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Biomedical subjects

E Endert

Publications and source records attributed to E Endert.

At least 109 records · Page 6Linked to original sources
PubMed1993

Non-insulin-mediated glucose uptake in human immunodeficiency virus-infected men.

1. One of the metabolic features of acquired immunodeficiency syndrome is increased tissue glucose uptake documented by euglycaemic-hyperinsulinaemic clamp studies, suggesting increased insulin sensitivity. However, these results may also be related to the confounding effect of increased non-insulin-mediated glucose uptake in acquired immunodeficiency syndrome, which will result in an erroneously presumed increased insulin sensitivity. To study the contribution of non-insulin-mediated glucose uptake to total tissue glucose uptake in acquired immunodeficiency syndrome, we conducted a hypoinsulinaemic clamp study in clinically stable human immunodeficiency virus-infected (Centers for Disease Control class IV) men (n = 7) and healthy subjects (n = 5). Glucose uptake was measured by a primed, continuous infusion of [3-3H]glucose in the postabsorptive state and during somatostatin-induced insulinopenia at euglycaemic (approximately 5.3 mmol/l) and hyperglycaemic (approximately 11 mmol/l) glucose concentrations. 2. Basal glucose concentration (patients, 5.2 +/- 0.1 mmol/l; control subjects, 5.3 +/- 0.1 mmol/l) and basal glucose tissue uptake (patients, 15.9 +/- 0.5 mumol min-1 kg-1 fat-free mass; control subjects, 15.2 +/- 0.4 mumol min-1 kg-1 fat-free mass) were not different between the two groups. 3. Euglycaemic glucose uptake during somatostatin infusion, reflecting non-insulin-mediated glucose uptake, decreased to 82 +/- 3% in patients and 78 +/- 2% in control subjects (not significant). Under hyperglycaemic (approximately 11 mmol/l) conditions with sustained insulinopenia, no differences in glucose uptake existed between the two groups (patients, 16.8 +/- 0.6 mumol min-1 kg-1 fat-free mass; control subjects, 16.1+/- 0.3 mumol min-1 kg-1 fat-free mass).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Indomethacin stimulates basal glucose production in humans without changes in concentrations of glucoregulatory hormones.

1. To investigate whether indomethacin affects basal glucose production, we measured hepatic glucose production in six healthy postabsorptive subjects on two occasions: once after administration of indomethacin (150 mg orally) and once after administration of placebo. 2. Glucose production was measured by primed, continuous infusion of [3-3H]-glucose. 3. Indomethacin administration resulted in an increase in glucose production from 10.9 (SEM 0.3) mumol min-1 kg-1 to a maximum of 16.5 (SEM 1.6) mumol min-1 kg-1 (P < 0.05) within approximately 1 h, whereas in the control experiment glucose production declined gradually (P < 0.01) (P < 0.05 indomethacin versus control). There were no differences in plasma concentrations of insulin, C-peptide and counter-regulatory hormones between the two experiments. 4. Since indomethacin administration resulted in an increase in glucose production in the absence of any changes in concentrations of glucoregulatory hormones, we conclude that indomethacin stimulates hepatic glucose production through other mechanisms.

Adult↗
PubMed1993

Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration.

Stable isotope tracers and indirect calorimetry were used to evaluate the regulation of endogenous fat and glucose metabolism in relation to exercise intensity and duration. Five trained subjects were studied during exercise intensities of 25, 65, and 85% of maximal oxygen consumption (VO2max). Plasma glucose tissue uptake and muscle glycogen oxidation increased in relation to exercise intensity. In contrast, peripheral lipolysis was stimulated maximally at the lowest exercise intensity, and fatty acid release into plasma decreased with increasing exercise intensity. Muscle triglyceride lipolysis was stimulated only at higher intensities. During 2 h of exercise at 65% VO2max plasma-derived substrate oxidation progressively increased over time, whereas muscle glycogen and triglyceride oxidation decreased. In recovery from high-intensity exercise, although the rate of lipolysis immediately decreased, the rate of release of fatty acids into plasma increased, indicating release of fatty acids from previously hydrolyzed triglycerides. We conclude that, whereas carbohydrate availability is regulated directly in relation to exercise intensity, the regulation of lipid metabolism seems to be more complex.

