Abstract:
Background: Metabolic Syndrome (MetS) is a non-communicable disorder caused by impaired management and storage of energy, primarily caused by unhealthy diets, sedentary lifestyle and stress. It is diagnosed when an individual exhibits any three of the following: obesity or insulin resistance (primary), dyslipidemia (low HDL, hypertriglyceridemia), hypertension, and hyperglycemia. Globally, MetS affects approximately 14–34% of the population. As a cluster of interrelated conditions, current therapies target individual components rather than the syndrome, often requiring multiple drugs and increasing the risk of drug–drug interactions.
Materials and Methods: This study evaluated the effects of a high-fat diet (HFD; 30% fat) combined with dexamethasone on Sprague Dawley rats. HFD was administered for 3 months, with dexamethasone given twice weekly from day 15 until day 90. Rats were randomly divided into two groups (n=8). During this period, rats were monitored for various biochemical, physiological, and molecular parameters, including blood glucose, insulin levels, lipid profile, blood pressure, markers of oxidative stress and inflammation, and relevant tissue-specific molecular changes, to comprehensively assess metabolic alterations associated with high-fat diet and dexamethasone.
Result: The administration of HDF and Dexamethasone increased obesity (body weight, Lee index, adiposity index), hypertension (blood pressure), dyslipidemia (cholesterol, triglycerides, LDL/HDL ratio), hyperglycemia (glucose, α-glucosidase), and insulin resistance. Markers of oxidative stress and inflammation were also elevated, indicating metabolic imbalance. Additionally, combined HFD and dexamethasone disrupted gut microbial balance, promoting gut dysbiosis, and collectively contributed to metabolic imbalance characteristic of metabolic syndrome.
Discussion: High-fat diet and dexamethasone co-administration promoted metabolic dysfunction, affecting multiple parameters associated with metabolic syndrome and replicating its pathological features. This approach may serve as a reliable experimental model to study MetS and its underlying mechanisms, offering a preclinical model mimicking human MetS pathology.
