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Glycogen cycling, i.e. simultaneous glycogen synthesis and glycogenolysis, affects estimates of glucose fluxes using tracer techniques and may contribute to hyperglycaemia in diabetic conditions. This study presents a new method for quantifying hepatic glycogen cycling in the fed state. Glycogen is synthesised from glucose by the direct and indirect (gluconeogenic) pathways. Since glycogen is also synthesised from glycogen, i.e. glycogen--glucose 1-phosphate--glycogen, that synthesised through the direct and indirect pathways does not account for 100% of glycogen synthesis. The percentage contribution of glycogen cycling to glycogen synthesis then equals the difference between the sum of the percentage contributions of the direct and indirect pathways and 100.The indirect and direct pathways were measured independently in nine healthy volunteers who had fasted overnight. They ingested (2)H(2)O (5 ml/kg body water) and were infused with [5-(3)H]glucose and acetaminophen (paracetamol; 1 g) during hyperglycaemic clamps (7.8 mmol/l) lasting 8 h. The percentage contribution of the indirect pathway was calculated from the ratio of (2)H enrichments at carbon 5 to that at carbon 2, and the contribution of the direct pathway was determined from the (3)H-specific activity, relative to plasma glucose, of the urinary glucuronide excreted between 2 and 4, 4 and 6, and 6 and 8 h.Glucose infusion rates increased (p0.01) to approximately 50 mumol kg(-1) min(-1). Plasma insulin and the insulin : glucagon ratio rose approximately 3.6- and approximately 8.3-fold (p0.001), respectively. From the difference between 100% and the sum of the direct (2-4 h, 54+/-6%; 4-6 h, 59+/-5%; 6-8 h, 63+/-4%) and indirect (32+/-3, 38+/-4, 36+/-3%) pathways, glycogen cycling was seen to be decreased (p0.05) from 14+/-4% (2-4 h) to 4+/-3% (4-6 h) and 1+/-3% (6-8 h).This method allows measurement of hepatic glycogen cycling in the fed state and demonstrates that glycogen cycling occurs most in the early hours after glucose loading subsequent to a fast.

Normal subjects, fasted 60 h, and patients with insulin-dependent diabetes mellitus (IDDM), withdrawn from insulin and fasted overnight, were given phenylacetate orally and intravenously infused with [3-14C]lactate and 13C-bicarbonate. Rates of hepatic gluconeogenesis relative to Krebs cycle rates were estimated from the 14C distribution in glutamate from urinary phenylacetylglutamine. Assuming the 13C enrichment of breath CO2 was that of the CO2 fixed by pyruvate, the enrichment to be expected in blood glucose, if all hepatic glucose production had been by gluconeogenesis, was then estimated. That estimate was compared with the actual enrichment in blood glucose, yielding the fraction of glucose production due to gluconeogenesis. Relative rates were similar in the 60-h fasted healthy subjects and the diabetic patients. Conversion of oxaloacetate to phosphoenolpyruvate was two to eight times Krebs cycle flux and decarboxylation of pyruvate to acetyl-CoA, oxidized in the cycle, was less than one-30th the fixation by pyruvate of CO2. Thus, in estimating the contribution of a gluconeogenic substrate to glucose production by measuring the incorporation of label from the labelled substrate into glucose, dilution of label at the level of oxaloacetate is relatively small. Pyruvate cycling was as much as one-half the rate of conversion of pyruvate to oxaloacetate. Glucose and glutamate carbons were derived from oxaloacetate formed by similar pathways if not from a common pool. In the 60-h fasted subjects, over 80 % of glucose production was via gluconeogenesis. In the diabetic subjects the percentages averaged about 45 %.

Quantification of gluconeogenesis (GNG) with carbon labeled tracers results in underestimation due to exchange and loss of tracer C in TCA cycle. We have reported the use of deuterium labeling of body water pool in order to label the glucogenic precursor phosphoenol pyruvate (JCI 95:172, 1995). The appearance of 2H on C-6 of glucose quantifies GNG from pyruvate, if correctred for incomplete equilibration of label at the pyruvate level, but does not include glycerol. Since 2H from water labels C-5 of glucose via pyruvate, and also labels C-2 of the triose phosphate pool, appearance of2 H on C-5 of glucose gives an estimate of total GNG, eliminating the uncertainty of incomplete equilibration and including glycerol.

In three experiments, subjects sorted 32-card decks with four stimuli into two classes using one relevant dimension with four levels. Relative and absolute similarity of the stimuli was manipulated through different forms of redundancy with respect to a second dimension. With nonintegral dimensions (circle size and diameter angle), redundancy had no effect on performance. With integral dimensions, form of redundancy affected performance, but the effects depended on the stimulus dimensions (dot positions vs. value and chroma) and on the relevant dimension (value vs. chroma). Results suggest that performance in a speeded classification task with integral stimuli can be only partially explained in terms of interstimulus similarity.

In Zusammenarbeit mit der Hals-Nasen-Ohren-Klinik Freiburg haben wir — neben klinischer Untersuchung, Modellanalyse, Fernrontgenauswertung — mittels Nasenwiderstandsmessungen mit dem Korperplethysmographen die Durchgangigkeit der oberen Luftwege bewertet. Wir konnten gewisse morphologische und funktionelle Besonderheiten beim Mundatmertyp erfassen und Ruckschlusse auf die Therapieplanung ziehen.

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We examined 143 ears in 89 patients before and after septum operation. We found that in 56.6% of the patients with negative pressure in the middle ear, this negative pressure was reduced by the operation. This result was supported by rhinomanometric examinations. The tubal resistance and the ability of opening the tubes actively were not influenced. This result indicates an improved pressure compensation between nose and middle ear after the operation, when a tympanic underpressure is present.