Adult↗
PubMed1993

Pulsatile thyrotropin release in patients with untreated pituitary disease.

Pulsatile and nocturnal TSH secretion was investigated in 16 healthy controls (group A) and 19 patients with untreated pituitary disease [7 were euthyroid without suprasellar extension (group B), 6 were euthyroid with suprasellar extension (group C) of pituitary lesions, and 6 were hypothyroid with or without suprasellar extension (group D)]. Pulse analysis was performed using Desade and Cluster algorithms. No changes were observed among groups A-D in mean 24-h TSH pulse amplitude [values given as mean +/- SD; Desade, 0.4 +/- 0.2 vs. 0.7 +/- 0.4 vs. 0.6 +/- 0.4 vs. 0.5 +/- 0.2 mU/L (P = NS); Cluster, 0.4 +/- 0.2 vs. 0.7 +/- 0.4 vs. 0.5 +/- 0.3 vs. 0.4 +/- 0.2 mU/L (P = NS)] or in the mean 24-h TSH pulse frequency (approximately 10 pulses/24 h). The mean 24-h TSH concentration was highly correlated to the mean 24-h TSH pulse amplitude in controls (r = 0.93; P < 0.001) and patients (r = 0.63; P < 0.01), but not to the mean 24-h TSH pulse frequency. The nocturnal TSH surge was similar in controls and euthyroid patients without suprasellar extension (group A, 1.0 +/- 0.6; group B, 1.3 +/- 1.3 mU/L; P = NS), but was decreased in euthyroid patients with suprasellar extension (group C, 0.3 +/- 1.0 mU/L; P < 0.05) and hypothyroid patients (group D, 0.4 +/- 0.4 mU/L; P < 0.05). The decreased nocturnal TSH surge was associated with a loss of the usual nocturnal increase in TSH pulse amplitude, whereas the usual nocturnal increase in TSH pulse frequency was maintained. In conclusion, 1) mean 24-h TSH pulse amplitude and frequency are unchanged in untreated patients with pituitary disease; and 2) patients with central hypothyroidism as well as euthyroid patients with suprasellar extension of pituitary lesions had a decreased nocturnal TSH surge associated with a loss of the usual nocturnal increase in TSH amplitude, but not TSH pulse frequency.

Adult↗
PubMed1993

Pulsatile thyrotropin secretion in nonthyroidal illness.

Pulsatile and nocturnal TSH secretion was investigated in 16 healthy controls (group A) and 21 patients with nonthyroidal illness (NTI; group B). Ten patients had normal plasma T3 and T4 values (group B1), and 11 patients had decreased plasma T3 with normal or low plasma T4 (group B2). Mean 24-h TSH secretion in NTI patients was higher than that in controls (3.1 +/- 0.7 vs. 1.7 +/- 0.7 mU/L; P < 0.01; mean +/- SD). This was associated with an increased TSH pulse amplitude in NTI patients relative to controls [Desade, 0.79 +/- 0.46 vs. 0.44 +/- 0.20 mU/L (P < 0.01); Cluster, 0.64 +/- 0.42 vs. 0.39 +/- 0.20 mU/L (P < 0.05)]. There was no difference in TSH pulse amplitude between subgroups B1 and B2. TSH pulse frequency was not different between NTI patients and controls (approximately 10 pulses/24 h). The mean 24-h TSH concentration was significantly related to the mean 24-h TSH pulse amplitude but not to the mean 24-h TSH pulse frequency. The absolute nocturnal TSH surge in NTI patients was lower than that in controls (0.6 +/- 0.6 vs. 1.0 +/- 0.6 mU/L; P < 0.05). The lower nocturnal TSH surge in patients with decreased plasma T3 (group B2) was associated with a loss of the usual nocturnal increase of TSH pulse amplitude; the usual nocturnal increase in TSH pulse frequency was preserved. This was also observed in the six patients (two in group B1 and four in group B2) in whom the nocturnal TSH surge was completely absent. The changes in nocturnal TSH secretion in NTI resemble those found in central hypothyroidism, suggesting that features of central hypothyroidism are involved in the euthyroid sick syndrome.

