid, and purifying the pale yellow solid by column chromatography (petroleum ether/ethyl acetate, 80:20, v/v) to give 0.32 g as a white solid, yield 80%,99% ee.

Example 5

(S, E) -2- (6- (((3, 7-dimethyloctyl-2, 6-dien-1-yl) oxy) -2, 3-dihydrobenzofuran-3-yl) acetic acid (II)

Geraniol (0.5 g, 3.3 mmol) was added in portions to a dichloromethane solution of previously cooled 5 ml thionyl chloride under ice bath, stirred well and then heated to reflux for reaction 1 h, the reaction solution was distilled off under reduced pressure to remove the excess thionyl chloride, the resulting brown oil was dissolved in 20 ml THF, the starting ester (1 eq), anhydrous potassium carbonate (3 eq) and catalytic amount KI were added, heated to 60 ℃ for reaction 8h, filtered, the solvent was distilled off under reduced pressure, the residue was dissolved in 30 ml water, extracted with ethyl acetate (20 ml ×3), the organic phases were combined, washed with saturated brine (15 ml ×2), dried over anhydrous sodium sulfate, filtered, the filtrate was distilled off under reduced pressure to remove the solvent, the residue was purified by column chromatography (petroleum ether/ethyl acetate, 5:1, v/v) to give a white solid, dissolved in 4 mL tetrahydrofuran, 6 mL methanol and 2 mL water, reacted at room temperature for 8h, distilled off under reduced pressure to remove tetrahydrofuran and methanol, dropwise added 1N hydrochloric acid under ice water, PH 2-3 was adjusted, the white solid was precipitated, and 99% white filtered solid was obtained as a white solid, and the white compound was dried.

¹ H NMR (300 MHz, DMSO-d ₆ ) δ 7.13 (d, J = 8.0 Hz, 1H), 6.56 – 6.27 (m, 2H), 5.41 – 5.35 (m,1H), 5.11 – 5.05 (m, 1H), 4.49 (d, J = 6.5 Hz, 2H), 4.25 – 4.17 (m, 1H), 3.75 – 3.63 (m, 1H), 2.81 – 2.63 (m, 1H), 2.58 – 2.35 (m, 2H), 2.16 – 1.92 (m, 4H), 1.68 (s, 3H), 1.65 (s, 3H), 1.57 (s, 3H). ¹³ C NMR (75 MHz, DMSO-d ₆ ) δ 173.74, 161.15, 159.75, 140.36, 131.52, 125.03, 124.26, 122.12, 120.25, 107.05, 96.96, 77.63, 64.94, 40.67, 39.86, 37.62, 26.25, 25.94, 18.01, 16.75. ESI-MS m/z: 329.1 [M-H] ^- .

Example 6

The in vitro receptor agonistic activity and in vivo hypoglycemic and lipid-regulating activity of the compounds of the invention can be measured by using the measuring system as described below.

The following biological test examples illustrate the invention.

The experimental methods for the specific conditions in the test cases of the present invention are generally conventional or according to the conditions recommended by the commercial manufacturers. The reagents of specific origin are not noted and are commonly used reagents purchased in the market.

Test example 1

Agonistic activity of the compounds of the invention on PPAR

The invention uses the following methods to determine the PPAR agonistic activity of the compounds of the invention:

transfection: HEK293 cells were grown at 5X 10 prior to transfection ⁴ Density of wells/density of wells was seeded in 96-well plates at 37℃with 5% CO ₂ One day (for pparγ and pparδ transfection) in cell culture; hepG2 cells at 6X 10 ⁴ Density of wells/density of wells was seeded in 96-well plates at 37℃with 5% CO ₂ One day (for pparα transfection); transfection was performed with FuGENE HD transfection reagent (available from Roche), respectively: 25 ng/well pBIND-PPARα or PPARδ or PPARγ, 25 ng/well pG5Luc, and 0.15 μl/well FuGENE HD.

Agonist activity assay: after 24h of transfection, the test compound was added to the post-transfection cell well plate, incubated for 18h, lysed by addition of 20. Mu.l of cell lysate and 30. Mu.l of luciferase assay reagent II (from Promega), mixed well, fluorescence measured, 2 seconds delay, read for 10 seconds. Transfection efficiency was corrected using the reference Renilla luciferase activity. All transfection experiments were independently repeated at least three times, at least 2 duplicate wells per experimental group. Relative fluorescence intensity = firefly fluorescence intensity/renilla fluorescence intensity. PPAR agonist activity (%) = [ (X-Min)/(Max-Min) ] ×100%, where X represents compound group relative fluorescence intensity, min represents blank group relative fluorescence intensity, max represents positive control compound group relative fluorescence intensity at a concentration of 10 μm. The examples of PPARα, PPARδ and PPARγ agonistic activity (all at 10 μM concentrations) are shown in Table 1.

Table 1: PPARα, PPARδ and PPARγ agonistic activity

Conclusion: the compound has good agonistic activity on PPARdelta and good receptor subtype selectivity on PPARalpha and PPARgamma, thereby avoiding potential side effects caused by activating PPARalpha and PPARgamma.

