Short Communication - Current Trends in Cardiology (2023) Volume 7, Issue 10
Glucose metabolic changes in heart failure: Beyond ATP ProductionSimei Sun*
Department of Laboratory Medicine, Chonnam National University, Medical School and Hospital, Gwangju, Republic of Korea
- *Corresponding Author:
- Simei Sun
Department of Laboratory Medicine
Chonnam National University
Medical School and Hospital
Gwangju, Republic of Korea
Received: 29-Sep-2023, Manuscript No. AACC-23-114287; Editor assigned: 03-Oct-2023, Pre QC No. AACC-23-114287(PQ); Reviewed: 18-Oct-2023, QC No. AACC-23-114287; Revised: 23-Oct-2023, Manuscript No. AACC-23-114287(R), Published: 30-Oct-2023,DOI:10.35841/aacc-7.10.215
Citation: Sun S. Glucose metabolic changes in heart failure: Beyond ATP production. J Cell Biol Metab. 2023;7(9):215
Heart failure is a complex and debilitating condition that affects millions of individuals worldwide. It occurs when the heart is unable to pump blood effectively, leading to a reduced supply of oxygen and nutrients to the body's tissues. While the role of glucose metabolism in providing adenosine triphosphate (ATP), the cellular energy currency, is well understood, recent research has revealed that glucose metabolic changes in heart failure go far beyond ATP production. These metabolic alterations play a pivotal role in the progression of heart failure, making them an important area of study in the quest for better treatment options and improved patient outcomes .
The role of glucose in the heart
The heart is a highly energy-demanding organ, and ATP is essential for its normal functioning. Under healthy conditions, the heart primarily relies on fatty acids as its main energy source. However, glucose metabolism also plays a crucial role in meeting the heart's energy demands, especially during periods of increased workload or stress .
Glucose metabolic changes in heart failure
In heart failure, several metabolic changes in glucose utilization become evident, contributing to the progression of the disease. These changes go beyond ATP production and have far-reaching implications for cardiac function. One of the prominent metabolic changes in heart failure is a shift in substrate preference. Instead of predominantly using fatty acids for energy, the failing heart increasingly relies on glucose as its primary fuel source. This shift is not necessarily beneficial, as it can impair cardiac function due to the reduced efficiency of ATP production from glucose.
Impaired mitochondrial function: Mitochondria, the energyproducing powerhouses of cells, play a crucial role in glucose metabolism. In heart failure, there is often mitochondrial dysfunction, which impairs oxidative phosphorylation and reduces ATP production. This dysfunction further exacerbates energy deficits in the failing heart .
Insulin resistance: Heart failure is associated with systemic metabolic changes, including insulin resistance. Insulin resistance reduces the ability of cells, including cardiac myocytes, to take up glucose, leading to increased blood glucose levels. Elevated blood glucose can exacerbate cardiac dysfunction and contribute to the progression of heart failure.
Increased lactate production: The shift towards glycolysis in the failing heart can lead to increased production of lactate, a byproduct of anaerobic metabolism. Elevated lactate levels can further compromise cardiac function and contribute to a state of metabolic acidosis, negatively impacting overall health.
Beyond ATP production: Implications for treatment
Understanding the broader implications of glucose metabolic changes in heart failure is essential for developing targeted therapies that address the underlying causes of the disease. While ATP production is crucial, addressing the multifaceted aspects of glucose metabolism can offer new avenues for treatment and potentially improve patient outcomes.
Metabolic modulators: Researchers are exploring various metabolic modulators that can optimize glucose utilization in the failing heart. These modulators aim to restore the balance between fatty acid and glucose oxidation, improving overall cardiac efficiency.
Mitochondrial therapies: Given the importance of mitochondrial dysfunction in heart failure, therapies aimed at restoring mitochondrial function are being investigated. These approaches seek to enhance oxidative phosphorylation and improve ATP production from glucose .
Targeting insulin resistance: Managing insulin resistance through lifestyle interventions and pharmacological treatments can help regulate blood glucose levels in heart failure patients. Improved glycemic control may alleviate some of the metabolic stress on the heart.
Reducing lactate accumulation: Strategies to reduce lactate production and accumulation in the heart are under investigation. These approaches may involve optimizing the balance between glycolysis and oxidative phosphorylation or improving lactate clearance mechanisms .
Glucose metabolic changes in heart failure extend beyond ATP production and have significant implications for the progression of the disease. Understanding these metabolic alterations opens the door to novel treatment strategies that address the root causes of heart failure and aim to improve cardiac function and overall patient outcomes. As research in this field continues to advance, we may see the development of more effective therapies that offer hope to the millions of individuals living with heart failure worldwide.
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