CN114731985B - Construction method of non-human primate model of metabolic-related fatty liver disease - Google Patents
Construction method of non-human primate model of metabolic-related fatty liver disease Download PDFInfo
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Abstract
The invention discloses a construction method of a non-human primate model of metabolic-related fatty liver disease, belonging to the technical field of experimental animals. The construction method of the invention relates to the following steps: by using a non-human primate, namely a cynomolgus monkey, as a model animal, the animal body weight is increased along with the feeding time by feeding high-fat high-sugar high-cholesterol feed, and the phenomenon of glycolipid metabolism disorder with remarkably increased blood glucose, cholesterol and triglyceride levels is caused, so that liver fat accumulation and fibrosis lesions are caused. The non-human primate model of the metabolic related fatty liver disease constructed by the invention can simulate the occurrence and development of the metabolic related fatty liver caused by improper diet in physiological and pathological processes of human beings, and provides a preclinical evaluation tool for developing nutrients and medicines in the related fields.
Description
Technical Field
The invention belongs to the technical field of experimental animals, and particularly relates to a construction method of a non-human primate model of metabolic-related fatty liver disease.
Background
Metabolic-related fatty liver disease (metabolic associated fatty liver disease, MAFLD), commonly known as non-alcoholic fatty liver disease (nonalcoholic fatty liver disease, NAFLD), has a global prevalence of up to 25%, severely jeopardizes human health and places a great economic burden on society. Unhealthy lifestyles such as sedentary hypokinesia, too high dietary calories, unreasonable dietary structure, and the like are closely related to the increasing of the incidence of MAFLD. MAFLD has become the second most chronic liver disease next to viral hepatitis in China, but the pathogenesis of MAFLD is not completely elucidated, and the MAFLD is lack of effective measures in treatment.
The animal model has important roles in the fields of exploring pathogenesis of diseases, evaluating and diagnosing methods, screening prevention and treatment medicines and the like. At present, the MAFLD disease model research at home and abroad is mainly based on NAFLD model construction methods, and the related methods mainly comprise three types: 1) A gene knockout or gene mutation model; 2) Nutritional, pharmaceutical, or toxicant induction models; 3) The composite model is mainly the combined application of a gene model and a nutrition model. The ob/ob mice are the most widely used gene-stick model at present, and their ob gene (leptin-encoding gene) spontaneously mutates, causing leptin synthesis disorders, manifested by obesity, hyperinsulinemia, hyperlipidemia, diabetes, fatty liver, etc., and although having characteristics consistent with human NAFLD, they cannot spontaneously develop NASH (nonalcoholic steatohepatitis). The most widely used nutrition-induced models, including MCD diet models (methionine deficiency), HFD diet models (high fat diet) and high carbohydrate diets, were modeled primarily for rodents. The model construction method is simple, but the severity of diet-related diseases is different among animals with different lines, strains, sexes and genetic backgrounds, so the model cannot completely cover the disease spectrum and pathogenesis of human MAFLD.
Based on the above, establishing an animal model which is similar to human lesions, has complete disease spectrum, is stable and reliable, and can better simulate the whole body metabolic disorder background when human MAFLD becomes a problem to be solved urgently. Non-human primates are very similar to humans in life habit, genetic background, and in particular in body immunity, and are the best model animals for studying clinical disease. The Chinese patent discloses a non-human primate model of non-alcoholic chronic steatohepatitis and a construction method and application thereof, but the construction method adopted by the model comprises high-fat diet, CCL4 chemical induction and alcohol drinking, and has a certain difference with the induction factors of fatty liver diseases related to human metabolism.
Disclosure of Invention
In order to overcome the problems in the prior art, the invention aims to provide a construction method of a non-human primate model of metabolic-related fatty liver disease.
The object of the invention is achieved by at least one of the following technical solutions.
The invention provides a construction method of a non-human primate model of metabolic related fatty liver disease, which is to feed the non-human primate with high-fat high-sugar high-cholesterol feed to cause the animal to generate glycolipid metabolic disorder and further induce the liver to generate fatty and fibrosis lesions, wherein the nutritional ingredients of the high-fat high-sugar high-cholesterol feed comprise 17-25wt% of crude protein, 30-45wt% of crude fat, 13-17wt% of crude fiber, 3-15wt% of fructose, 1-3wt% of cholesterol, 1-4wt% of calcium, 0.7-1wt% of phosphorus, 0.2-0.7wt% of vitamin and 0.3-5wt% of mineral substances according to mass percentage.
