Refined Carbohydrate-Rich Diet Promotes Early Myocardial Dysfunction Associated with Adiponectin Reduction, Inflammation, and Impaired Ca2+ Handling in Female Rats.

Introduction

Diets rich in refined carbohydrates are associated with cardiometabolic dysfunction, but the mechanisms linking metabolic disturbances to myocardial impairment in females remain unclear. This study investigated the effects of short-term consumption of a refined carbohydrate-rich diet on papillary muscle contractility in female rats.

Methods

Adult female Wistar rats were assigned to either a control diet (CT) or a high-carbohydrate diet (HCD) for 15 days. The HCD consisted of 45% sweetened condensed milk, 10% refined sugar, and 45% standard chow. Metabolic, inflammatory, functional, and molecular parameters were evaluated. Myocardial contractility and intracellular Ca2+ handling were assessed in isolated left ventricular papillary muscles, while phospholamban (PLB), SERCA2a, and NCX1 protein expression were analyzed.

Results

The HCD increased ovarian adipose tissue, triglyceride levels, glucose intolerance, and TNF-α levels, while decreasing HDL cholesterol and circulating adiponectin. Leptin and MCP-1 levels were unchanged. Functional assessments revealed impaired cardiac contractility, evidenced by reduced papillary muscle force and lower positive force derivative (dF/dt+). HCD also decreased post-pause potentiation and post-rest contraction, indicating impaired sarcoplasmic reticulum (SR) Ca2+ storage and release, as well as potentially reduced extracellular calcium influx. At the molecular level, PLB expression was increased, whereas SERCA2a and NCX1 expression remained unchanged.

Conclusions

Short-term consumption of a refined carbohydrate-rich diet induces early cardiac contractile dysfunction in female rats, associated with impaired Ca2+ handling, reduced adiponectin, and increased inflammation, suggesting that metabolic and inflammatory disturbances precede structural cardiac alterations and may promote cardiometabolic disease development.