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Biomedical subjects

J Wahren

Publications and source records attributed to J Wahren.

At least 109 records · Page 6Linked to original sources
PubMed1990

Meal-induced thermogenesis in previously obese patients.

Meal-induced thermogenesis is reported to be reduced in obese patients and the purpose of this study was to find out whether thermogenesis after a mixed meal differs between previously obese (post-obese) subjects and non-obese controls. Nine post-obese patients (body mass index 27 +/- 1) and nine age- and sex-matched non-obese volunteers (body mass index 22 +/- 1) were studied with continuous indirect calorimetry in the basal state and after the ingestion of a standardized test meal. Following treatment with vertical banded gastroplasty for the obesity, the weight of the patients had decreased by an average of 44 +/- 5 kg. Basal oxygen uptake and energy expenditure did not differ between the post-obese and the controls. After the meal, energy expenditure increased rapidly, becoming relatively constant after 60 min; the average increase above basal was in the post-obese 30.5 +/- 1.8% and in the non-obese controls 29.5 +/- 2.3% (NS). In absolute terms, the increments above basal were also similar in the two groups. The heart rate was higher in the post-obese group throughout the study period. It is concluded that the thermogenic response to a mixed meal is much the same in post-obese subjects and in non-obese controls. These findings support the notion that a decreased meal-induced thermogenesis is a secondary phenomenon rather than a primary pathogenic factor in human obesity.

Adult↗
PubMed1990

Plasma lipolytic activity and substrate oxidation after intravenous administration of heparin and a low molecular weight heparin fragment.

This study examines the effects of heparin and a low molecular weight heparin (LMWH) fragment on plasma lipolytic activity and substrate oxidation. Indirect calorimetry was performed continuously in healthy male subjects receiving a constant infusion of fat emulsion (0.2 g min-1) and glucose (0.8 g min-1) during a period of 4 h. After 2 h an infusion of heparin (n = 6) or LMWH (n = 6) (100 antifactor Xa units kg-1) or saline (n = 6) was given over 1 h. Plasma concentration of the fat emulsion decreased by 76 +/- 5% with heparin and by 12 +/- 7% with LMWH (P less than 0.01). In the case of LMWH the initial fall was followed by a consistent rise in fat emulsion concentration for the entire remaining study period. Compared to the control experiments, plasma FFA increased five times with heparin and three times with LMWH (P less than 0.05). The average respiratory quotient (RQ) and energy expenditure (EE) increased constantly during the study period and did not differ significantly between the groups. In all groups the average increase in glucose oxidation was 40-50%, while fat oxidation decreased to a comparable extent. Infusions of heparin and LMWH had no effect on RQ or EE. A microcalorimetric study on isolated rat adipocytes in buffer solutions containing glucose, fat emulsion, heparin or LMWH was also made. The heat output from the adipocytes was not influenced by the presence of heparin or LMWH. In conclusion, infusion of heparin resulted in a pronounced increase in FFA availability, whereas LMWH exerted a less marked lipolytic effect. However, the heparin-induced elevations in plasma FFA were not accompanied by measurable rises in lipid oxidation rate.

Adult↗
PubMed1990

Diminished meal-induced thermogenesis in elderly man.

The purpose of this study was to examine the possible influence of age on thermogenic response to a mixed meal in healthy subjects. Twenty-five healthy male subjects participated in the study and they were divided into three groups, comprising 10 young subjects with an average age of 27 years (22-35 years), seven middle-aged individuals (51 years, 42-60 years) and eight elderly men (70 years, 67-74 years). They were all studied with continuous indirect calorimetry in the basal state and for 3 h after the ingestion of a mixed meal in liquid form. The size of the meal corresponded to 60% of the individually computed 24-h basal energy expenditure. Resting energy expenditure was lower in the elderly men than in the young ones when expressed in absolute values (P less than 0.001) as well as in relation to body weight (P less than 0.01) and body surface area (P less than 0.01). After the meal energy expenditure increased rapidly and reached a relatively constant level after 60 min in all groups; the average increase above the basal level during the whole postprandial period was less in the elderly (21.1 +/- 2.5%, P less than 0.01) and the middle-aged (24.2 +/- 1.7%, P less than 0.05) than in the young (28.6 +/- 1.6%) men. It is concluded that the thermogenic response during the first 3 h following a mixed meal decreases with age and that this diminished meal-induced thermogenesis may contribute to lower nutrient requirements in old age.

