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Animal and culture studies have indicated a neuroprotective role for brain glycogen during glucose deprivation, which could not be tested in the human brain due to lack of non-invasive methodology until recently. Using in vivo [sup 13]C NMR spectroscopy we have shown that the human brain stores 3-4 µmol/g glucose units in the form of glycogen, but turns this store over slowly at euand slight hyperglycemia (turnover time constant ∼ 1 day). We hypothesized that glycogen represents a significant glucose reservoir in the brain which can be mobilized to support cerebral energy metabolism during hypoglycemia. To test this hypothesis, we administered IV 186 g of 99% enriched [1-[sup 13]C]glucose to 4 healthy volunteers (3 M / 1 F, age 41 ± 14, BMI 24 ± 2 kg/m²) over 11 ± 1 h to pre-label glycogen. Average blood glucose levels during the infusion were 133 ± 17 mg/dL and average isotopic enrichment of plasma glucose 70 ± 10% (by GC-MS). Following the infusion (5 ± 1 h after), each participant underwent a 2 h long hyperinsulinemic, euglycemic (96 ± 3 mg/dL blood glucose) and a 2 h long hyperinsulinemic, hypoglycemic (.53 ± 5 mg/dL blood glucose) clamp separated by at least one week. Counterregulation was demonstrated by measurement of serum glucagon (basal 57 a: 28 (mean ± SD) pg/mL vs. peak 159 ± 89 pg/mL), growth hormone (basal 3 ± 3 ng/mL vs. peak 34 ± 17 ng/mL), cortisol (basal 13 ± 4 µg/dL vs. peak 38 ± 14 µg/dL) and catecholamines (norepinephrine basal 153 ± 118 pg/mL vs. peak 226 ± 152 pg/mL; epinephrine basal 26 ± 22 pg/mL vs. peak 301 ± 176 pg/mL) during hypoglycemia. [1-[sup 13]C]glycogen concentration in the brain was measured by [sup 13]C NMR at 4 tesla during the clamps. The rate of label wash-out from [1-[sup 13]C]glycogen was higher during hypoglycemia (0.12 ± 0.05 µmol/g/h) than during euglycemia (0.01 ± 0.05 µmol/g/h, p = 0.02) indicating mobilization of glucose units from glycogen during moderate hypoglycemia. This is the first evidence for glycogen utilization in the human brain during hypoglycemia. Together with our previous results regarding very slow turnover of bulk brain glycogen under normal physiology, they support the hypothesis that brain glycogen supports energy metabolism when glucose supply from the blood is inadequate. [ABSTRACT FROM AUTHOR]

The article discusses the results of a clinical study examining the risk of glucose intolerance and diabetes among hemipancreas donors. The authors have hypothesized that about 25% of hemipancreas donors since 1997 would display abnormal glucose tolerance on follow-up. The study involved 21 subjects who undergone hemipancreatectomy between 1997-2003.