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L-diabetes--causes, pathogenesis and therapy.

Franz-Peter Liebel·Elke Zimmermann
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Abstract

L-diabetes represents a subtype of non-autoimmunopathic and non-adipose diabetes mellitus. It is hypothesized that ATP-sensory brain centres measure the cerebral ATP concentration and announce a hypoglycaemia if the setpoint is undercut. The disease involves a decreased ATP formation in the CNS that is independent of blood glucose levels, and that leads to a "hypoglycaemia" false alarm. UGT1-polymorphisms, a sensitive sympathetic system, an IgM deficit and an increased porousity of the mucous membrane of the small intestine have been postulated in its etiology. These causative factors bring about increasing amounts of toxins and radicals which impair the ATP generation in the CNS so that through the announcement of a non-existing hypoglycaemia the release of the insulin antagonists hGH, cortisol and adrenaline is induced.

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Adenosine TriphosphateDiabetes MellitusEpinephrineFeedback, PhysiologicalGlucuronosyltransferaseGrowth HormoneHumansHydrocortisoneHypoglycemiaImmunoglobulin MInsulin AntagonistsModels, BiologicalMucous MembranePolymorphism, GeneticSympathetic Nervous SystemTelencephalonJournal Article

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Franz-Peter Liebel, Elke Zimmermann. 2006-06-02. L-diabetes--causes, pathogenesis and therapy.. https://doi.org/10.1016/j.mehy.2006.02.048

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