Further, in the construction method, the non-human primate is a single cage-reared cynomolgus monkey 5-25 years old.
Further, in the construction method, the non-human primate is a single cage-reared cynomolgus monkey 5-23 years old.
Further, in the construction method, the non-human primate is a cynomolgus monkey, the age range is 5-20 years, and the feeding mode is single cage feeding.
Further, in the construction method, enough high-fat high-sugar high-cholesterol feed is supplied, the supply of the high-fat high-sugar high-cholesterol feed to the cynomolgus monkey is unlimited, and the animals eat freely for 3-12 months.
Further, in the construction method, the main nutritional raw materials of the high-fat high-sugar high-cholesterol feed comprise more than one of soybean meal, fish meal and chicken meal to provide protein; one or more of corn oil, sunflower seed oil and lard oil is used for providing fat; one or more of corn starch, flour, and rice flour provides carbohydrate; one or more of bran and rice bran provides crude fiber.
Further, in the construction method, the high-fat high-sugar high-cholesterol feed comprises 2-3wt% of cholesterol in percentage by mass.
Further, in the construction method, the high-fat high-sugar high-cholesterol feed caloric composition comprises: 680-1011 Kcal/kg protein, 2700-4050 Kcal/kg fat, 960-1160 Kcal/kg carbohydrate, and total calories of 4660-5850 Kcal/kg.
Further, in the construction method, the high-fat high-sugar high-cholesterol feed caloric composition comprises: 960-1120 Kcal/kg carbohydrate.
Further, in the construction method, the fatty acid composition in the high-fat high-sugar high-cholesterol feed is as follows in percentage by mass: 30-65wt% of saturated fatty acid, 10-30wt% of monounsaturated fatty acid and 15-30wt% of polyunsaturated fatty acid.
Further, in the construction method, the fatty acid composition in the high-fat high-sugar high-cholesterol feed comprises the following components in percentage by mass: 51.53 to 57.85 percent of saturated fatty acid, 23.78 to 29.95 percent of monounsaturated fatty acid and 18.58 to 28.64 percent of polyunsaturated fatty acid.
Further, the fatty acid composition in the high-fat high-sugar high-cholesterol feed comprises: 51.85 to 57.85wt% of saturated fatty acid.
Further, in the construction method, the ratio of the chain length of the fatty acid in the high-fat high-sugar high-cholesterol feed comprises the following components in percentage by mass: 6.8 to 27.3 weight percent of medium chain fatty acid (fatty acid with the carbon number of 6 to 12 on a carbon chain) and 72.2 to 93.2 weight percent of long chain fatty acid (fatty acid with the carbon number of more than 12 on a carbon chain).
Further, in the construction method, the high-fat high-sugar high-cholesterol feed is fed for 3-12 months to form a model, the Cheng Mo rate reaches 72%, the weight of a model animal is obviously increased, and the total cholesterol content and the triglyceride content of blood reflecting abnormal liver lipid metabolism are obviously increased; a magnetic resonance imaging scan reflecting liver fat accumulation, the fat accumulation of the model animal is obvious; biopsies reflecting liver metabolic diseases appear as severe steatosis accompanied by a degree of fibrotic pathological changes.
Compared with the prior art, the invention has the following advantages and beneficial effects:
1. the liver glycolipid metabolism abnormality of the model can be found after the cynomolgus monkey is fed for 3-12 months by the non-human primate model of the metabolism-related fatty liver disease, and the liver tissue is subjected to steatosis and fibrosis lesion, so that the disease progress condition of liver steatosis caused by the glycolipid metabolism abnormality of human beings is successfully simulated.
2. According to the non-human primate model for the metabolic-related fatty liver disease, provided by the invention, the non-human primate model for the metabolic-related fatty liver disease can be obtained only by feeding the cynomolgus monkey with a simple feed without adopting a gastric lavage or drug injection means, so that the non-human primate model for the metabolic-related fatty liver disease accords with animal ethics, and various symptoms of the metabolic-related fatty liver disease of human beings are simulated, so that a theoretical basis is provided for research on the human-related disease, and the non-human primate model for the metabolic-related fatty liver disease has important significance in developing nutrients and drugs in the related fields.
Drawings
FIG. 1 is a flow chart of the construction of a non-human primate model of metabolic-related fatty liver disease according to the present invention.
FIG. 2 is a bar graph of modeling rate for three groups of high fat, high sugar and high cholesterol feeds of examples 1-3 in a non-human primate model of metabolic fatty liver disease 12 months after modeling.
