Carbohydrate and lipid oxidation was measured in normal and diabetic human beings by means of continuous indirect calori metry in the course of a 100-gm. oral glucose tolerance test.
After the glucose load, the carbohydrate (CHO) oxidation rate of 10 control subjects gradually rose, from 30 to 180 minutes, during the decline of plasma glucose and immunoreactive insulin (IRI). The lipid oxidation rate decreased during the same period.
Diabetics were divided into two groups. In a group of six nonobese maturity-onset diabetics with a slight IRI response to glucose load and a fall in plasma free fatty acid (FFA) levels, the CHO oxidation rate was found to be of the same order of magnitude as in normal subjects, but this occurred at a high plasma concentration of glucose. The lipid oxidation rate decreased as in normal subjects.
Conversely, in a group of four juvenile-type diabetics with no IRI response to glucose load and no fall in FFA levels, the CHO oxidation rate was markedly diminished and the lipid oxidation rate presented only a slight fall after glucose load.
In the group of maturity-onset diabetics, a slight insulin secretion seemed to be sufficient to prevent lipolysis and to allow normal rates of lipid and CHO oxidation in response to glucose load. On the other hand, in the group of juvenile-type diabetics, the lack of endogenous insulin secretion seemed to be responsible for increased lipolysis, leading to decreased responses of lipid and CHO oxidation to glucose load.