Adult↗
PubMed1993

Thyroxine administration to infants of less than 30 weeks' gestational age does not increase plasma triiodothyronine concentrations.

Very preterm infants (less than 30 weeks' gestational age) were treated with thyroxine in three different dosage schemes: 10, 8 and 6 micrograms.kg-1 birthweight.day-1 during the first 6 weeks of life. The aim was to prevent transient hypothyroxinemia of the preterm infant. Plasma levels of thyroxine, free thyroxine, triiodothyronine, reverse triiodothyronine, thyroxine-binding globulin and thyrotropin were measured weekly. Thyroxine administration increased thyroxine and free thyroxine levels most properly in the 8-micrograms supplementation group. It did not result in a change in plasma triiodothyronine levels. Levels of reverse triiodothyronine increased in relation to the thyroxine dosage. Thyrotropin secretion was suppressed in the 6- and 8-micrograms groups during the first 2 weeks, while in the 10-micrograms group suppression lasted 4 weeks. No clinical adverse effects of thyroxine administration were seen. We conclude that 8 micrograms thyroxine.kg-1 birthweight.day-1 for 6 weeks prevents transient hypothyroxinemia. The finding that plasma triiodothyronine concentrations are not influenced by thyroxine administration suggests a specific maturation process in the deiodination of thyroxine.

Aging↗
PubMed1993

Soluble receptors for tumour necrosis factor: a putative marker of disease progression in HIV infection.

OBJECTIVE: To assess the value of concentrations of soluble receptors for tumour necrosis factor (sTNFR) as markers for disease progression in HIV infection. DESIGN: We measured concentrations of sTNFR in the serum of 32 HIV-infected male patients in various stages of disease and in 12 healthy male control subjects. Correlations between the levels of sTNFR and CD4+ lymphocyte counts were calculated. RESULTS: Serum levels of sTNFR p55 and p75 were elevated in parallel with severity of clinical stage. sTNFR p55 levels were higher at later stages of HIV infection (Centers for Disease Control stage IV) with or without concurrent illness, whereas sTNFR p75 was already elevated in asymptomatic carriers, compared with controls. There was an inverse correlation between sTNFR concentrations and CD4+ lymphocyte counts. CONCLUSIONS: Our results suggest that sTNFR concentrations could be potential markers for disease progression in HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Dehydroepiandrosterone as predictor for progression to AIDS in asymptomatic human immunodeficiency virus-infected men.

The steroid hormone dehydroepiandrosterone (DHEA) has been reported to protect against certain viral infections in animal models and to be a modest inhibitor of human immunodeficiency virus type 1 (HIV-1) infection in vitro. Serum DHEA levels were determined in 41 asymptomatic HIV-1-seropositive subjects, who progressed to AIDS within 5 years after entering a cohort study, in 41 HIV-1-seropositive controls, who remained asymptomatic, and in 41 HIV-1-seronegative controls. At entry, DHEA levels were higher in the seronegative group (median, 13.3 nmol/l) than in either the seropositive nonprogressors (median, 9.2 nmol/l; P = .01) or the progressors (median, 7.2 nmol/l; P less than .001). DHEA levels in the progressors approximately 5 months before the diagnosis of AIDS were lower than the levels in the nonprogressors after the same follow-up (median, 5.6 vs. 8.8 nmol/l; P = .007). DHEA levels less than 7 nmol/l and CD4+ cell counts less than 0.5 x 10(9)/l both proved to be independent predictors for disease progression in HIV-1-infected men.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Circadian changes in pulsatile TSH release in primary hypothyroidism.

