KETOSIS RESISTANCE IN FIBROCALCULOUS PANCREATIC DIABETES .2. HEPATIC KETOGENESIS AFTER ORAL MEDIUM-CHAIN TRIGLYCERIDES

A majority of patients with fibrocalculous pancreatic diabetes (FCPD) do not become ketotic even in adverse conditions. It is not clear whet her this ketosis resistance is due td reduced fatty acid release from adipose tissue dr to impaired hepatic ketogenesis. We tested hepatic k etogenesis in FCPD patients using a ketogenic challenge of oral medium -chain triglycerides (MCTs) and compared it with that in matched insul in-dependent diabetes mellitus (IDDM) patients and healthy controls. A fter oral MCTs, FCPD patient; showed only a mild increase in blood 3-h ydroxybutyrate (3-HB) concentrations (median: fasting, 0.13 mmol/L; pe ak, 0.52) compared with IDDM patients (fasting, 0.44; peak, 3.39) and controls (fasting, 0.04; peak, 0.75). Plasma nonesterified fatty acid (NEFA) concentrations were comparable in the two diabetic groups (FCPD : fasting, 0.50 mmol/L; peak, 0.79; IDDM: fasting, 0.91; peak, 1.04). Plasma C-peptide concentrations were low and comparable in the two dia betic groups. Plasma glucagon concentrations were higher in IDDM patie nts in the fasting state, but declined to levels comparable to those i n FCPD patients after oral MCTs; Plasma carnitine concentrations were comparable in the two groups of patients. It is concluded that the fai lure to stimulate ketogenesis under these conditions could be partly d ue to inhibition of a step beyond fatty acid entry into the mitochondr ia. Copyright (C) 1997 by W.B. Saunders Company