Adult↗
PubMed1990

Total and net muscle protein breakdown in infection determined by amino acid effluxes.

The present investigation was undertaken to study whether, in human infection of varying severity, peripheral 3-methylhistidine efflux and urinary excretion are associated with net protein degradation and to estimate the protein synthesis rate from the combined effluxes of 3-methylhistidine, tyrosine, and phenylalanine. Quadruplicate femoral arteriovenous differences of 3-methylhistidine, tyrosine, and phenylalanine were multiplied by leg plasma flow in 15 infected patients. Leg effluxes for 3-methylhistidine, tyrosine, and phenylalanine were -0.074 +/- 0.011, -2.57 +/- 0.43, and -3.17 +/- 0.44 mumol/min, respectively. There was a significant linear relationship (P less than 0.01) between the effluxes of tyrosine and phenylalanine and the efflux and urinary excretion of 3-methylhistidine. A significant release of tyrosine and phenylalanine was observed in patients studied at the 3-methylhistidine level seen in normal healthy subjects. It is concluded that in infection 1) there is an increased breakdown of skeletal muscle protein and a reduced rate of protein synthesis, with the latter being relatively more important in patients with mild disease; and 2) urinary 3-methylhistidine excretion is associated with net skeletal muscle protein degradation for the patient group studied.

Abdomen↗
PubMed1990

Regulation of amino acid metabolism by epinephrine.

The effect of epinephrine on amino acid (AA) metabolism was examined in 33 healthy volunteers who participated in four studies. Nine subjects participated in study I, which consisted of four parts: euglycemic insulin clamp, insulin plus epinephrine, insulin plus epinephrine plus propranolol, and insulin plus propranolol. In study II six subjects received epinephrine with hepatic-femoral venous catheterization. In study III five individuals received epinephrine with somatostatin plus basal insulin replacement. In study IV quadriceps muscle biopsy was performed in six subjects after epinephrine or insulin infusion. Both epinephrine and insulin caused a generalized decline in all plasma AA except alanine. With combined epinephrine-insulin infusion, the decrease in plasma AA was additive. Propranolol blocked the hypoaminoacidemic effect of epinephrine but failed to alter the AA lowering action of insulin. Epinephrine, while maintaining basal insulinemia, reduced the catechol's hypoaminoacidemic effect by 39%. After epinephrine, splanchnic alanine uptake increased, but plasma alanine remained constant because of a parallel rise in muscle alanine production. Plasma/intracellular concentrations of branched-chain amino acids (BCAA) and all gluconeogenic amino acids, except alanine, decreased after both epinephrine and insulin. In summary, the effect of epinephrine on plasma/intracellular total, gluconeogenic, and BCAA concentrations is similar to insulin.

Adult↗
PubMed1990

Fructose-6-phosphate cycling and the pentose cycle in hyperthyroidism.

Hepatic fructose-6-phosphate (fructose-6-P) cycling and pentose cycle activity were quantified in hyperthyroid patients. A measure of the fructose-6-P cycle was the incorporation of 14C, on administering [3-3H,6-14C]galactose, into carbon 1 of blood glucose and the 3H/14C ratio in blood glucose. The measure of the pentose cycle was the randomization of 14C to carbon 1 of blood glucose on administering [2-14C]galactose. [2-3H]Galactose was also administered, so the 3H/14C ratio in blood glucose measured the extent of equilibration of glucose-6-P with fructose-6-P. Patients given [3-3H,6-14C]galactose were restudied when euthyroid. Of the 14C from [3-3H,6-14C]galactose, 7.7-9.5% was in carbon 1 of glucose in both states. 3H/14C ratios were also the same in both states. Fructose-6-P cycling was estimated to be 13 +/- 1% the rate of glucose turnover in the euthyroid and 15 +/- 1% that in the hyperthyroid state. The pentose cycle contributed about 2% to glucose utilization, similar to previous estimates in healthy humans. As in healthy individuals, about 25% of 3H was retained in the conversion of [2-3H]glucose-6-P to glucose. Thus, the fractions of glucose turnover participating in hepatic fructose-6-P and pentose cycling are similar in hyperthyroid and healthy subjects. As a result, augmented fructose-6-P cycling does not substantially contribute to increased hepatic oxygen consumption in hyperthyroidism.

