C. Muller et al., ENDOGENOUS GLUCOSE-PRODUCTION, GLUCONEOGENESIS AND LIVER-GLYCOGEN CONCENTRATION IN OBESE NONDIABETIC PATIENTS, Diabetologia, 40(4), 1997, pp. 463-468
Resting, post-absorptive endogenous glucose production (EGP), fraction
al gluconeogenesis and liver glycogen concentration were assessed in 6
lean and 5 obese non-diabetic subjects undergoing elective abdominal
surgery. During the 2 days preceding these measurements, 0.3 g/day U-C
-13 glucose had been added to their usual diet to label their endogeno
us glycogen stores. On the morning of day 3, EGP was measured with 6,6
-H-2 glucose. Their endogenous C-13 glycogen enrichment was calculated
from (CO2)-C-13 and respiratory gas exchanges. Fractional gluconeogen
esis was assessed as 1-(C-13 glucose/C-13 glycogen). 100. EGP was simi
lar in lean subjects (113 +/- 5 mg/min) and in obese subjects (111 +/-
6). Fractional gluconeogenesis was higher in obese (59 +/- 10%) than
in lean subjects (29 +/- 8%). However, overall EGP remained constant d
ue to a decrease in glycogenolysis. Since an increased gluconeogenesis
and a decreased glycogenolysis may both contribute to increase liver
glycogen concentration in obesity, hepatic glycogen concentrations wer
e assessed in hepatic needle biopsies obtained during surgery. Hepatic
glycogen concentrations were increased in obese patients (515 +/- 38
mg/g protein) compared to lean subjects (308 +/- 58, p < 0.05). It is
concluded that in obese patients: a) fractional gluconeogenesis is inc
reased; b) overall EGP is unchanged due to a proportional inhibition o
f glycogenolysis; c) liver glycogen concentration is increased.