Abstract: Objective The objective is to develop a better mouse model of post-prandial hypertriglyceridemia that closely resembles the dietary habits of humans. This model will serve as a reference for studying traditional Chinese medicine for preventing and treating post-prandial hypertriglyceridemia and related diseases. Additionally, it will aid in the development of healthcare products and drugs related to this condition. Method Thirty-two SPF-grade 5-week-old male ICR mice were randomly divided into 4 groups of 8 mice each after 1 week of adaptive feeding on standard diets, including the group of gavage 0. 9% NaCl solution, the group of gavage edible oil, the group of combined gavage edible oil and 30% fructose in water, and the group of intraperitoneal injection of P-407. According to the relevant references of the lipid tolerance experiment, it was decided to take the material after 120 min of gavage, and the relevant serological indexes ( TG, TC, HDL and LDL) were detected by
using a fully automatic biochemistry instrument. According to the experimental result, subsequent
experiments were conducted; 24 SPF grade 5-week-old male ICR mice were randomly divided into 12
blank groups and 12 model groups after being acclimatized to standard chow for 1 week. In the blank
group, 0. 7 mL of 0. 9% NaCl solution was given by gavage, and in the model group, 0. 5 mL of peanut
oil and 0. 2 mL of 30% fructose water were given by gavage. After 120 min of gavage, the material was
taken and the glycolipid-related biochemical indexes ( TG, TC, HDL, LDL, AST, ALT, GLU and ALP)
were detected by fully automatic biochemistry instrument; the levels of serum SOD and MDA were
detected by the superoxide dismutase ( SOD) and malondialdehyde ( MDA) kits to assess the level of
oxidative stress; the hepatic pathological conditions were observed by HE staining and oil red O staining;
the liver was observed by transmission electron microscopy. The liver pathology was observed by HE and
oil red O staining; mitochondrial morphology in hepatocytes was observed by transmission electron
microscopy. Result
The combined gavage of edible oil and fructose water was more consistent with the
mechanism of post-prandial lipid elevation in humans. It could significantly increase the TG level in mice
after meals. In the follow-up experiments, serum TG, LDL, GLU, ALT, AST and ALP were significantly
increased and HDL was significantly decreased in the model group. Serum SOD level was significantly
reduced and MDA level was significantly increased in the model group. HE staining of hepatocytes in the
model group showed slight structural changes, lipid droplet aggregation was seen in hepatic oil red O
staining, and the phenomenon of mitochondrial endoplasmic reticulum following lipid droplets in
hepatocytes was seen in transmission electron microscopy. Conclusion A modified postprandial hypertriglyceridemic mouse model can be successfully established by gavage with a combination of peanut oil and 30% fructose water, and this disorder of glycolipid metabolism may be related to oxidative stress and mitochondrial function.
