PubMed HealthSearch

Biomedical subjects

J Wahren

Publications and source records attributed to J Wahren.

At least 19 recordsLinked to original sources

Effects of C-peptide on blood flow, capillary diffusion capacity and glucose utilization in the exercising forearm of type 1 (insulin-dependent) diabetic patients.

Microvascular dysfunction is frequently seen in patients with Type 1 (insulin-dependent) diabetes. The present study was undertaken to examine whether skeletal muscle microcirculation in Type 1 diabetic patients is influenced by C-peptide. Forearm blood flow, capillary diffusion capacity and substrate exchange were studied during strenuous rhythmic forearm exercise on a hand ergometer. Measurements were made before and during i.v. infusion for 60 min of C-peptide or 0.9% NaCl in Type 1 diabetic patients and healthy subjects. During infusion the C-peptide levels in the diabetic patients increased from less than 0.05 nmol/l to 1.32 +/- 0.08 nmol/l. Prior to infusion forearm blood flow and capillary diffusion capacity during exercise were lower in the diabetic patients than the control subjects. During C-peptide infusion both variables increased in the diabetic patients (blood flow +27 +/- 4%, capillary diffusion capacity +52 +/- 9%) to levels similar to those in the healthy subjects, while no significant change was seen in the healthy control subjects or the diabetic patients given NaCl. Forearm uptake of oxygen and glucose in the diabetic patients increased markedly after C-peptide administration but were unchanged after NaCl infusion. Significant uptake of C-peptide to the deep forearm tissues was observed in the resting state; approximately 7 +/- 2% of the arterial C-peptide concentration was extracted by forearm tissues in diabetic patients as well as in healthy control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

The influence of human C-peptide on renal function and glucose utilization in type 1 (insulin-dependent) diabetic patients.

The possible influence of C-peptide administration on renal function and whole body glucose utilization was examined in 11 patients (Group 1) with Type 1 (insulin-dependent) diabetes mellitus. They were given an i.v. insulin infusion during the night before the study and were euglycaemic at the time of examination. The glomerular filtration rate and effective renal plasma flow were measured by clearance techniques using constant-rate infusions of inulin and sodium para-aminohippurate. After baseline measurements C-peptide was infused during two periods of 60 min at rates of 5 and 30 pmol.kg-1.min-1. In a control study 0.9% NaCl was infused during two 60 min periods in ten Type 1 diabetic patients (Group 2). Glomerular filtration rate decreased by 7% (p less than 0.001), effective renal plasma flow increased by 3%, (p less than 0.05) and whole-body glucose utilization rose by approximately 25% (p less than 0.05) above basal during low-dose C-peptide infusion. Group 2 showed an unaltered glomerular filtration rate, effective renal plasma flow and glucose utilization during 60 min of NaCl infusion. The differences between Group 1 and Group 2 in glomerular filtration rate and glucose utilization were statistically significant. It is concluded that short-term administration of C-peptide in physiological amounts to patients with Type 1 diabetes may reduce the glomerular filtration rate and increase whole-body glucose utilization. The results suggest the possibility that short-term C-peptide administration may exert a regulatory influence on renal function and stimulate glucose utilization in Type 1 diabetic patients.

Adult

Heat leakage across the abdominal wall and meal-induced thermogenesis in normal-weight and obese subjects.

The mechanism behind the meal-induced increase in energy expenditure in humans and its reduction in obesity was examined in 15 normal-weight and seven obese subjects. The subjects were studied by indirect calorimetry in the basal state and during 2 hours after a mixed meal corresponding to 40% of the 24-hour basal energy requirement. Artificial thermal insulation was applied over the abdominal area before the study in seven of the normal-weight subjects. Thermistor catheters were inserted into a hepatic vein, the pulmonary artery, and a systemic artery for blood sampling and recording of blood temperatures. Basal hepatic venous drainage of heat in relation to the splanchnic oxygen uptake in the normal-weight subjects was low (12 +/- 1 J/mL O2) and became even lower after the meal (5 +/- 3 J/mL). In the obese individuals and the insulated subjects, blood-drained splanchnic heat amounted to 19 to 21 J/mL oxygen both before and after the meal. The postprandial increase in whole body energy expenditure was diminished both in the obese (12% +/- 1% above basal) and in the insulated subjects (15% +/- 1%) compared with the noninsulated controls (22% +/- 2%). In normal-weight subjects, there is a leakage of heat across the abdominal wall. Reduction or prevention of this leakage by artificial thermal insulation or by obesity is accompanied by a reduction of the postprandial increase in energy expenditure.

