Search

Intracellular glucose concentration in skeletal muscle of awake rats was determined under conditions of hyperglycemic (10.2 ± 0.6 mM) hyperinsulinemia (∼1,200 pM) and hyperglycemic (20.8 ± 1.5 mM) hypoinsulinemia (13C nuclear magnetic resonance (NMR) spectroscopy during a prime-constant infusion of [1-13C]glucose and [1-13C]mannitol with either insulin (10 mU ⋅ kg−1⋅ min−1) or somatostatin (1.0 μg ⋅ kg−1⋅ min−1). Intracellular glucose was calculated as the difference between the concentrations of total tissue glucose (calculated from the in vivo13C NMR spectrum with mannitol as an internal concentration standard) and extracellular glucose, corrected by the ratio of intra- and extracellular water space. Extracellular concentration was corrected for an interstitial fluid-to-plasma glucose concentration gradient of 0.83 ± 0.07, determined by open-flow microperfusion. The mean ratio of intra- to extracellular glucose space, determined from the relative NMR signal intensities and concentrations of mannitol and total creatine, was 9.2 ± 1.1 (hyperglycemic hyperinsulinemia, n = 10), and 9.0 ± 1.7 (hyperglycemic hypoinsulinemia, n= 7). Mean muscle intracellular glucose concentration was

Whether liver glycogen synthesis and breakdown occur simultaneously during net glycogen synthesis was assessed in fed and fasted healthy humans. The peak intensity of the carbon-1 (C1) resonance of the glycosyl units of glycogen was monitored with 13C nuclear magnetic resonance spectroscopy during [1-13C]glucose infusion followed by unlabeled glucose infusion. The C1 peak intensity increased almost linearly during the [1-13C]glucose infusion, reflecting a near linear rate of glycogen synthesis. When switched to unlabeled glucose, the C1 peak intensity reached a plateau in the fasted subjects and declined in the fed subjects, reflecting active glycogenolysis during a time of net glycogen synthesis. We conclude that liver glycogen synthesis and degradation occur simultaneously in humans under conditions of net glycogen synthesis. The relative turnover rate was significantly higher in the fed (57 +/- 3%) than in the fasted state (31 +/- 8%; P < 0.01). The results indicate that glycogen may regulate its rate of breakdown and that liver glycogen turnover may be an important factor in limiting the accumulation of liver glycogen in humans.