Adult↗
PubMed1990

Gut exchange of glucose and lactate in basal state and after oral glucose ingestion in postoperative patients.

Glucose uptake by the intestine and its conversion into 3-carbon compounds in the human intestine in the basal state and after an oral glucose load are not understood. Consequently, we studied the arterial and portal venous concentration differences (A-PV) for glucose and glucogenic substrates in the basal state and 3 h after the ingestion of a 100-g glucose load with the catheter technique. Five patients were studied 3-11 days after surgery for gallbladder disease or cancer of the colon or liver. A-PV for glucose in the basal state was 0.12 +/- 0.02 mM (P less than 0.01), indicating net glucose uptake by extrahepatic splanchnic tissues. No net exchange of lactate or pyruvate was detected, but there was release of alanine and uptake of glutamine. After glucose ingestion, glucose was released by the gut, reflecting absorption of the load (mean A-PV for glucose -2.10 +/- 0.04 mM, P less than 0.01). The arterial glucose concentration rose gradually from 4.6 +/- 0.1 mM before glucose ingestion to a plateau at 9.5 +/- 0.7 mM from 90 to 180 min. Glucose ingestion was accompanied by net lactate and alanine release (A-PV -0.16 +/- 0.06 mM and -48 +/- 7 microM, respectively), whereas A-PV for pyruvate did not change. We conclude that, in postoperative patients, there is a significant net glucose uptake by the gastrointestinal tract in the basal state. Glucose ingestion is accompanied by a small release of lactate and alanine from the intestine. However, the estimated net gut formation of lactate and alanine can play only a minor role in the disposal of an oral glucose load.

3-Hydroxybutyric Acid↗
PubMed1989

N-acetyl-L-tyrosine and N-acetyl-L-cysteine as tyrosine and cysteine precursors during intravenous infusion in humans.

The usefulness of N-acetyl-L-tyrosine (NAT) and N-acetyl-L-cysteine (NAC) as tyrosine and cysteine precursors during intravenous infusion was investigated in humans. Plasma levels and urinary excretion of NAT, tyrosine, NAC, and total cysteine were determined, and the site of deacetylation was examined by measuring the splanchnic and renal balances. Eleven healthy volunteers were given 5 g of either NAT or NAC as a 4-hour intravenous infusion. Plasma levels of NAT and NAC increased rapidly, accompanied by a 25% increase in tyrosine levels and a 35% decrease in total cysteine. Urinary excretion of NAT and NAC in 4 hours accounted for 56% and 11% of the infused amount, respectively. No net production of tyrosine or cysteine was found from the splanchnic area, but from the kidneys there was a small release of both tyrosine (10 +/- 3 mumol/min) and cysteine (64 +/- 3 mumol/min). We conclude that under these conditions the usefulness of NAT and NAC as precursors for the corresponding amino acids in humans is not apparent.

Acetylcysteine↗
PubMed1989

Utilization of intravenously administered N-acetyl-L-glutamine in humans.

