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Effects of Obesity and Diabesity on Ventricular Muscle Structure and Function in the Zucker Rat

(1) Background: Cardiovascular complications are a leading cause of morbidity and mortality in diabetic patients. The effects of obesity and diabesity on the function and structure of ventricular myocytes in the Zucker fatty (ZF) rat and the Zucker diabetic fatty (ZDF) rat compared to Zucker lean (Z...

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Detalles Bibliográficos
Autores principales: Sultan, Ahmed, Adeghate, Ernest, Emerald, Bright Starling, Qureshi, Muhammad A., Minhas, Saeed Tariq, Howarth, Frank Christopher
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9410105/
https://www.ncbi.nlm.nih.gov/pubmed/36013400
http://dx.doi.org/10.3390/life12081221
Descripción
Sumario:(1) Background: Cardiovascular complications are a leading cause of morbidity and mortality in diabetic patients. The effects of obesity and diabesity on the function and structure of ventricular myocytes in the Zucker fatty (ZF) rat and the Zucker diabetic fatty (ZDF) rat compared to Zucker lean (ZL) control rats have been investigated. (2) Methods: Shortening and intracellular Ca(2+) were simultaneously measured with cell imaging and fluorescence photometry, respectively. Ventricular muscle protein expression and structure were investigated with Western blot and electron microscopy, respectively. (3) Results: The amplitude of shortening was increased in ZF compared to ZL but not compared to ZDF myocytes. Resting Ca(2+) was increased in ZDF compared to ZL myocytes. Time to half decay of the Ca(2+) transient was prolonged in ZDF compared to ZL and was reduced in ZF compared to ZL myocytes. Changes in expression of proteins associated with cardiac muscle contraction are presented. Structurally, there were reductions in sarcomere length in ZDF and ZF compared to ZL and reductions in mitochondria count in ZF compared to ZDF and ZL myocytes. (4) Conclusions: Alterations in ventricular muscle proteins and structure may partly underlie the defects observed in Ca(2+) signaling in ZDF and ZF compared to ZL rat hearts.