OBJECTIVE: We evaluated pulsatile and circadian TSH secretion in primary hypothyroidism. DESIGN: In a prospective study, blood was sampled every 10 minutes during 24 hours for assay of TSH (IRMA). Thyroid hormones and TSH responsiveness to TRH were then measured. SUBJECTS: Nine patients with overt primary hypothyroidism, seven patients with subclinical hypothyroidism and 16 healthy controls. MEASUREMENTS: Computer-assisted analysis by the Desade and Cluster programs. RESULTS: Both computer-assisted programs revealed an increased TSH pulse amplitude in both overt and subclinical hypothyroidism versus controls (Desade: 36.9 +/- 31.4 (mean +/- SD) (P < 0.001) and 2.8 +/- 1.9 (P < 0.001) vs 0.4 +/- 0.2 mU/l; Cluster: 25.6 +/- 25.1 (P < 0.001) and 2.4 +/- 1.4 (P < 0.001) vs 0.4 +/- 0.2 mU/l). TSH pulse frequency remained unchanged with approximately 10 pulses/24 hours. A highly significant correlation was found between the mean 24-hour TSH concentration and the TSH pulse amplitude in all controls and patients but not to TSH pulse frequency. The nocturnal TSH surge was absent in six out of nine patients with overt primary hypothyroidism. The deficient nocturnal rise of TSH in primary hypothyroidism vs controls (22 +/- 51 vs 82 +/- 41%, P < 0.001), was associated with a loss of the usual nocturnal increase in TSH pulse amplitude and frequency. CONCLUSIONS: Mean 24-hour TSH pulse amplitude is increased in primary hypothyroidism, but TSH pulse frequency remains unchanged. The decrease of the nocturnal TSH increase in primary hypothyroidism is associated with a loss of the usual nocturnal increase in TSH pulse amplitude and frequency.

Adult↗
PubMed1992

The nocturnal thyroid-stimulating hormone surge is absent in overt, present in mild primary and equivocal in central hypothyroidism.

UNLABELLED: The nocturnal TSH surge was studied in controls, in 34 patients with hypothalamic/pituitary disease and in 21 patients with primary hypothyroidism. It was absent in 5/12 hypothyroid patients and in 5/22 euthyroid patients with hypothalamic/pituitary disease (42% vs 23%, NS). Central hypothyroidism relative to euthyroidism was associated with a lower absolute (0.3 +/- 0.4 vs 0.9 +/- 1.0 mU/l, p less than 0.05) and relative (24 +/- 31 vs 63 +/- 51%, p less than 0.05) nocturnal rise in TSH. In primary hypothyroidism, the nocturnal TSH surge was absent in eight of ten patients with overt, in one of five patients with mild and in none of six patients with subclinical hypothyroidism. The relative nocturnal rise in TSH was normal in mild (54 +/- 33%) and subclinical (92 +/- 69%), but decreased in overt hypothyroidism (2 +/- 10%). Plasma T4 was positively and 09.00 plasma TSH negatively related to the relative nocturnal TSH surge in primary hypothyroidism, but not in central lesions. In both conditions, however, a positive relationship was observed between the relative nocturnal TSH surge and the relative increase of TSH to TRH. IN CONCLUSION: (a) The nocturnal TSH surge is usually absent in overt hypothyroidism but present in mild primary hypothyroidism and equivocal in central hypothyroidism. This limits its usefulness as an adjunct in the diagnosis of central hypothyroidism. (b) The magnitude of the nocturnal TSH surge in patients with hypothalamic/pituitary disease or primary hypothyroidism is directly related to the TSH response to TRH, and thus appears to be determined by the directly releasable TSH pool of the pituitary.

Circadian Rhythm↗
PubMed1991

Improved method for the determination of serotonin in plasma by high-performance liquid chromatography using on-line sample pre-treatment.

An improved method for the determination of serotonin in platelet-rich plasma (PRP) and platelet-poor plasma (PPP), by reversed-phase high-performance liquid chromatography with electrochemical detection and direct plasma injection, is described. The chromatographic system comprises a strong cation-exchange pre-column and a C18 analytical column. The method is selective, rapid, simple and sensitive, and offers good reproducibility and recovery. Reference values for serotonin concentrations in healthy adults (n = 10) are 31 nM for PPP and 6 nmol per 10(9) platelets for PRP. The conditions used for the preparation of PRP and PPP may influence the serotonin concentration in PRP.