FIG. 3 is a bar graph of body weight change in the non-human primate model of comparative example 1 for 0-12 months of the three groups of high fat, high sugar and high cholesterol feeds of examples 1-3 induced metabolic fatty liver disease.
FIG. 4 is a bar graph showing the results of serum glucose changes in the normal diet of comparative example 1 and the three groups of high fat, high sugar, high cholesterol diet of examples 1-3 induced metabolic fatty liver disease non-human primate models over a period of 0-12 months.
FIG. 5 is a bar graph showing the results of changes in serum total cholesterol in the normal diet of comparative example 1 and the three groups of high fat, high sugar, high cholesterol diet of examples 1-3 induced metabolic fatty liver disease non-human primate models for 0-12 months.
FIG. 6 is a bar graph showing the results of serum triglyceride changes in the normal diet of comparative example 1 and the three groups of high fat, high sugar, high cholesterol diet of examples 1-3 induced metabolic fatty liver disease non-human primate models over a period of 0-12 months.
Fig. 7 is a magnetic resonance imaging scan of liver after 12 months in a non-human primate model of comparative example 1 with normal diet feed and three groups of high fat high sugar high cholesterol feeds of examples 1-3 induced metabolic fatty liver disease.
FIG. 8 is a graph showing the results of HE staining of liver of a non-human primate model of comparative example 1 after 12 months of induction of metabolic fatty liver disease by the normal diet and the three groups of high fat, high sugar and high cholesterol feeds of examples 1-3.
FIG. 9 is a graph showing the results of liver Masson staining of a non-human primate model of comparative example 1 after 12 months of induction of metabolic fatty liver disease with the normal diet feed of examples 1-3 with the three groups of high fat, high sugar and high cholesterol feeds.
Detailed Description
Specific implementations of the invention are further described below with reference to the drawings and examples, but the implementation and protection of the invention are not limited thereto. It should be noted that the following processes, if not specifically described in detail, can be realized or understood by those skilled in the art with reference to the prior art. The reagents or apparatus used were not manufacturer-specific and were considered conventional products commercially available.
FIG. 1 is a flow chart of the construction of a non-human primate model of metabolic-related fatty liver disease according to the present invention.
Example 1
Taking adult cynomolgus monkey as an example, a non-human primate model of metabolic-related fatty liver disease with abnormal glycolipid metabolism and further with liver fatty and fibrotic lesions is constructed.
The experiment firstly prepares a high-fat high-sugar high-cholesterol feed-F1, wherein the nutritional ingredients of the feed comprise 25wt% of crude protein, 30wt% of crude fat, 17wt% of crude fiber, 3wt% of fructose, 1wt% of cholesterol, 4wt% of calcium, 1wt% of total phosphorus, 0.7wt% of vitamin and 5wt% of mineral matter; the caloric composition of the high-fat high-sugar high-cholesterol feed is as follows: 1000Kcal/kg of protein, 2700Kcal/kg of fat, 960Kcal/kg of carbohydrate, 4660Kcal/kg of total energy; the fatty acid composition of the high-fat high-sugar high-cholesterol feed is as follows: 51.58% by weight of saturated fatty acid, 27.78% by weight of monounsaturated fatty acid and 20.64% by weight of polyunsaturated fatty acid, wherein the medium chain fatty acid and the long chain fatty acid in the high-fat high-sugar high-cholesterol feed account for 6.8% by weight and 93.2% respectively.
In the experiment, 25 cynomolgus monkeys aged 5-21 are selected, the weight of the cynomolgus monkeys is 5.25-9.2 kg, and the cynomolgus monkeys are placed in a single cage, and enough high-fat, high-sugar and high-cholesterol feed is fed daily, so that the cynomolgus monkeys can eat and drink water freely.
The animals were weighed periodically (at 0, 3, 6, 9, 12 months respectively) and were monitored for glucose metabolism and lipid metabolism disturbance by blood sampling of the extremities to measure the serological changes; magnetic resonance imaging scanning and liver biopsy pathology detection are carried out regularly, and are used for judging pathological processes of liver steatosis and fibrosis.
Example 2
Taking adult cynomolgus monkey as an example, a non-human primate model of metabolic-related fatty liver disease with abnormal glycolipid metabolism and further with liver fatty and fibrotic lesions is constructed.
