Construction and evaluation of a rat model for glycolipid metabolic disorder
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1. Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing 100010, China;2. Beijing Institute of Traditional Chinese Medicine, Beijing 100010, China

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    Abstract:

    Objective To establish a model of glycolipid metabolic disorder model in Zucker diabetic fatty (ZDF) rats induced by Purina 5008 feed, and to evaluate its pathological characteristics to provide a preclinical model tool for mechanistic research and drug development. Methods Twelve-week-old male ZDF rats were selected as the model group and Zucker lean(ZL) rats served as the normal control group (n= 9 rats per group). Rats in the model group were fed Purina 5008 feed, while normal control rats received standard feed for 7 weeks. Observations included physical sign scores, body mass, Lee’ s index, food and water intake, fasting blood glucose, oral glucose tolerance, serum total cholesterol ( TC), triglycerides ( TG), low-density lipoprotein cholesterol ( LDL-C), high-density lipoprotein cholesterol ( HDL-C), alanine aminotransferase ( ALT), aspartate aminotransferase ( AST),insulin levels, and homeostasis model assessment of insulin resistance ( HOMA-IR). Pathological changes in the liver, pancreas, and aorta were analyzed by hematoxylin-eosin(HE) and oil red O staining. Results Compared with the normal control group, model rats showed typical signs such as excessive drinking and eating, dull hair ( P<0. 01), and their body mass, Lee’s index, food / water intake increased significantly (P<0. 01), and fasting blood glucose, blood lipid and HOMA-IR all increased significantly (P<0. 01). Pathological examination revealed severe hepatic steatosis, vacuolar degeneration of pancreatic islet cells, and disorganized aortic wall structure with uneven thickening in the model group. Conclusions A ZDF rat model induced by Purina 5008 feed can stably simulate the core pathological features of glycolipid metabolic disorders, including metabolic dysregulation, insulin resistance, and multi-organ damage, offering a reliable platform for future mechanistic studies and therapeutic evaluation.

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  • Received:April 21,2025
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  • Online: March 05,2026
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