Publications by authors named "Sebastian T Thrane"
Article Synopsis
- The diabetic heart exhibits changes that lead to a higher risk of contractile failure, with chronic sympathetic activation being a key factor in heart failure development.
- In a study using a diabetic rat model, researchers tested how repeated β-adrenergic stimulation (via isoprenaline) affected heart metabolism and mitochondrial function, hypothesizing that type 1 diabetic hearts would handle this stress better.
- The results indicated that while both diabetes and isoprenaline impaired heart mitochondrial respiration, the diabetic rats showed resilience and improved energy status when subjected to isoprenaline, suggesting that adrenergic stimulation could have protective effects in type 1 diabetes.
Cardiovascular and renal complications are the predominant causes of morbidity and mortality amongst patients with diabetes. Development of novel treatments have been hampered by the lack of available animal models recapitulating the human disease. We hypothesized that experimental diabetes in rats combined with a cardiac or renal stressor, would mimic diabetic cardiomyopathy and nephropathy, respectively.
View Article and Find Full Text PDFDiabetic nephropathy (DN) is associated with albuminuria and loss of kidney function and is the leading cause of end-stage renal disease. Despite evidence of sex-associated differences in the progression of DN in human patients, male mice are predominantly being used in preclinical DN research and drug development. Here, we compared renal changes in male and female uninephrectomized (UNx) db/db C57BLKS mice using immunohistochemistry and RNA sequencing.
View Article and Find Full Text PDFBackground: The trans-fat containing AMLN (amylin liver non-alcoholic steatohepatitis, NASH) diet has been extensively validated in C57BL/6J mice with or without the Lep/Lep () mutation in the leptin gene for reliably inducing metabolic and liver histopathological changes recapitulating hallmarks of NASH. Due to a recent ban on trans-fats as food additive, there is a marked need for developing a new diet capable of promoting a compatible level of disease in and C57BL/6J mice.
Aim: To develop a biopsy-confirmed mouse model of NASH based on an obesogenic diet with trans-fat substituted by saturated fat.