O. Ye. Akimov¹*, A. O. Mykytenko², V. O. Kostenko¹

¹Department of Pathophysiology, Poltava State Medical University, Poltava, Ukraine;
*e-mail: o.akimov@pdmu.edu.ua;
²Department of Biological and Bioorganic Chemistry,
Poltava State Medical University, Poltava, Ukraine

Received: 22 May 2025; Revised: 24 July 2025;
Accepted: 12 September 2025; Available on-line: 17 September 2025

The populace of Ukraine shows a trend of increasing percentage of persons with obesity, complicated by metabolic syndrome (MetS), which causes damage to the heart extracellular matrix. According to recent studies chromium, picolinate (CrPIC) has the potential to attenuate lipid metabolism disorders and protect the extracellular matrix from degradation. The aim of this research was to estimate the blood lipid profile and the content of glycosaminoglycans, L-hydroxyproline and sialic acids in the heart of rats with simulated metabolic syndrome under Chromium picolinate administration. Mature male Wistar rats were divided into 4 groups of 6 animals each – control; metabolic syndrome induction; CrPIC administration; metabolic syndrome + CrPIC administration. Metabolic syndrome was reproduced by using a 20% fructose solution as the only source of water for 60 days. CrPIC was administered orally at a dose of 80 µg/kg daily for 60 days. The concentration of the heart extracellular matrix degradation proteins was determined spectrophotometrically in a 10% heart homogenate. CrPIC administration to healthy animals stimulated the accumulation of glycosaminoglycans chondroitin fraction in the rat heart. Metabolic syndrome modeling resulted in an increase in TG, TC and LDL-C blood levels, intensification of collagenolysis, degradation of glycoproteins and glycosaminoglycans with a predominance of the keratan-dermatan fraction. CrPIC administration to animals with metabolic syndrome reduced collagenolysis and glycoproteins degradation, changed the dominating fraction of glycosaminoglycans from keratan-dermatan to chondroitin in rat heart connective tissue indicating its potential to prevent cardiac tissue remodeling during metabolic syndrome.