Syndrome-AC: noninsulin-dependent diabetes mellitus and the anabolic/catabolic paradox

Abstract 

When an organism is starving, infected or injured, the body initiates a catabolic response that, among other things, creates insulin resistance. While many possible mechanisms and numerous loci of insulin resistance have been studied, a theme of inappropriately activated components of catabolic chemistry emerges. Patients with noninsulin-dependent diabetes mellitus (NIDDM) have elevated blood levels of glucagon, cortisol, fatty acids, protein, glucose and possibly acute phase reactants. Recent studies hint that this can occur with meals, resulting in a multilevel, multiorgan interference with glucose handling. This implies NIDDM is the result of the dietary activation of catabolic chemistry simultaneously with that of anabolic chemistry. We review the possibility that this is caused by the consumption of body tissue, the substance ordinarily endogenously released in starvation or injury. Activating the catabolic pathways when eating creates a hormonal paradox, forcing exaggerated insulin levels to compensate. Five case studies are reviewed.

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