Abdominal Muscles

Thermogenic response to intravenous nutrition in patients with cirrhosis.

Energy expenditure was determined using continuous indirect calorimetry in the basal state and during 3 h of total parenteral nutrition (TPN) in 8 patients with cirrhosis and 8 healthy volunteers. TPN consisted of glucose, fat and amino acids and had a glucose/fat ratio of 50:50. The infusion rate was set to provide energy corresponding to 62.5% of the individually measured 24-h resting energy expenditure. In the basal state energy expenditure was similar in patients and controls while the respiratory quotient (RQ) was lower in the patients (0.78 +/- 0.01 vs. 0.82 +/- 0.01, mean +/- SEM, p < 0.05). During TPN, energy expenditure increased progressively during the 3-h infusion period. The average rise in energy expenditure was similar in patients (19.1 +/- 1.2%) and in controls (21.4 +/- 1.6%, n.s.). The RQ rose in both groups, but more in the patients with cirrhosis. At the end of the study, RQ was higher in patients (0.89 +/- 0.01) than in controls (0.85 +/- 0.01, p < 0.05). It is concluded that the nutrient-induced rise in energy expenditure during TPN is not significantly different in patients with cirrhosis and control subjects. Furthermore, the results indicate that the increased fat utilization in overnight fasting cirrhotic patients is rapidly shifted to an augmented carbohydrate oxidation during TPN, possibly as a consequence of marked hyperinsulinemia.

Adult

Use of 14CO2 in estimating rates of hepatic gluconeogenesis.

Estimating the rate of hepatic gluconeogenesis in vivo from the incorporation of 14C from 14CO2 into glucose requires determination of the rates in liver of equilibration of oxaloacetate with fumarate, conversion of oxaloacetate to phosphoenolpyruvate (PEP), and conversion of PEP to pyruvate, all relative to the rate of tricarboxylic acid cycle flux. With the use of a model of mitochondrial metabolism and gluconeogenesis, expressions are derived relating specific activity of carboxyl of PEP from 14CO2 to those rates and specific activity of mitochondrial CO2. If those rates and specific activity of mitochondrial CO2 are known, specific activity of PEP, calculated using the expressions, should, on a mole basis, be one-half the specific activity of the glucose formed. At steady state, in the 60-h fasted individual, where glucose formation is solely by gluconeogenesis, twice estimated specific activity of PEP should then approximate that of blood glucose. Estimates of relative rates in 60-h fasted humans, previously made from distribution of 14C in glutamate from phenylacetylglutamine excreted when [3-14C]lactate and phenylacetate were given, were applied to the expressions. Specific activity of mitochondrial CO2 was equated to that of CO2 expired by 60-h fasted subjects given NaH14CO3 and alpha-[1-14C]ketoisocaproate. Predicted specific activities approximated actual specific activities of blood glucose when NaH14CO3 was administered. alpha-[1-14C]ketoisocaproate administrations gave underestimates. This is attributable to differences between specific activities of hepatic mitochondrial CO2 and expired CO2, which is evidenced by higher incorporations of 14C in glucose than in expired CO2 from alpha-[1-14C]ketoisocaproate than from NaH14CO3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Noninvasive tracing of Krebs cycle metabolism in liver.

