Abstrakt
Purpose of review Stores of glucose (Glc) in our body are small compared with protein and lipid. Therefore, at times of famines or trauma/disease-related starvation, glucose utilization must be limited only to pathways that can only run with glucose carbon as substrate.
We will try to outline how insulin resistance drives these pathways and inhibits glucose oxidation in the stressed organism. Recent findings Glc is a basic substrate for a variety of other biomolecules like nucleic acids, amino acids, proteoglycans, mucopolysaccharides and lipids.
It is essential for the formation of reducing equivalents, indispensable for anabolic, antioxidative, regulatory and immune processes. As a result, a continuous Glc turnover/cycle is essential to secure at all times the Glc requirements for nonoxidative pathways mentioned above but then requires introduction of extra glucose or other intermediates into the cycle.
The production of ATP through complete Glc oxidation occurs only when Glc intake is higher than required for its nonoxidative metabolism. Insulin resistance and decreased Glc oxidation indicate that requirements of Glc for anabolic pathways are high.
Glc is an important building block for anabolic reactions and substrate for reducing equivalents formation. Insulin resistance prevents irreversible Glc oxidation and stimulates Glc production during stress or growth.
Glc is only oxidized when intake is in excess of its anabolic requirements.