ArticleAnimal models and experimental medicine2026
Chronic high-fat diet induces multi-organ dysfunction and metabolic homeostasis disruption in Macaca fascicularis.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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- Chronic high-fat diet induces multi-organ dysfunction and metabolic homeostasis disruption in Macaca fascicularis.Animal models and experimental medicine · 2026Article
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Abstract
backgroundThe aim of the study was to develop a non-human primate model of metabolic dysfunction in Macaca fascicularis using chronic high-fat diet (HFD) to mimic clinical disease progression.
methodsThirty-five male macaques aged 10-15 years underwent an 18-month HFD intervention. Physiological parameters (BMI, BP, hematology), liver fat fraction (evaluated by ultrasound/MRI), cardiac function (assessed by echocardiography), and histopathology (using liver biopsy) were measured before and after the intervention. Serum proteomics with KEGG/STRING analyses identified molecular mechanisms.
resultsWithin 6 months, HFD induced dyslipidemia (elevated TG, TCHO, HDL-C, LDL-C). After 18 months, metabolic dysfunction-associated steatohepatitis (MASH) was confirmed by histopathology in 57.14% (16/28) of macaques, diabetes (elevated FPG/HbA1c) in 17.86% (5/28), and myocardial hypertrophy (elevated LVMass/LAD) in 46.43% (13/28). Proteomics identified Bile acid-CoA: amino acid N-acyltransferase (BAAT) as a MASH hallmark protein, the level of which was inversely correlated with the degree of fibrosis. For diabetes, citrate synthase (CS) and malate dehydrogenase 1 (MDH1) impaired glucose oxidation via the TCA cycle, while hexose-6-phosphate dehydrogenase (H6PD) disrupted gluconeogenesis. Myocardial hypertrophy was associated with the downregulation of SRC proto-oncogene, non-receptor tyrosine kinase (SRC), mitogen-activated protein kinase 14 (MAPK14), emerin (EMD), and integrin subunit beta 1 (ITGB1).
conclusionsAn 18-month HFD successfully established a translational M. fascicularis model replicating key metabolic disorders (MASH, diabetes, cardiac hypertrophy). BAAT, CS/MDH1/H6PD, and SRC/MAPK14/EMD/ITGB1 were identified as mechanistic biomarkers for these conditions.
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