To quantify intrahepatic Krebs cycle metabolism, phenyl acetate, excreted in urine as a glutamine conjugate, was given to healthy subjects infused with [3-14C]lactate. They were studied after 60 h of fasting and when given glucose after an overnight fast. Distributions of 14C in glutamate from urinary phenylacetylglutamine and blood glucose were determined. Corrections to the distributions because of the fixation of 14CO2 formed from the [3-14C]lactate were determined by administering [14C]bicarbonate. Comparisons of distributions in glucose and glutamate support the assumption that the glutamate distributions reflect those in hepatic alpha-ketoglutarate. From the distributions in glutamate, the extent of exchange of labeled with unlabeled carbons and relative flow rates in the cycle in liver were estimated. Dilution of 14C by 12C in the cycle was found in the fasted but not the fed state. In the fasted state, pyruvate carboxylation was estimated to be at least twice the rate of Krebs cycle flux and the rate of pyruvate's decarboxylation less than 1/25 the rate of its carboxylation. In the fed state, the rate of decarboxylation was estimated to be between one-sixth and one-half the rate of carboxylation. The rate of conversion of oxalacetate to fumarate in both states appeared to be greater than 6 times the rate of Krebs cycle flux.

Adult

Metabolism of [2-14C]acetate and its use in assessing hepatic Krebs cycle activity and gluconeogenesis.

To examine the fate of the carbons of acetate and to evaluate the usefulness of labeled acetate in assessing intrahepatic metabolic processes during gluconeogenesis, [2-14C]acetate, [2-14C]ethanol, and [1-14C]ethanol were infused into normal subjects fasted 60 h and given phenyl acetate. Distributions of 14C in the carbons of blood glucose and glutamate from urinary phenylacetylglutamine were determined. With [2-14C]acetate and [2-14C]ethanol, carbon 1 of glucose had about twice as much 14C as carbon 3. Carbon 2 of glutamate had about twice as much 14C as carbon 1 and one-half to one-third as much as carbon 4. There was only a small amount in carbon 5. These distributions are incompatible with the metabolism of [2-14C]acetate being primarily in liver. Therefore, [2-14C]acetate cannot be used to study Krebs cycle metabolism in liver and in relationship to gluconeogenesis, as has been done. The distributions can be explained by: (a) fixation of 14CO2 from [2-14C]acetate in the formation of the 14C-labeled glucose and glutamate in liver and (b) the formation of 14C-labeled glutamate in a second site, proposed to be muscle. [1,3-14C]Acetone formation from the [2-14C]acetate does not contribute to the distributions, as evidenced by the absence of 14C in carbons 2-4 of glutamate after [1-14C]ethanol administration.

Acetates

Renal and splanchnic exchange of human biosynthetic C-peptide in type 1 (insulin-dependent) diabetes mellitus.

Biosynthetic human C-peptide or NaCl (154 mmol.l-1) was given intravenously to 13 Type 1 (insulin-dependent) diabetic patients to determine the renal and splanchnic exchange of C-peptide. Catheters were inserted percutaneously into an artery and a renal and hepatic vein. Infusions of C-peptide were given for 60 min at two dose levels (5 and 30 pmol.kg-1.min-1). Insulin was infused throughout the study (0.5 mU.kg-1.min-1) and plasma glucose was kept constant by a variable glucose infusion. The regional blood flows were measured by indicator dilution techniques. In 11 of the 13 patients basal C-peptide levels were not detectable. The arterial steady-state C-peptide concentration was 0.81 +/- 0.10 nmol.l-1 and 2.33 +/- 0.30 nmol.l-1 at the low and high rate infusions, respectively. Renal uptake was 124 +/- 18 pmol.min-1 at the low infusion corresponding to 39% of the infused amount. At the higher dose C-peptide infusion renal uptake increased to 155 +/- 21 pmol.min-1 (p less than 0.05). Urinary excretion of C-peptide was 7 +/- 2 pmol.min-1 at the low dose infusion and increased to 34 +/- 6 pmol.min-1 at the high dose infusion (p less than 0.01). The proportions of infused amount excreted were fairly constant and between 2% and 3%. No net exchange of C-peptide was found across the splanchnic vascular bed. The rate of glucose infusion had to be increased by 35% during the low dose C-peptide, but not during NaCl infusion in order to maintain a constant plasma glucose concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Normalization of hepatic glucose regulation despite systemic insulin delivery. Studies in patients with pancreatic transplantation for type 1 (insulin-dependent) diabetes mellitus.

