Myocardial Disorders in BDNF-Deficient Rats: Limited Recovery Post-Moderate Endurance Training DOI Creative Commons

Norbert Grzelak,

Dominik Kaczmarek,

Krystian Poziemba

и другие.

Diabetes Metabolic Syndrome and Obesity, Год журнала: 2024, Номер Volume 17, С. 4649 - 4660

Опубликована: Дек. 1, 2024

Introduction: The study aimed to determine whether heterozygous BDNF-deficient (BDNF-knockout, SD-BDNF) rats exhibit pathological changes in the myocardium and assess a 5-week moderate-intensity endurance training program can reverse adverse heart muscle. Methods: Experiments were conducted on four groups of rats: control wild-type, BDNF knockout, trained wild-type knockout. Knockout selected due presence symptoms resembling metabolic syndrome serum liver while moderate was used as an intervention targeted at restoring function. Measurements BDNF/Trk-B concentrations molecules levels activities, such cardiac specific enzymes like creatine kinase myocardial band, lipids total cholesterol, low-density lipoprotein triglycerides, including alanine aminotransferase, aspartate gamma-glutamyl transferase lactate dehydrogenase interleukin-1 carried out homogenates. Results: In rats, showed significantly reduced lipid concentrations, decreased enzyme activity, elevated Trk-B levels, all which are indicative ischemia or hypoxia. These critical biomarkers consistent with those earlier observed livers suggesting link between Moderate led increase activity increased production utilization energy required for contraction knockout populations rats. Discussion: exhibited numerous abnormalities, most not reversible after training. findings provide basis deeper understanding mechanisms underlying disorders appear be suitable model studying various aspects disorders. Keywords: BDNF, Trk-B, gene-deficiency heart,

Язык: Английский

(Epi)genetic Aspects of Metabolic Syndrome Pathogenesis in Relation to Brain-derived Neurotrophic Factor Expression: A Review DOI Creative Commons
Н. М. Тодосенко, K. А. Yurova, О. Г. Хазиахматова

и другие.

Gene Expression, Год журнала: 2024, Номер 23(2), С. 127 - 138

Опубликована: Май 8, 2024

A key element in the pathogenesis of metabolic syndrome (MetS) is reprogramming hypothalamic cells at genetic level (in prenatal phase), which leads to neuroinflammation. We hypothesize that alterations structure neurons mediated by (epi)genetic are directly related impaired expression/production neurotrophins and neurotransmitters control metabolism substances brain periphery, including brain-derived neurotrophic factor (BDNF). The aim this review describe molecular epigenetic role BDNF development MetS. Articles entered into National Library Medicine Medline database via PubMed interface were used create review. attempted include as much literature possible, reviews, animal studies, cell culture clinical trials. Studies on point its processes, glucose, insulin, cholesterol homeostasis. Evidence-based studies show multiple genes close proximity involved aimed analyzing diseases using different biological samples will reveal clear pathophysiological links between processes periphery.

Язык: Английский

Процитировано

2
Myocardial Disorders in BDNF-Deficient Rats: Limited Recovery Post-Moderate Endurance Training DOI Creative Commons

Norbert Grzelak,

Dominik Kaczmarek,

Krystian Poziemba

и другие.

Diabetes Metabolic Syndrome and Obesity, Год журнала: 2024, Номер Volume 17, С. 4649 - 4660

Опубликована: Дек. 1, 2024

Introduction: The study aimed to determine whether heterozygous BDNF-deficient (BDNF-knockout, SD-BDNF) rats exhibit pathological changes in the myocardium and assess a 5-week moderate-intensity endurance training program can reverse adverse heart muscle. Methods: Experiments were conducted on four groups of rats: control wild-type, BDNF knockout, trained wild-type knockout. Knockout selected due presence symptoms resembling metabolic syndrome serum liver while moderate was used as an intervention targeted at restoring function. Measurements BDNF/Trk-B concentrations molecules levels activities, such cardiac specific enzymes like creatine kinase myocardial band, lipids total cholesterol, low-density lipoprotein triglycerides, including alanine aminotransferase, aspartate gamma-glutamyl transferase lactate dehydrogenase interleukin-1 carried out homogenates. Results: In rats, showed significantly reduced lipid concentrations, decreased enzyme activity, elevated Trk-B levels, all which are indicative ischemia or hypoxia. These critical biomarkers consistent with those earlier observed livers suggesting link between Moderate led increase activity increased production utilization energy required for contraction knockout populations rats. Discussion: exhibited numerous abnormalities, most not reversible after training. findings provide basis deeper understanding mechanisms underlying disorders appear be suitable model studying various aspects disorders. Keywords: BDNF, Trk-B, gene-deficiency heart,

Язык: Английский

Процитировано

0