L-glutamine is too unstable for inclusion in solutions for parenteral nutrition, but its acetylated analogue, N-acetyl-L-glutamine is not. The purpose of this three-part study was to investigate the utilization of intravenously (IV) administered acetylglutamine in humans. In study 1, nine healthy postabsorptive subjects were given 9.4 g acetylglutamine IV during four hours. In study 2, five healthy subjects were studied on two occasions following an overnight fast. They were given 9.4 g of acetylglutamine or an equivalent amount of glutamine as part of a total parenteral nutrition (TPN) regimen during 7.2 hours. A control group of five subjects was given the same TPN regimen, but without acetylglutamine or glutamine. The nutrient solution included glucose, amino acids, and a fat emulsion, supplying 9.4 g nitrogen and 6,300 kJ in a total volume of 1.8 L. In study 3, four patients were studied the day after major surgery. They were given the same TPN regimen as in study 2, containing 9.4 g acetylglutamine, during 7.2 hours. Plasma concentrations and urinary excretion of acetylglutamine and glutamine were measured in all three studies, and so were splanchnic and renal exchange of acetylglutamine and glutamine in study 1. In study 1, the plasma concentration of glutamine rose from 594 +/- 28 mumol/L to 728 +/- 26 mumol/L (P less than .001), whereas plasma levels of acetylglutamine exceeded 1,000 mumol/L in all subjects at the end of infusion. The eight-hour urinary excretion of acetylglutamine and glutamine corresponded to 18% of the infused amount of acetylglutamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Protein and amino acid metabolism during early starvation as reflected by excretion of urea and methylhistidines.

Endogenous excretion of nitrogenous products was studied during early starvation in six healthy, nonobese subjects after six days on a well-defined diet, designed to achieve net protein balance and an adequate calorie supply. The diet contained 0.5 g myofibrillar-free protein and 35 kcal/kg body weight. The subjects then fasted for three days. Urine was collected for 24-hour periods and analyzed for urea, ammonia, 3-methylhistidine, and 1-methylhistidine. Blood glucose and serum urea levels were measured daily. In a second group of subjects, muscle biopsies for determination of free amino acid concentrations were taken in the overnight fasted state and after three days of fasting. During the period with a balanced diet, urea production fell initially and stabilized after two to three days at a level of 146 +/- 15 mmol/24 h. During the period of fasting, serum urea increased from 3.0 +/- 0.4 to a maximum value of 6.2 +/- 0.7 mmol/L and urea production rose markedly, to a peak of 293 +/- 16 mmol/24 h. Ammonia excretion was 24 +/- 2 mmol/24 h before and 71 +/- 13 mmol/24 h after three days of fasting. 3-Methylhistidine excretion was stable before fasting and then rose from 154 +/- 17 to 198 +/- 17 mumol/24 h. 1-Methylhistidine excretion was unchanged during fasting. Blood glucose levels were stable at 4.8 +/- 0.2 mmol/L before fasting and then fell to 3.7 +/- 0.3 mmol/L. Intracellular concentrations of amino acids in skeletal muscle decreased markedly during fasting; after three days of fasting the glutamine concentration had fallen by 34%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Pathways of hepatic glycogen formation in humans following ingestion of a glucose load in the fed state.

The relative contributions of the direct and the indirect pathways to hepatic glycogen formation following a glucose load given to humans four hours after a substantial breakfast have been examined. Glucose loads labeled with [6-(14)C]glucose were given to six healthy volunteers along with diflunisal (1 g) or acetaminophen (1.5 g), drugs excreted in urine as glucuronides. Distribution of 14C in the glucose unit of the glucuronide was taken as a measure of the extent to which glucose was deposited directly in liver glycogen (ie, glucose----glucose-6-phosphate----glycogen) rather than indirectly (ie, glucose----C3-compound----glucose-6-phosphate----glycogen). The maximum contribution to glycogen formation by the direct pathway was estimated to be 77% +/- 4%, which is somewhat higher than previous estimates in humans fasted overnight (65% +/- 1%, P less than 0.05). Thus, the indirect pathway of liver glycogen formation following a glucose load is operative in both the overnight fasted and the fed state, although its contribution may be somewhat less in the fed state.

Acetaminophen↗
PubMed1989

Effect of carnitine supplemented TPN on turnover and muscle utilisation of free fatty acids in patients with persistent post-operative infection.