With current surgical techniques for pancreatic transplantation, the graft is anastomosed to the iliac vessels, resulting in delivery of insulin to the systemic circulation rather than to the portal vein as in healthy man. The possible influence of the altered route of insulin delivery on the regulation of splanchnic glucose metabolism was studied in four patients with Type 1 (insulin-dependent) diabetes mellitus at 6-19 months after combined pancreatic and kidney transplantation. Four non-diabetic, age-matched renal transplant recipients and two groups of age-matched healthy subjects served as controls. The studies were carried out in the basal state and during two rates of intravenous glucose infusion (2 and 4 mg.kg-1.min-1). Fasting arterial glucose and splanchnic glucose output was similar in all groups. Basal hyperinsulinaemia was present in pancreatic graft recipients compared to healthy subjects. During low rate intravenous glucose infusion splanchnic glucose output decreased to a similar extent in all groups. With the higher glucose infusion rate (4 mg.kg-1.min-1) a net glucose uptake was observed which was similar in all three groups. Peripheral glucose uptake was unchanged at the lower glucose infusion rate but increased by 45-55% at the higher rate. It is concluded that despite systemic insulin delivery from a heterotopic pancreatic graft, hepatic glucose metabolism appears normal both in the post-absorptive state and in response to glucose-stimulated endogenous insulin secretion. Portal insulin delivery is thus not necessary for normal hepatic glucose metabolism in the Type 1 diabetic patient.

Adult

Effect of medium- and long-chain triglyceride infusion on lipoprotein and hepatic lipase in healthy subjects.

Plasma lipolytic activity and hydrolysis of intravenous fat were studied in six healthy subjects during infusion of a long-chain triglyceride (LCT) fat emulsion (Intralipid 20%) or of a medium-chain triglyceride (MCT)/LCT emulsion (Lipofundin MCT 20%). The fat emulsions were infused continuously at a rate of 0.17 g triglyceride kg-1 body weight (BW)h-1 for 6 h in random order at 7-day intervals. A continuous infusion of glucose (0.18 g kg-1 BW h-1) was administered for a period of 7 h and was started 1 h before the lipid infusion. Infusions of both types of fat increased plasma triglyceride (TG), free fatty acid (FFA) and lipoprotein lipase (LPL) levels and steady-state values were present during the 3rd to 5th h of infusion. MCT/LCT infusion resulted in higher plasma levels at steady-state of TG (3.63 +/- 0.45 [SEM] vs 2.73 +/- 0.45 mmol l-1; P less than 0.05), FFA (1.05 +/- 0.08 vs 0.54 +/- 0.04 mmol l-1; P less than 0.01) and LPL (4.6 +/- 0.6 vs 2.6 +/- 0.5 mU ml-1; P less than 0.05) in comparison with LCT administration. There was a positive correlation between plasma LPL activity and TG concentration (r = 0.77; P less than 0.001) when data for the two infusions were combined. Although the same amount of fat was infused on a weight basis, the molar infusion rate was 40% higher with MCT/LCT than with LCT infusion, due to differences in molecular weights (634 vs 885 Da).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Influence of a mixed meal on splanchnic and interscapular energy expenditure in humans.

Pulmonary, splanchnic, and interscapular O2 uptake was studied in 14 male volunteers before and for 90 min after a mixed meal. Thermistor catheters were inserted into a hepatic vein, the azygous vein, the pulmonary artery, and the aorta. Systemic and regional blood flows were determined during indirect calorimetry measurements and recordings of blood temperature. After the meal, pulmonary O2 uptake rose by 33-49 ml/min and splanchnic O2 uptake increased by 16-25 ml/min. In the azygous region O2 uptake did not increase significantly. Cardiac output increased after the meal by 1.1-1.5 l/min and splanchnic blood flow rose by 0.4-0.9 l/min. Azygous venous blood flow increased from 130 +/- 19 ml/min to 163 +/- 23 ml/min. In relation to splanchnic O2 uptake, the blood-drained splanchnic heat was low, 11 +/- 1 J/ml, and decreased to 7 +/- 1 J/ml after the meal. We conclude that after a mixed meal approximately one-half of the rise in O2 uptake occurs in the splanchnic organs; azygous-drained tissues, including possible interscapular brown adipose tissue, contribute minimally. The amount of heat drained with blood from the splanchnic region was low in relation to the splanchnic O2 uptake, indicating that splanchnic heat may be dissipated by routes other than the perfusing blood.

