Mechanisms underlying electro-mechanical dysfunction in the Zucker diabetic fatty rat heart: a model of obesity and type 2 diabetes

Abstract

Diabetes mellitus (DM) is a major and worsening global health problem, currently affecting over 450 million people and reducing their quality of life. Type 2 diabetes mellitus (T2DM) accounts for more than 90% of DM and the global epidemic of obesity, which largely explains the dramatic increase in the incidence and prevalence of T2DM in the past 20 years. Obesity is a major risk factor for DM which is a major cause of morbidity and mortality in diabetic patients. The electro-mechanical function of the heart is frequently compromised in diabetic patients. The aim of this review is to discuss the pathophysiology of electro-mechanical dysfunction in the diabetic heart and in particular, the Zucker diabetic fatty (ZDF) rat heart, a well-studied model of T2DM and obesity.

1H‐NMR‐based metabolomics reveals the preventive effect of Enteromorpha prolifera polysaccharides on diabetes in Zucker diabetic fatty rats

“…Enteromorpha prolifera polysaccharide (EP) has been extensively studied for its various biological activities, such as anticoagulant, antioxidant, immunoregulatory, anti‐inflammatory, antitumor, antiaging, and hypolipidemic effects (Chen et al., 2022 ; Zhong et al., 2020 ). In this work, we investigated the hypoglycemic effect of EP in male Zucker diabetic fatty (ZDF) rats, which are known to be spontaneously obese and hyperglycemic due to defects in the leptin receptor and low inherited insulin promoter activity (Sultan et al., 2020 ). Our results showed that the EP group exhibited lower FBG, fasting insulin, and HbA1c levels than the DM group, indicating that EP effectively prevents the continuous increase in blood glucose levels associated with functional defects.…”

Oxidative stress signaling in the pathogenesis of diabetic cardiomyopathy and the potential therapeutic role of antioxidant naringenin

“…In animal models of heart failure, the impairment of systolic and diastolic cardiac function was associated with increased ROS levels in cardiomyocytes [ 37 , 38 ]. ROS generation and activation of the antioxidant system were detected in cardiomyocytes of leptin receptor deficient db/db mice, severe hyperglycemia, and type 2 diabetes [ 39 , 40 ]. Excessive ROS production caused damage to cellular proteins, nucleic acids, lipids and other biomolecules [ 41 , 42 ], and also destroyed cellular antioxidant defense system, resulting in disturbance of apoptosis-related molecular signaling pathways [ 43 , 44 ].…”