Using 13C MRS, it was shown that, while fasting hepatic glycogen concentrations were similar between MODY-2 patients and controls, glucokinase-deficient MODY-2 patients had a 30–60% lower net increment of hepatic glycogen and relatively elevated hepatic gluconeogenesis after meals [47]. The gene discussed is GCK; the disease is maturity-onset diabetes of the young type 2.