Test example 2

The present invention uses the following method to determine the agonist activity of FFA1-CHO stable cells of the compounds of the present invention:

FFA1-CHO stable cells at 3X 10 ⁴ Density of wells/density of wells was seeded in 96-well plates at 37℃with 5% CO ₂ Overnight culture in a cell incubator; the medium was discarded, and after washing with 100 ul of HBSS (Beyotime) per well, 100 ul Fluo-4 (Invitrogen) dye solution containing Probenecid (Invitrogen) was added and incubated for 90 min at 37 ℃. After the incubation, the Fluo-4 dye solution was aspirated, 100. Mu.l of HBSS buffer was added, and the dye was washed away; 100 mu HBSS containing Probenecid is added to each well and incubated for 10 min at 37 ℃; different concentrations of drug were added to each well of the 96-well plate and read FLIPR (Molecular Devices) according to the parameter set-up table. And analyzing the experimental result. Agonist activity = (compound pore fluorescence value-blank Kong Yingguang value)/(linoleic acid pore fluorescence value-blank Kong Yingguang value) ×100% and the results are shown in table 2.

Table 2: FFA1 agonistic Activity

Conclusion: the compound has good agonistic activity on FFA1, and the agonistic efficiency is higher than that of a partial agonist GW9508.

Test example 3

The in vivo hypolipidemic activity of the compounds of the invention can be determined by using the assay system described below:

ICR mice, male, randomized, 6 in each group, were dosed (ip, 50 mg/kg) after 12 h non-fasting, injection of Triton WR-1339 for molding (400 mg/kg) after 20min, recovery of normal diet after 2h, and orbital bleeding after 24h (including 12 h fasting) and blood lipid levels in mice were measured with a full-automatic biochemical analyzer. The in vivo lipid-lowering activity of each compound is expressed as the rate of decrease (%) of TG or TC, i.e. TG or TC rate (%) = (model group TG or TC content-experimental group TG or TC content)/TG or TC content x 100.

Table 3: hypolipidemic activity in vivo

± SD，n = 6）/>

Conclusion: the compound disclosed by the invention can be used for remarkably improving the hyperlipidemia level, has a lipid-lowering effect stronger than that of a classical lipid-lowering drug fenofibrate, and has a wide development prospect.

Test example 4

The in vivo hypoglycemic lipid-regulating activity of the compounds of the invention can be determined by using the assay system described below:

8 weeks of ageob/obMice, males, were randomly divided into 5 groups, 6 mice per group, a blank control group (blank vehicle: 0.5% sodium carboxymethyl cellulose solution), a test compound I group (20 mg/kg), a test compound II group (10, 20, 40 mg/kg) were respectively given by gastric administration of the blank vehicle and the test compound once daily for 15 consecutive days, oral glucose tolerance (OGTT) of the mice was measured on the 15 th day of administration, the mice were fasted without water interruption for 12 hours before the experiment, blood was taken by tail breaking, and blood glucose level was measured (recorded as-30 min). The vehicle and test compound were then administered by gavage, respectively, and blood glucose was measured for 30 min and recorded as 0min, immediately thereafter, 3 g/kg glucose aqueous solution was administered by gavage, and blood glucose was measured at 15, 30, 60, 120 min. OGTT results are shown in Table 4. On day 16, the mice were collected with a hollow blood and serum was collected, and the blood lipid level of the mice was measured by a full-automatic biochemical analyzer, and the results are shown in Table 5.

Table 4: pairs of inventive compoundsob/obEffect of oral glucose tolerance in mice

±SD，n=6）

Note that: * P.ltoreq.0.05 and p.ltoreq.0.01 are results of Student's t test against the blank.

The OGTT results indicate that: both compounds I and II can be significantly improvedob/obThe oral glucose tolerance of mice shows better in vivo blood sugar reducing effect.

Table 5: pairs of inventive compoundsob/obInfluence of blood lipid level of mice

±SD，n=6）

The results show that: compound I, II can improve remarkablyob/obThe blood lipid level of mice is obviously improved on TC, TG and LDL levels, which shows that the mice have obvious effect of improving lipid metabolism.

Claims

1. The compound with the functions of reducing blood sugar and regulating lipid is characterized by being a compound with a structure shown in a formula I and a formula II and pharmaceutically acceptable salts, wherein the structures shown in the formula I and the formula II are as follows:

。

2. the compound with the functions of reducing blood glucose and regulating lipid according to claim 1, wherein the pharmaceutically acceptable salt is potassium salt, sodium salt or organic acid-base salt containing a basic group.

3. A preparation of the compound with the effect of reducing blood sugar and regulating lipid according to claim 1 or 2, which is characterized in that the compound with the effect of reducing blood sugar and regulating lipid is added with pharmaceutically acceptable auxiliary materials to prepare tablets, capsules, powder, pills or injections.

4. Use of a compound having a hypoglycemic lipid-regulating effect as claimed in claim 1 or 2, characterized in that the compound having a hypoglycemic lipid-regulating effect is prepared as a FFA1/pparδ dual agonist.

5. The use of a compound having a hypoglycemic and lipid-regulating effect as claimed in claim 1 or 2, characterized in that the use of the compound having a hypoglycemic and lipid-regulating effect for the preparation of a medicament for preventing and/or treating abnormal glucose metabolism and/or abnormal lipid metabolism.

6. The use according to claim 5, wherein the compound having the function of reducing blood glucose and regulating lipid is used for preparing medicines for preventing and/or treating diabetes, diabetic nephropathy, obesity, hyperlipidemia, atherosclerosis and fatty liver.