Effect of a 3-day fast on glucose storage and oxidation in obese hyperinsulinemic diabetics

Glucose disposal was measured for a 3-hr period after a 100-g oral glucose load by means of a new adaptation of continuous indirect calorimetry in 6 obese hyperinsulinemic diabetics and 5 nonobese normal subjects who served as the control. While total glucose oxidized during the 3-hr test was not significantly lower in the obese diabetic group (31 ± 3 g) than in the control group (37 ± 3 g), a marked impairment of net glucose storage was observed in the former group (26 ± 7 g) in comparison to the control group (64 ± 3 g; p < 0.001). This marked decrease in net glucose storage suggests that a limited capacity for glucose storage might play a major role in glucose intolerance in these cases of obese hyperinsulinemic diabetes. In the obese diabetic group, after a 3-day fast supplemented with protein, the plasma glucose values dropped significantly both in the fasting state and in response to the glucose load. This was accompanied by a marked improvement of glucose storage (52 ± 9 versus 26 ± 7 g before the fast; p < 0.001), a decrease in glucose urinary loss (5 ± 1 g versus 14 ± 4 g prior to fast), but a marked impairment in glucose oxidation (13 ± 1 g versus 31 ± 3 g before fast; p < 0.001). In the control group, a moderate impairment of glucose tolerance was observed, probably related to the important decrease in glucose oxidation (12 ± 3 g versus 37 ± 3 g prior to fast), in spite of the increase in glucose storage (82 ± 4 g versus 64 ± 3 g prior to fast). These observations suggest that glucose intolerance observed in obese hyperinsulinemic diabetics in the postabsorptive state might result at least in part from deficiency in net glucose storage capacity. The marked lowering of the plasma glucose tolerance curve in the same subjects after a 3-day period of fast is probably a consequence of the overall effect of a decrease in the glucose pool and an increase in net glucose storage in spite of a decrease in glucose oxidation and in urinary glucose loss. It does not exclude, however, other factors, such as changes in tissue insulin sensitivity.