Adult↗
PubMed1991

Glucose and fat metabolism during short-term starvation in cirrhosis.

To evaluate the metabolic consequences of short-term (i.e., less than 24 hours) starvation, glucose and fat metabolism were studied in eight healthy subjects and in eight patients with stable cirrhosis after 16-hour and again after 22-hour starvation by 3-[3H]glucose and [14C]palmitate turnover and by indirect calorimetry. Although patients and controls showed significant increases in free fatty acid concentration (respectively, 48% +/- 12% and 53% +/- 17%) and turnover (55% +/- 14% and 71% +/- 21%) during short-term starvation, the values after 16- and after 22-hour starvation were higher in cirrhosis. Fat oxidation was enhanced in the patients, but did not increase during fasting in contrast to controls (increase 19% +/- 17%, P less than 0.05). Net glucose oxidation was decreased in postabsorptive cirrhotics (P less than 0.05). Although postabsorptive glucose turnover was not different from controls, starvation induced a greater decrease in glucose turnover in the patients (25% +/- 3% vs. 10% +/- 3%, P less than 0.05). This was not reflected in plasma glucose concentrations. In conclusion, the effects of starvation on glucose and fat metabolism are enhanced in cirrhosis; fasting hypoglycemia is prevented by decreased use of glucose. It remains to be established whether these changes are merely explained by defective liver function, per se.

Adult↗
PubMed1991

Insulin sensitivity and insulin clearance in human immunodeficiency virus-infected men.

To test whether clinically stable human immunodeficiency virus (HIV) infection, like other infections, is associated with insulin resistance and increased insulin clearance, we measured the sensitivity to insulin and insulin clearance using the euglycemic insulin clamp technique in 10 clinically stable outpatients with symptomatic HIV infection (Centers for Disease Control [CDC] group IV) and 10 healthy controls. During administration of 0.8 and 4 mU insulin.kg-1.min-1, HIV-infected men had 40% (P less than .02) and 83% (P less than .01) higher rates of insulin clearance when compared with healthy controls. Despite significantly lower steady-state insulin concentrations (42 +/- 2 v 52 +/- 4 microU/mL, P less than .05, and 255 +/- 17 v 392 +/- 14 microU/mL, P less than .001, patients v controls), patients and controls had similar total glucose uptake (7.99 +/- 0.81 v 7.92 +/- 0.44 mg.kg-1.min-1 and 14.00 +/- 0.81 v 13.65 +/- 0.65 mg.kg-1.min-1, patients v controls). In the postabsorptive state, no differences were found between patients and controls in insulin levels (7 +/- 1 microU/mL in both) and endogenous glucose production (2.52 +/- 0.07 and 2.24 +/- 0.17 mg.kg-1.min-1, respectively), but plasma glucose levels in the patients (5.02 +/- 0.15 mmol/L) were significantly lower when compared with controls (5.46 +/- 0.14 mmol/L, P less than .05). The results indicate that HIV-infected men have increased rates of insulin clearance and increased sensitivity of peripheral tissues to insulin, which makes HIV infection unique with regard to glucose and insulin metabolism.

Adult↗
PubMed1991

Sex- and time-dependent changes in neurochemical and hormonal variables induced by predictable and unpredictable footshock.

Previous experiments have revealed sex-dependent effects of inescapable shock in rats. Behavior of male rats was more severely disrupted by inescapable shock than behavior of female rats. These sex differences were found after 1- and 24-hour intervals but not after a 72-hour interval. The present experiment was designed to study various physiological parameters at 1-, 4- and 24-hour intervals after inescapable footshock. The predictability of shock was manipulated by adding a compound light and tone stimulus that preceded shock presentation for one group but was not correlated with shock presentation for another group of subjects. Noradrenaline, dopamine, serotonin, and metabolites of these 3 transmitters were measured in the frontal cortex. Transient shock-induced increments in dopamine and metabolites of dopamine and serotonin were found, but the sex of the animal did not differentially affect this neurotransmitter response. In addition to neurotransmitter concentrations in the frontal cortex, levels of corticosterone were measured in plasma. The pituitary-adrenal axis was activated for a longer period in females than males after shock. The present data do not provide evidence that behavioral sex differences induced by inescapable shock are paralleled by sex differences in neurotransmitter activity. In addition, sex-dependent effects of predictability of shock on neurotransmitter activity were not detected. The relevance of the observed sex-dependent responses in the pituitary-adrenal system is discussed.