The effect of L-carnitine on FFA turnover and regional utilisation over the leg was investigated using infusion of 14C-oleic acid and measurement of the respiratory quotient (RQ) in eight artificially ventilated patients with severe post-operative infection and at least 2 weeks of carnitine free TPN. Carnitine or placebo was added to the daily infusion of lipid during two consecutive 4-day periods in a randomised cross-over fashion. The total dose of carnitine was 110 mg/kg over 4 days. Before carnitine supplementation, total plasma carnitine levels ranged between 39 and 152 micromol/l. The RQ was 0.87 +/- 0.02 (SEM). The turnover (185 +/- 64 micromol/min) and fractional turnover (0.39 +/- 0.04/min) of oleic acid as well as the uptake (31 +/- 10 micromol/min) and fractional uptake (0.46 +/- 0.05) over the leg were similar to previously reported values in healthy subjects. Carnitine supplementation, despite a doubling of the average plasma carnitine level, did not influence the RQ or the whole body turnover and regional exchange of oleic acid. The present results suggest that four days of carnitine supplementation in patients with persistent post-operative infection has no measurable effect on FFA utilisation, indicating that the patients' carnitine reserves were sufficient to maintain normal FFA utilisation.

Journal Article↗
PubMed1989

Intravenous and subcutaneous administration of a long-acting somatostatin analogue: effects on glucose metabolism and splanchnic haemodynamics in healthy subjects.

The effect of SMS 201-995, a long-acting somatostatin analogue, on splanchnic blood flow and glucose metabolism, was investigated in five groups of healthy subjects. Groups A (n = 4), B (n = 5), C (n = 5) and D (n = 5) were studied before, during and after a 60-min intravenous infusion of SMS (1.7, 0.8, 0.2 and 0.1 micrograms min-1, respectively). Group E (n = 6) was investigated before and for 6 h after a subcutaneous injection of 25 micrograms of SMS. The splanchnic blood flow decreased by 20-25% in all groups in response to SMS and remained low during the entire observation periods. Arterial concentrations of glucose showed a 15-20% decline during SMS infusion in Groups A and B (P less than 0.05-0.01) and a less pronounced decrease in the other groups. Fifteen minutes after the end of infusion the glucose levels started to rise and in group A, the levels were significantly higher than basal (+25%, P less than 0.05-0.01) at 90-180 min after the end of infusion. The net splanchnic glucose production, determined in groups A and B, decreased by 65-75% in response to SMS infusion. Towards the end and immediately after the infusions, however, the net glucose output increased, but decreased again at 30-60 min after the end of infusion. Arterial, insulin and glucagon concentrations decreased significantly during infusion in all groups. This decline was more pronounced for insulin (50%) than for glucagon (20-25%) and insulin concentrations remained low for a longer period after the end of infusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Diet-induced thermogenesis in patients with liver cirrhosis.

Diet-induced thermogenesis after ingestion of a mixed meal was investigated in eight patients with documented liver cirrhosis and in eight age- and sex-matched healthy controls. Respiratory gas exchange was measured continuously for one hour in the basal state and for three hours after ingestion of a mixed liquid meal, consisting of 17% kJ protein, 28% kJ lipids and 55% kJ carbohydrates and dispensed to correspond to 60% of the individually computed energy expenditure. Arterial substrate and hormone concentrations were determined before and at timed intervals for three hours after the meal. Urine was collected for determination of nitrogen excretion. The patients' oxygen uptake, energy expenditure and respiratory quotient were similar to those of the controls in the basal state. After the meal, pulmonary oxygen uptake and energy expenditure rose markedly in both groups during the first hour and were subsequently stable. The average increase in oxygen uptake above basal during the whole study period was 21.2 +/- 1.8% and 22.3 +/- 1.2% (NS) in patients and controls, respectively. The corresponding increase in energy expenditure was 24.8 +/- 2.0% in the patients and 24.9 +/- 1.4% in the controls (NS). The respiratory quotient was elevated throughout the postprandial period in both groups but the quotient was significantly higher in the patients (P less than 0.05-0.001), suggesting a greater proportion of carbohydrate oxidation. The basal arterial concentrations of insulin and glucagon were significantly higher in the patients. After the meal the insulin level increased 10- to 20-fold in both groups. Glucose concentration rose significantly in both groups to a maximum of 8.82 +/- 1.00 and 8.03 +/- 0.95 mmol/l in patients and controls, respectively, at 60 min after the meal. This was accompanied by a fall in the levels of glycerol and ketone bodies in both groups, indicating decreased lipolysis. It is concluded that both the basal energy expenditure and the thermogenic response to a mixed meal are similar in patients with liver cirrhosis and in healthy controls. The patients' carbohydrate oxidation rose to a greater extent after the meal, probably as a consequence of excessive increases in insulin concentration, demonstrating that insulin resistance in these patients may be compensated for by postprandial hyperinsulinaemia.

