Ketosis resistance in fibrocalculous pancreatic diabetes: II. 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 whether this ketosis resistance is due to reduced, fatty acid release from adipose tissue or to impaired hepatic ketogenesis. We tested hepatic ketogenesis in FCPD...

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Published in:	Metabolism, clinical and experimental Vol. 46; no. 1; pp. 1 - 4
Main Authors:	Yajnik, C.S., Sardesai, B.S., Bhat, D.S., Naik, S.S., Raut, K.N., Shelgikar, K.M., Orskov, H., Alberti, K.G.M.M., Hockaday, T.D.R.
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 1997 Elsevier
Subjects:	Adipose Tissue - metabolism Administration, Oral Adult Biological and medical sciences Blood Glucose - analysis C-Peptide - blood Carnitine - blood Diabetes Complications Diabetes Mellitus - blood Diabetes Mellitus - metabolism Diabetes Mellitus, Type 1 - blood Diabetes Mellitus, Type 1 - metabolism Diabetes. Impaired glucose tolerance Diabetic Ketoacidosis - prevention & control Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fatty Acids - metabolism Fatty Acids, Nonesterified - blood Female Glucagon - blood Glycerol - blood Humans Hydroxybutyrates - blood Ketones - metabolism Liver - metabolism Male Medical sciences Triglycerides - administration & dosage Triglycerides - therapeutic use Endocrinopathy Human Ketogenesis Pathophysiology Ketose Diabetes mellitus Metabolic diseases Medium chain Metabolism Triglyceride Target tissue resistance Fibrosis Endocrine pancreatic diseases Pancreas
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Summary:	A majority of patients with fibrocalculous pancreatic diabetes (FCPD) do not become ketotic even in adverse conditions. It is not clear whether this ketosis resistance is due to reduced, fatty acid release from adipose tissue or to impaired hepatic ketogenesis. We tested hepatic ketogenesis in FCPD patients using a ketogenic challenge of oral medium-chain triglycerides (MCTs) and compared it with that in matched insulin-dependent diabetes mellitus (IDDM) patients and healthy controls. After oral MCTs, FCPD patients, showed only a mild increase in blood 3-hydroxybutyrate (3-HB) concentrations (median: fasting, 0.13 mmol/L; peak, 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 diabetic groups. Plasma glucagon concentrations were higher in IDDM patients in the fasting state, but declined to levels comparable to those in FCPD patients after oral MCTs. Plasma carnitine concentrations were comparable in the two groups of patients. It is concluded that the failure to stimulate ketogenesis under these conditions could be partly due to inhibition of a step beyond fatty acid entry into the mitochondria.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ISSN:	0026-0495 1532-8600
DOI:	10.1016/S0026-0495(97)90158-X