The experiment firstly prepares a high-fat high-sugar high-cholesterol feed-F2, wherein the nutritional ingredients of the feed comprise 22wt% of crude protein, 35wt% of crude fat, 14wt% of crude fiber, 15wt% of fructose, 2wt% of cholesterol, 2wt% of calcium, 1wt% of total phosphorus, 0.2wt% of vitamin and 0.5wt% of mineral matter; the caloric composition of the high-fat high-sugar high-cholesterol feed is as follows: protein 880Kcal/kg, fat 3150Kcal/kg, carbohydrate 1160Kcal/kg, total energy 5190Kcal/kg; the fatty acid composition of the high-fat high-sugar high-cholesterol feed is as follows: 57.58% by weight of saturated fatty acid, 23.78% by weight of monounsaturated fatty acid and 28.64% by weight of polyunsaturated fatty acid, and the medium chain fatty acid and the long chain fatty acid in the high-fat, high-sugar and high-cholesterol feed account for 21.7% by weight and 78.3% by weight respectively.
25 cynomolgus monkeys 7-17 years old are selected, the weight of the cynomolgus monkeys is 5.4-8.5 kg, the cynomolgus monkeys are placed in a single cage, and enough high-fat, high-sugar and high-cholesterol feed is fed daily, so that the cynomolgus monkeys can eat and drink water freely.
The animals were weighed periodically (at 0, 3, 6, 9, 12 months respectively) and were monitored for glucose metabolism and lipid metabolism disturbance by blood sampling of the extremities to measure the serological changes; magnetic resonance imaging scanning and liver biopsy pathology detection are carried out regularly, and are used for judging pathological processes of liver steatosis and fibrosis.
Example 3
Taking adult cynomolgus monkey as an example, a non-human primate model of metabolic-related fatty liver disease with abnormal glycolipid metabolism and further with liver fatty and fibrotic lesions is constructed.
The experiment firstly prepares a high-fat high-sugar high-cholesterol feed-F3, wherein the nutritional ingredients of the feed comprise 17wt% of crude protein, 45wt% of crude fat, 13wt% of crude fiber, 15wt% of fructose, 3wt% of cholesterol, 4wt% of calcium, 0.7wt% of total phosphorus, 0.48wt% of vitamin and 0.6wt% of mineral matter; the caloric composition of the high-fat high-sugar high-cholesterol feed is as follows: 680Kcal/kg of protein, 4050Kcal/kg of fat, 1120Kcal/kg of carbohydrate, 5850Kcal/kg of total energy; the fatty acid composition of the high-fat high-sugar high-cholesterol feed is as follows: 51.53% by weight of saturated fatty acid, 29.95% by weight of monounsaturated fatty acid and 18.52% by weight of polyunsaturated fatty acid, and the medium chain fatty acid and the long chain fatty acid in the high-fat, high-sugar and high-cholesterol feed account for 27.3% by weight and 72.7% by weight respectively.
In the experiment, 25 cynomolgus monkeys aged 6-23 are selected, the weight of the cynomolgus monkeys is 5.0-9.5 kg, and the cynomolgus monkeys are placed in a single cage, and enough high-fat, high-sugar and high-cholesterol feed is fed daily, so that the cynomolgus monkeys can eat and drink water freely.
The animals were weighed periodically (at 0, 3, 6, 9, 12 months respectively) and were monitored for glucose metabolism and lipid metabolism disturbance by blood sampling of the extremities to measure the serological changes; magnetic resonance imaging scanning and liver biopsy pathology detection are carried out regularly, and are used for judging pathological processes of liver steatosis and fibrosis.
Comparative example 1
The normal diet feed for the cynomolgus monkey, namely N, comprises the following nutritional ingredients of 21wt% of crude protein, 15wt% of crude fat, 40wt% of crude fiber, 2wt% of fructose, 14wt% of calcium, 10wt% of total phosphorus, 0.7wt% of vitamin and 0.3wt% of mineral matter; the caloric composition of the cynomolgus monkey normal diet feed is as follows: 840Kcal/kg of protein, 1350Kcal/kg of fat, 1680Kcal/kg of carbohydrate, 3870Kcal/kg of total energy; the normal diet feed for the cynomolgus monkey comprises the following fatty acids: 31.68wt% of saturated fatty acid, 21.67wt% of monounsaturated fatty acid and 46.65wt% of polyunsaturated fatty acid, wherein the medium chain fatty acid and the long chain fatty acid in the normal diet feed of the cynomolgus monkey account for 6.7wt% and 93.3wt%.