Adult↗
PubMed1989

Diet-induced thermogenesis in well-trained subjects.

The purpose of this study was to examine the possible relationship between the thermogenic response to a mixed meal and the aerobic capacity in healthy subjects. Fourteen male subjects participated, and their maximal oxygen uptake was determined on a bicycle exercise ergometer. Two groups, each comprising seven individuals, were compared: a well-trained group, with an oxygen uptake of 58 +/- 2 ml min-1 kg-1 and a sedentary group, with an oxygen uptake of 39 +/- 2 ml min-1 kg-1. Respiratory gas exchange was measured continuously for 1 h in the basal state and then for 3 h postprandially. The subjects ingested a test meal in liquid form, consisting of 17% kJ protein, 28% kJ lipids and 55% kJ carbohydrates, and corresponding to 60% of the individually computed 24-h basal energy expenditure. Basal oxygen uptake and energy expenditure were similar in the two groups. After the meal, pulmonary oxygen uptake and energy expenditure rose rapidly and reached a plateau after 1 h. The responses were no different in the two groups: the average rise in pulmonary oxygen uptake above basal during the whole study period was 24.0 +/- 2.1% in well-trained and 26.7 +/- 1.5% in sedentary subjects (NS); the corresponding values for energy expenditure were 25.0 +/- 2.1% and 29.0 +/- 1.6% (NS). Also, when expressed in absolute terms the increments above basal were not significantly different. There was no discernible relationship between the individual thermogenic response and maximal oxygen uptake. In conclusion, the present findings do not indicate that diet-induced thermogenesis is proportional to aerobic capacity in healthy young men.

Adolescent↗
PubMed1989

Beta-adrenergic blockade does not influence the thermogenic response to a mixed meal in man.

The sympathetic nervous system has been implicated in the regulation of glucose-induced thermogenesis in man. The present study was undertaken to examine the influence of a pharmacological beta blockade on the thermogenic response after ingestion of a mixed meal. Ten healthy male volunteers were examined on two occasions, once during intravenous administration of beta-blocking agent (Series 1) and once without (Series 2). Five subjects received propranolol and the other five atenolol. Two subjects were also studied on a third occasion after 1 week of other propranolol medication (Series 3). Continuous respiratory gas exchange measurements were carried out for 1 h in the basal state and then for 3 h postprandially. The subjects ingested a standardized test meal in liquid form. After the meal oxygen uptake and energy expenditure both rose markedly during the first hour and then reached a relatively stable plateau. The average increase in oxygen uptake above basal during the whole study period was 27.0 +/- 1.4 vs. 26.7 +/- 1.4% (NS) in Series 1 and 2, respectively. The corresponding values for energy expenditure were 28.6 +/- 1.4 vs. 28.6 +/- 1.6%. Also in absolute terms, the increments above basal did not differ between the two series. Moreover, the basal measurements and the response to the meal were no different in the subjects in Series 1 receiving the selective beta-1 antagonist and the non-selective blocker, respectively. In conclusion, the present findings indicate that in healthy man, beta-adrenergically mediated sympathetic nervous system activity does not significantly influence the magnitude of the thermogenic response to a mixed meal.

Adult↗