Chronic sucrose consumption in mice reveals organ-specific metabolic disruptions

Researchers at the Advanced Research Unit on Metabolism, Development & Aging (ARUMDA), in the Tata Institute of Fundamental Research (TIFR, Mumbai and TIFR Hyderabad), have recently conducted a groundbreaking study on the detrimental effects of sugar-sweetened beverages (SSBs) on human health. Using a preclinical mouse model that closely resembles human consumption patterns, the study aimed to provide a comprehensive understanding of the impact of chronic sucrose intake on various physiological processes.

Published in The Journal of Nutritional Biochemistry, the study revealed how chronic sucrose-water consumption at a 10% concentration can lead to significant alterations in key physiological, molecular, and metabolic processes across multiple organs. These changes can ultimately contribute to the development of diseases such as diabetes and obesity.

One of the key findings of the study was the identification of the small intestine as a central player in metabolic dysregulation caused by excessive sucrose consumption. The researchers discovered that chronic intake of sucrose can create a “molecular addiction” in the intestinal lining, leading to imbalanced absorption of glucose over other essential nutrients like amino acids and fats. This disruption in nutrient uptake can disrupt energy metabolism and exacerbate dysfunction in other organs such as the liver and muscles.

Additionally, the study highlighted the differences in physiological responses under fed and fasted states due to chronic sucrose intake. The researchers observed distinct anabolic and catabolic responses in fed versus fasted states, underscoring the importance of nutrient allocation and resource mobilization in systemic metabolic disorders.

Furthermore, the study shed light on the effects of chronic sucrose consumption on the liver and skeletal muscles. Despite increased glucose absorption, the liver did not exhibit altered gene expression related to glucose metabolism. Instead, systemic insulin resistance was triggered, leading to metabolic imbalance. In skeletal muscles, mitochondrial dysfunction and reduced efficiency in glucose utilization were observed, contributing to the impaired metabolic state.

The implications of these findings for public health are significant, emphasizing the urgent need for policies and awareness campaigns to reduce SSB consumption, particularly among vulnerable populations. The identification of tissue-specific effects provides a roadmap for developing targeted therapies to address the global burden of metabolic diseases associated with high sugar intake.

By understanding the tissue-specific mechanisms at play, researchers suggest that targeting intestinal nutrient transport pathways and mitochondrial function across tissues could be potential strategies to mitigate the metabolic effects of SSB consumption. This study contributes valuable insights to the ongoing efforts to combat the metabolic disorders linked to excessive sugar consumption on a global scale.