25 cynomolgus monkeys 7-24 years old are selected, weighing 5.05-9.7 kg, placed in a single cage, and fed with enough normal diet feed daily as a high-sugar high-fat high-cholesterol feed control, and fed with water freely.
The animals were weighed periodically (at 0, 3, 6, 9, 12 months respectively) and were monitored for glucose metabolism and lipid metabolism disturbance by blood sampling of the extremities to measure the serological changes; magnetic resonance imaging scanning and liver biopsy pathology detection are carried out regularly, and are used for judging pathological processes of liver steatosis and fibrosis.
Experimental results
Fig. 2 is a bar graph of the success rate of non-human primate models of metabolic fatty liver disease 12 months after molding the three high fat, high sugar, high cholesterol feeds of example 1, example 2, and example 3. As shown in FIG. 2, different high-fat, high-sugar and high-cholesterol feeding induction can obtain non-human primate models of the fatty liver disease related to metabolism, and the molding rate can reach 72% at the lowest.
FIG. 3 is a bar graph of the change in body weight of the normal diet of comparative example 1, the three groups of high fat, high sugar, high cholesterol diet of examples 1-3, induced metabolic fatty liver disease non-human primate model for 0-12 months (A1: normal body weight, A2: F1 body weight, A3: body weight, A4: F3 body weight). As can be seen from fig. 3, the weight of the cynomolgus monkey fed with the high-fat, high-sugar and high-cholesterol diet was significantly increased compared with the normal diet, and the weight increase showed F1 < F2 < F3, and further, the F3 high-fat, high-sugar and high-cholesterol diet could cause significant weight change after 3 months of feeding, due to the increase of the fat, fructose and cholesterol contents contained in the diet.
FIG. 4 is a bar graph showing the results of serum glucose changes in the non-human primate model of the three groups of high fat, high sugar and high cholesterol feeds of comparative example 1 and examples 1-3 over a period of 0-12 months (B1: normal glucose, B2: F1 glucose, B3: F2 glucose, and B4: F3 glucose). FIG. 5 is a bar graph showing the results of serum total cholesterol changes in the normal diet of comparative example 1 and the three groups of high fat, high sugar, high cholesterol diet of examples 1-3 in a non-human primate model of induced metabolic fatty liver disease over a period of 0-12 months (C1: normal total cholesterol, C2: F1 total cholesterol, C3: F2 total cholesterol, C4: F3 total cholesterol). FIG. 6 is a bar graph showing the results of serum triglyceride changes in the normal diet of comparative example 1, and the three groups of high fat, high sugar, high cholesterol diet of examples 1-3, in a non-human primate model of induced metabolic fatty liver disease over 0-12 months (D1: normal triglycerides, D2: F1 triglycerides, D3: F2 triglycerides, D4: F3 triglycerides). As can be seen from fig. 4 to fig. 6, the increase of total cholesterol content occurred 3 months before molding (0 months per se), and the significant increase of triglyceride and glucose occurred 6 to 9 months after molding, which indicates that the model liver had been in disorder of glycolipid metabolism.
FIG. 7 is a 12 month magnetic resonance imaging scan of liver from a non-human primate model of comparative example 1, a normal diet feed, and three groups of high fat, high sugar, and high cholesterol feeds of examples 1-3 (E: normal liver, G: F1 liver, H: F2 liver, I: F3 liver). Magnetic Resonance Imaging (MRI) techniques are widely used for liver fat quantification, where Proton Density Fat Fraction (PDFF) techniques are highly accurate, stable and reproducible, and therefore are used to assess liver steatosis using magnetic resonance imaging proton density fat fraction (MRI-PDFF). From the results of fig. 7, it is clear that 12 cynomolgus monkeys were subjected to magnetic resonance imaging with the high-fat, high-sugar and high-cholesterol feed model, and that the white areas of the fatty liver images of the model animals were more than those of normal livers, and that fat accumulation occurred in the livers of the instant cynomolgus monkeys (G, H, I in fig. 7).
FIG. 8 is a 12-month liver pathology biopsy HE color-staining photograph (J: normal liver, K: F1 liver, L: F2 liver, M: F3 liver) of the normal diet feed of comparative example 1 and the three groups of high-fat, high-sugar and high-cholesterol feeds of examples 1-3 induced metabolic fatty liver disease non-human primate model.
