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Measurements of pyruvate and ketones bodies (acetoacetate and 3-hydroxybutyrate) are essential to the investigation of intermediary metabolism. Indeed, their blood levels reflect energy balance influenced by nutritional status. This balance can be disturbed in certain diseases such as diabetes and some inherited metabolic disorders. We have developed methods for assays on open automated biochemistry analyser, Konelab 20 XT (ThermoFischer, Whaltham USA), using kits marketed by Sobioda (Montbonnot, France) for pyruvate and Wako Chemicals GmbH (Neuss, Germany) for ketones, on deproteinised blood sample. We have validated the performance of these three quantitative methods using NF EN ISO 15189 (range B) standard criteria. We obtain satisfactory results concerning fidelity (precision measured as within and between batch CVs are respectively less than 7% and less than 6%), measuring ranges (from 7.7 to 228 μmol/L for pyruvate and from 22.6 to 650 μM for total ketone bodies), accuracy (10.4 μmol/L in physiological range for pyruvate and 7.1 μmol/L for 3-hydroxybutyrate) and comparing methods (versus manual assay with spectrophotometry on Uvikon XL). Establishment of reference ranges (35 to 74 μmol/L for pyruvate, less than 100 μM for 3-hydroxybutyrate and less than 44 μmol/L for acetoacetate) and reagents stability study (up to 12 weeks if frozen) have enabled us to finalize method validation and to add these assays to our routine laboratory repertoire.

Most textbooks advise that newly diagnosed insulin dependent mellitus be admitted to the hospital for starting carefully insulin treatment. We report a pilot study for starting an outpatient insulin using continuous subcutaneous insulin infusion. In 40 newly IDDM (glycaemia over 16.5 mM/l, CO2 over 15 mM/l), intensive therapy was done by CSII = basal rate 1 unit/hour, bolus 5 units per meal. After a long explanatory talk (4 hours) with the physician and the nurse on hypo, hyperglycaemia, on blood glucose sensor and pump, 21 patients agreed to start insulin at home and 19 remained in hospital for 2 or 7 days. At days 3, 30 and 365, clinical and biological evaluation was done and at D30 patient education program for 5 days was undergone. Never emergency even was reported in any patient, and no difference appeared between the in and out patient in D1, D3 and D365 normalisation of blood glucose (3 days) or level cetone body (2 days) and total insulin dose. Our results suggest that outpatient is a safe and cost effective IDDM onset therapy.

Severe ketoacidosis sometimes develops in chronic alcoholics after increased alcohol intake associated with dietary restriction. This particular case was unusual from two standpoints: a considerable, prolonged and unexplained increase in serum free fatty acid, and discordance between the degree of ketonaemia and an abundant liver glycogen load.

In fed geese, plasma levels of glucose and alanine were 1.9 g.l-1 and 560 mumol.l-1, respectively. During a long fast (40 days), plasma glucose and alanine were maintained at a high level (1.5-1.8 g.l-1 and 370-540 mumol.l-1, respectively). Plasma level of acetoacetate was very low (40 mumol.l-1); by contrast, plasma level of beta hydroxybutyrate reached very high values (20 mmol.l-1) after about 20 days of fasting, then it decreased. Plasma levels of lactate and pyruvate decreased along the course of the fast, from 2 500 to 2 000 mumol.l-1 and 220 to 170 mumol.l-1, respectively.

The medium chain acyl-CoA deshydrogenase defect: a new inherited metabolic disorder. This enzymatic defect blocks the catabolism of non esterified fatty acids during fasting. Thus, this disease is revealed by a coma due to hypoglycemia in a young child; the presence of dicarboxylic aciduria in such a situation is the main evidence for this diagnosis. Finally, the enzymatic studies performed on skin fibroblasts show a defect in medium chain acyl-CoA deshydrogenase. When a child is investigated away from a coma episode, the ketotic diet induces dicarboxylic aciduria but must be performed in an intensive care unit for its dangers.

Salbutamol-induced diabetic ketoacidosis having recently been reported, the authors have studied the metabolic changes produced by the drug in 6 nondiabetic patients. All patients received a 3-hour infusion of salbutamol (S) 20 z g/minm. On the following day, three of these were given somatostatin (SRIF) 100 mg/hour mixed with S infused at the same rate, whilst the remaining 3 patients received SRIF alone. On the 3rd day, patients of the first sub-group received the same infection of S and SRIF as before plus exogenous glucagon 90 ng/kg/hour. Somatostatin is know to inhibit insulin and glucagon secretion. Exogenous glucagon was given in order to reproduce the metabolic conditions of insulin-deficient diabetes mellitus. Salbutamol alone induced a small rise in blood glucose and insulin, free fatty acids, glycerol and ketonic bodies, but no changes in endogenous glucagon. SRIF alone produced no significant metabolic variations. In the presence of SRIF, all salbutamol-induced metabolic changes were increased. Adding glucagon mainly resulted in high levels of ketonic bodies. All variations correlated with each other. Thus, whilst the hyperglycaemic, lipolytic and ketogenic effects of S in non-diabetic patients are partly masked by insulin hypersecretion, they are enhanced in the absence of insulin and, to an even greater extent, by an excess of glucagon. Diabetic patients treated with salbutamol should therefore be under close surveillance and have their insulin dosage increased.

In the young rabbit, immunoreactive serum insulin (IRI) significantly rises during the first 5 min after suckling and then 20-60 min later, at which time the maximum level is reached. Blood glucose levels remain stable, blood ketone bodies increase 2.7 times and the liver glycogen levels decrease. Replacement of maternal milk by an equal volume of 0.9% NaCl, 2% lactose or 3.5% glycerol does not induce any change in IRI. IRI significantly rises if solutions of bovine milk proteins or skimmed rabbit's milk are administered. This effect is quickened and strengthened by the addition of coconut oil or lipids of rabbit's milk whereas sunflower oil is ineffective. It is suggested that medium-chain fatty acids, major components of rabbit's milk lipids, play an important role in the regulation of insulin secretion in the young rabbit.