Adult

Ventilation-perfusion inequality in patients with non-alcoholic liver cirrhosis.

Ventilation-perfusion relationships were studied in patients with non-alcoholic liver cirrhosis. Spirometry was essentially normal but the transfer factor of the lung (DLCO) was reduced by an average 34% of predicted. Arterial oxygen tension (PaO2) ranged from normal down to 6.9 kPa. Varying degrees of ventilation-perfusion (VA/Q) abnormalities (multiple inert gas elimination technique) were observed with increased dispersion of the perfusion distribution (log SDQ, 0.90; range 0.32-1.71; upper normal limit, 0.60) and the presence of both regions of low VA/Q ratios (between 0.1 and 0.005) (mean 4.1%; range 0-18.8%) and shunt (VA/Q ratios below 0.005) (mean 3.9%; range 0.19.8%). There was a close similarity between measured and calculated PaO2 in normoxaemic patients, but calculated values exceeded measured PaO2 in hypoxaemic patients. The difference between calculated and measured PaO2 correlated inversely to DLCO (r = 0.65, p less than 0.05). An inverse correlation was also noted between DLCO and the sum of shunt and low VA/Q regions (r = 0.87, p less than 0.001). It is concluded that hypoxaemia in non-alcoholic liver cirrhosis patients can be accounted for by intrapulmonary shunting and VA/Q mismatch, and possibly a "diffusion-perfusion" defect in patients with more severe gas exchange impairment.

Adult

Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: evidence for a hepatopulmonary syndrome.

To examine the effect of liver transplantation on the respiratory and cardiovascular functions, ventilation/perfusion relationships were determined by multiple inert gas elimination technique in six patients with end-stage liver disease 1 to 19 mo before and 2 to 6 mo after liver transplantation. Cardiac output and pulmonary vascular pressures were measured after catheterization of the pulmonary artery. All patients had normal spirometry and chest x-ray films before transplantation. PaO2 before transplantation was 78.8 +/- 7.4 mm Hg (range = 51.8 to 102.8 mm Hg). All patients had perfusion of poorly ventilated lung regions (low ventilation/perfusion relationships) varying from 3% to 19% of cardiac output (mean = 8.5% +/- 2.4% of cardiac output) and two patients had intrapulmonary shunting (3% and 20% of cardiac output). Measured and calculated PaO2 agreed closely, indicating absence of pulmonary diffusion abnormality, as well as of extrapulmonary shunting. After transplantation, PaO2 normalized in all patients, and both shunting and low ventilation/perfusion relationships disappeared. Cardiac output decreased from 9.1 +/- 1.4 to 6.6 +/- 0.5 L/min (p less than 0.05), and the pulmonary vascular resistance increased from 0.69 +/- 0.14 to 1.64 +/- 0.43 mm Hg/L/min (p less than 0.05). The systemic vascular resistance also increased (before = 8.7 +/- 1.0; after = 15.3 +/- 1.1 mm Hg/L/min; p less than 0.001). Normalization of respiratory and cardiovascular alterations, after liver transplantation, in patients with end-stage liver disease indicates that these changes have a direct functional relationship to the diseased liver. It is hypothesized that this is part of a "hepatopulmonary syndrome,' which in similarity to the hepatorenal syndrome disappears with improved liver function.

Adult

Protein synthesis in skeletal muscle during starvation and refeeding: comparison of data from intact muscle and muscle biopsy material.