FIG. 9 is a 12-month liver Masson color-sensitive photograph (N: normal liver, O: F1 liver, P: F2 liver, QF3 liver) of a non-human primate model of the three groups of high-fat, high-sugar and high-cholesterol feeds of comparative example 1 and examples 1-3 induced metabolic fatty liver disease. As is clear from FIG. 8, the high-fat, high-sugar and high-cholesterol feeds used in the mold for 12 months caused steatosis of the liver (O, P, Q in FIG. 8), and as is clear from FIG. 9, the high-fat, high-sugar and high-cholesterol feeds used in the mold for 12 months caused fibrosis pathological changes (K, L, M in FIG. 9).
The animal model of metabolic fatty liver disease constructed by the high-fat high-sugar high-cholesterol feed can truly simulate the physiological and pathological process of liver steatosis and fibrosis pathological changes caused by abnormal metabolism of glycolipid due to unreasonable diet of human beings. The model construction method is simple and convenient, has good stability, fills the blank of a non-human primate model in the field of metabolic fatty liver disease, and has important significance for developing nutrients and medicines in the related fields.
The above examples are preferred embodiments of the present invention, but the embodiments of the present invention are not limited to the above examples, and any other changes, modifications, substitutions, combinations, and simplifications that do not depart from the spirit and principle of the present invention should be made in the equivalent manner, and the embodiments are included in the protection scope of the present invention.
Claims (8)
1. A method for constructing a non-human primate model of metabolic-related fatty liver disease, characterized in that the method comprises feeding a non-human primate with a high-fat, high-sugar and high-cholesterol feed, wherein the animal is abnormal in glycolipid metabolism and causes liver fatty lesions and fibrosis, the non-human primate is a cynomolgus monkey, and the high-fat, high-sugar and high-cholesterol feed comprises the following nutritional ingredients in percentage by mass: 17-25 wt% of crude protein, 30-45 wt% of crude fat, 13-17 wt% of crude fiber, 3-15 wt% of fructose, 1-3 wt% of cholesterol, 1-4 wt% of calcium, 0.7-1 wt% of phosphorus, 0.2-0.7 wt% of vitamins and 0.3-5 wt% of minerals, wherein the ingestion mode of the high-fat high-sugar high-cholesterol feed for the non-human primate is as follows: and (3) supplying enough high-fat high-sugar high-cholesterol feed, and enabling animals to eat freely for 3-12 months to mold.
2. The method of claim 1, wherein the non-human primate has an age ranging from 5 to 23 years.
3. The method of claim 1, wherein the non-human primate model is a single-cage animal.
4. The method for constructing a non-human primate model of metabolic-related fatty liver disease according to claim 1, wherein the nutritional main raw materials of the high-fat, high-sugar and high-cholesterol feed are as follows: the protein is one or more of soybean meal, fish meal and chicken meal, the fat is one or more of corn oil, sunflower seed oil and lard, the carbohydrate is one or more of corn starch, flour and rice flour, and the crude fiber is one or more of bran and rice bran.
5. The method for constructing a non-human primate model of metabolic-related fatty liver disease according to claim 1, wherein the caloric composition of the high-fat, high-sugar and high-cholesterol feed is as follows: 680-1011 Kcal/kg of protein, 2700-4050 Kcal/kg of fat, 960-1160 Kcal/kg of carbohydrate, and 4660-5850 Kcal/kg of total calories.
6. The method for constructing a non-human primate model of metabolic-related fatty liver disease according to claim 1, wherein the fatty acid composition in the high-fat, high-sugar and high-cholesterol feed is as follows by mass percent: 30-65% of saturated fatty acid, 10-30% of monounsaturated fatty acid and 15-30% of polyunsaturated fatty acid.
7. The method for constructing a non-human primate model of metabolic-related fatty liver disease according to claim 1, wherein the ratio of fatty acid chain length in the high-fat, high-sugar and high-cholesterol feed is as follows by mass percent: 6.8-27.3 wt% of medium-chain fatty acid and 72.7-93.2 wt% of long-chain fatty acid.
8. The method for constructing a non-human primate model of metabolic-related fatty liver disease according to any one of claims 1-7, wherein the model is produced by feeding a high-fat, high-sugar and high-cholesterol feed for 3-12 months, the Cheng Mo rate reaches 72%, the weight of the model animal is significantly increased, and the glucose content, total cholesterol content and triglyceride content in the blood reflecting abnormal liver lipid metabolism are significantly increased; in a magnetic resonance imaging scan reflecting liver fat accumulation, model animal fat accumulation is evident.
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