Metabolic Dysregulation in Microgravity: A Focus on Carbohydrate Utilization during Space Missions

Résumé

Exposure to microgravity during spaceflight induces significant physiological adaptations that disrupt metabolic homeostasis, particularly carbohydrate metabolism. This study reviews current evidence on the effects of microgravity on glucose regulation, insulin sensitivity, skeletal muscle function, and hepatic glucose metabolism. Findings from human spaceflight and ground-based analogs, such as bed rest and head-down tilt studies, consistently demonstrate the development of peripheral insulin resistance under microgravity conditions. This is largely attributed to skeletal muscle unloading, which leads to muscle atrophy, reduced mitochondrial oxidative capacity, and impaired insulin signaling, particularly along the IRS-1/PI3K/Akt pathway, resulting in decreased GLUT4 mediated glucose uptake. In addition, the suppression of contraction-mediated glucose transport further limits glucose utilization in skeletal muscle. Compensatory increases in hepatic glucose production, driven by enhanced gluconeogenesis and glycogenolysis and influenced by hormonal changes, including elevated cortisol and glucagon levels, contribute to altered glucose homeostasis. Although fasting glucose levels often remain within normal ranges, postprandial hyperglycemia and reduced insulin sensitivity are commonly observed. These metabolic alterations closely resemble early features of insulin resistance and type 2 diabetes, albeit developing over a much shorter timescale in microgravity. Current countermeasures, including exercise and nutritional interventions, provide partial mitigation but do not fully restore metabolic function during prolonged exposure. This review highlights the need for integrated strategies to preserve carbohydrate metabolism in long-duration space missions. It underscores the relevance of microgravity research in understanding and managing metabolic disorders on Earth

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