The intact extensor digitorum longus (EDL) preparation in rat is a well-documented model for assessing protein synthesis in skeletal muscle. Human muscle biopsy material has also been used, but the extent to which biopsy material is representative for evaluation of muscle protein synthesis has not been established. Therefore, the aim of this study was to compare protein synthesis in intact muscle and in muscle biopsy material simultaneously in rats. The animals (70 g) were divided into three groups: fed (n = 22), starved for 36 hours (n = 22), and refed for 24 hours (n = 19). Protein synthesis and RNA content were measured in each group. Protein synthesis was determined as the incorporation of 14-C-phenylalanine into muscle protein in the intact EDL muscle from one leg and in a muscle biopsy from the contralateral EDL muscle. The incorporation of 14-C-phenylalanine was linear over time in both preparations, but was consistently lower in the muscle biopsy compared with the intact muscle. The relative change in incorporation, in % of that obtained in the fed state, showed a decrease in incorporation after 36 hours of starvation, in both intact muscle and in muscle biopsy material, 33% +/- 10% and 42% +/- 6%, respectively. After 24 hours of refeeding, an overshoot in protein synthesis was seen, to 136% +/- 6% in the intact muscle and to 133% +/- 6% in the muscle biopsy, as compared with the fed state. The RNA content decreased during the starvation period from 21.6 +/- 0.7 to 14.5 +/- 0.4 mg RNA/g protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Simulation and evaluation of nicotine intake during passive smoking: cotinine measurements in body fluids of nonsmokers given intravenous infusions of nicotine.

The technique of monitoring cotinine concentrations in body fluids as a means of measuring nicotine intake during passive smoking has been evaluated in two studies, both of which used intravenous infusion to stimulate nicotine intake. In the first study, nicotine and cotinine were given separately, for 1 hour in four different intravenous doses (3.2, 15.4, 30.9, and 61.7 nmol/min) to each nonsmoker. In the second study, nicotine and cotinine were infused for 4 hours; each subject received five different doses of nicotine (1.5, 3.1, 6.2, 10.8, and 15.4 nmol/min) and one of cotinine (10.8 nmol/min). The concentration of cotinine was constant in both plasma and saliva from 1 to 4 hours after the nicotine infusion; the plateau levels of cotinine were found to be linearly and directly related to the nicotine intake. The ratio of salivary to plasma cotinine was 1:1.27. A linear relationship was also found between nicotine and cotinine infusion rates and the AUC values for cotinine. The fraction metabolized to cotinine was found to be about 0.5. The results from these studies show that: (1) there is a linear relationship between the plateau concentration of cotinine and the amount of nicotine infused over a period of 1 up to 4 hours; (2) salivary cotinine provides the same information on nicotine intake as does plasma cotinine; and (3) single measurements of either plasma or salivary cotinine concentrations at 1 to 4 hours after the exposure could be used to predict the nicotine intake during 1 to 4 hours of environmental tobacco smoke exposure.

Adult

Effect of in vivo contact between blood and dialysis membranes on protein catabolism in humans.

To investigate whether the contact between blood and dialysis membranes might induce muscle protein degradation, the exchange of free amino acids across leg tissues was measured by catheterization technique in three groups of healthy subjects before and after a 150 minute sham-hemodialysis procedure (SHDP), that is, in vivo passage of blood (100 ml/min) through a dialyzer but with no circulating dialysate. Dialyzers with either regenerated cellulose membrane (group CU, N = 10 and group CU-IND, N = 6) or polyacrylonitrile membrane (group AN, N = 8) were used in group CU-IND indomethacin was administered before (100 mg) and at the end (50 mg) of SHDP. Leg blood flow was measured by venous occlusion plethysmography. In group CU net leg release of tyrosine and phenylalanine increased from 3.4 +/- 0.8 and 3.6 +/- 0.8 nmol/min/100 g tissue, respectively, before SHDP to 7.8 +/- 1.8 and 8.3 +/- 1.8 nmol/min/100 g tissue, respectively, at 345 minutes after the start of SHDP (P less than 0.01). The total release of all measured amino acids increased from 148 +/- 31 to 309 +/- 50 nmol/min/100 g tissue (P less than 0.01). The results indicate that interaction between blood and regenerated cellulose membranes leads to accelerated net protein breakdown. In group CU-IND no change in leg amino acid release was observed following SHDP, suggesting that the increased net protein catabolism is mediated by prostaglandins. Sham hemodialysis using AN membranes did not result in increased amino acid efflux from leg tissues, implying that the protein catabolic effect of blood-membrane contact depends on the biochemical properties of dialyser.

Acrylic Resins

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