Abstract

1. 1. Only when glucose is presented orally does the liver account for a major proportion of glucose uptake, indicating the presence of some factor in the gut that can augment the effects of insulin and/or hyperglycemia on the liver. 2. 2. It is proposed that glucose in the gut produces a reflex activation of hepatic parasympathetic nerves. These nerves produce a dramatic and rapid uptake of glucose and in the absence of cholinergic stimulation the liver is weakly affected by insulin, a state similar to that of the liver of the maturity-onset diabetic. 3. 3. Selective parasympathetic neuropathy is seen at the very early stages of diabetes. It is proposed that hepatic parasympathetic neuropathy results in a reduction of the liver's ability to trap glucose. 4. 4. This would account for the postprandial hyperglycemia seen in the maturity-onset diabetic. This hyperglycemia leads, in turn, to hyperinsulinism and thence to peripheral insulin resistance.

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