Science is still searching for readily available, cost-effective biomarkers to assess metabolic disorders occurring before the onset and during the development of type-2 diabetes (T2DM). The aim of the present study was to induce T2DM in rats through a high-fat diet, followed by a single administration of low dose streptozotocin (STZ), and make an assessment of the development of the disease. The rats were divided into two groups—experimental and control—and were monitored for a period of 10 days. Changes in anthropometric parameters, glucose, insulin, lipids, uric acid, advanced oxidation protein products (AOPP), as well as the histological changes in the liver and pancreas, were recorded. To assess insulin resistance, we used the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and beta cell function (HOMA-β) and visceral obesity—adiposity index (AI). The data demonstrate that the increasing values of glucose, HOMA-IR, AI, total cholesterol, triacylglycerols, low- and very-low-density lipoproteins are important markers of the pre-diabetic state. The stable hyperglycemia and increased levels of TC, TG, VLDL, LDL, uric acid and AOPP in experimental rats strongly suggest the development of T2DM. HOMA-IR, HOMA-β, AI, and uric acid are reliable criteria for T2DM in rats.

Background: The aim of the present study is to compare the potential of a high-fat diet, a high-carbohydrate diet, and a high-fat, high-carbohydrate diet to induce liver injury and visceral obesity within a period of five weeks, identify the pattern and degree of hepatic changes at the tissue level, identify the earliest metabolic markers of specific liver changes induced by each type of diet, and to test the possible beneficial effects of steviol glycosides in a rat experimental model. Methods: Wistar rats (n = 56) were divided into seven groups as follows: group BD (before diet), group SD (standard diet), group HFD (high-fat diet), group HCHD (high-carbohydrate diet), group HFHCHD (high-fat high-carbohydrate diet), group SDS (standard diet supplemented with Stevia extract), and group HFDS (high-fat diet supplemented with Stevia extract). Results: Total cholesterol concentrations (2.02 ± 0.22 mmol/L) increased in the HFD group (2.56 ± 0.82 mmol/L) and in the HFDS group (2.89 ± 0.48 mmol/L). The VLDL values before diets were 0.27 ± 0.11 mmol/L and increased most significantly in the HFHCHD group—1.14 ± 0.62 mmol/L. The baseline ALT values (88.4 ± 10.6 U/L) increased in the HFD group (128.13 ± 19.5 U/L) and the HFDS group (127.00 ± 17.74 U/L). Similar increases were registered in the AST/ALT ratio and ALP. Total bilirubin (7.10 ± 1.39 μmol/L) increased in HFD group (27.86 ± 17.01 μmol/L). Serum NO had the lowest values in groups fed diets supplemented with steviol glycosides. All high-calorie diets induced hepatocellular injury. The mass of the perirenal fat depot and cross-sectional area of adipocytes were highest in HFD, HFHCHD, and HFDS groups. Conclusion: High-calorie diets have the potential to induce visceral obesity and hepatocellular injury within a very short period of time, which produces characteristic histological changes and specific biochemical profile. Steviol glycosides may alleviate some aspects of the inflammatory response, but findings about lipid profile parameters and liver enzymes are controversial.