Increased gluconeogenesis in rats exposed to hyper-G stress

Area of Science:

• Physiology
• Biochemistry
• Gravitational Biology

Background:

• Hyper-G stress, or radial acceleration, significantly impacts physiological systems.
• Understanding metabolic responses to G-force is crucial for aerospace medicine and physiology.
• Gluconeogenesis is a key pathway for glucose production, particularly during fasting or stress.

Purpose of the Study:

• To determine the role of gluconeogenesis in elevated plasma glucose and liver glycogen during hyper-G stress.
• To investigate the involvement of epinephrine in these metabolic changes.

Main Methods:

• Rats were injected with 14C-labeled lactate, alanine, or glycerol and exposed to 3.1G for varying durations.
• 14C incorporation into plasma glucose and liver glycogen was measured.
• Gluconeogenesis was inhibited using 5-methoxyindole-2-carboxylic acid; adrenergic blockade was achieved with propranolol; adrenal medulla removal was performed.

Main Results:

• Hyper-G stress significantly increased 14C incorporation from all substrates into plasma glucose and, at later time points, into liver glycogen.
• Inhibition of gluconeogenesis blocked the observed increases in glucose and glycogen.
• Adreno-demedullation and beta-adrenergic blockade abolished or suppressed the glucose and glycogen increases.

Conclusions:

• The rapid increase in plasma glucose and liver glycogen under hyper-G stress is primarily due to enhanced gluconeogenesis.
• Epinephrine plays a dominant role in mediating these early metabolic responses to centrifugation stress.