Animals↗
PubMed1991

Basal fuel homoeostasis in symptomatic human immunodeficiency virus infection.

1. In eight clinically stable symptomatic human-immunodeficiency-virus-infected patients and in seven healthy control subjects, glucose and fat metabolism were studied, using indirect calorimetry and primed continuous infusions of [3-3H]glucose and [14C]palmitate. 2. Studies were performed in the post-absorptive state (16 h of overnight fasting) and again after 22 h of overnight fasting. 3. In the post-absorptive state, net fat oxidation and triacylglycerol ('triglyceride') concentrations were significantly higher in the patients, but concentrations and turnover of free fatty acids were not significantly different between patients and control subjects. After 22 h of overnight fasting, free fatty acid turnover in the patients rose to significantly higher levels when compared with the control subjects. 4. Post-absorptive glucose oxidation, glucose turnover and glucose clearance did not differ between patients and control subjects. Although fasting induced a significantly greater decline in glucose turnover in the patients, plasma glucose concentrations decreased comparably in patients and control subjects. 5. No differences were found in plasma concentrations of insulin or of the counter-regulatory hormones between patients and control subjects. 6. It is concluded that the metabolic adaptation to short-term starvation in clinically stable human-immuno-deficiency-virus-infected patients differs from that in healthy control subjects. Short-term starvation results in a significantly greater fall in glucose turnover, whereas fat metabolism is clearly stimulated. These alterations cannot be explained by differences in the concentrations of insulin or of the counter-regulatory hormones.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Resting energy expenditure and substrate oxidation in human immunodeficiency virus (HIV)-infected asymptomatic men: HIV affects host metabolism in the early asymptomatic stage.

To study the effect of persistent human immunodeficiency virus (HIV) infection on host metabolism, we performed indirect calorimetry in 11 asymptomatic HIV-infected patients (Centers for Disease Control group II or III) who were seropositive for greater than or equal to 1 y, but who still had normal numbers of circulating CD4+ T cells, and in 11 healthy control subjects of similar age and relative body composition. HIV-infected patients had 8% (P less than 0.05) higher rates of resting energy expenditure than did control subjects. Fat-oxidation rates were significantly higher in the patients (means +/- SE: 2.90 +/- 0.08 vs 2.19 +/- 0.17 g.kg FFM-1.d-1, patients vs control subjects, P less than 0.01) whereas no significant differences in carbohydrate-oxidation rates between patients and control subjects were found. These alterations in metabolism were not associated with increased concentrations of catecholamines, cortisol, or thyroid hormones. Mean concentrations of interleukin 6 in the patients were increased only twofold when compared with healthy control subjects. The results indicate that HIV infection affects host metabolism in the early asymptomatic stage, before CD4+ T cell numbers start to decline.

Adult↗
PubMed1991

Effects of interpleurally administered bupivacaine 0.5% on opioid analgesic requirements and endocrine response during and after cholecystectomy: a randomized double-blind controlled study.

In 30 patients undergoing cholecystectomy, a randomized double-blind saline-controlled study was performed using interpleural 0.5% bupivacaine with or without epinephrine (5 micrograms.ml-1) in combination with 0.8% halothane inspired concentration in oxygen. The aim of the study was to investigate whether interpleural 0.5% bupivacaine could decrease the intraoperative opioid requirements and attenuate the metabolic endocrine response to surgical stress. Patients were randomly allocated to one of three groups: Group 1: 0.5% bupivacaine; Group 2: 0.5% bupivacaine with epinephrine (5 micrograms.ml-1); and Group 3: saline. The interpleural catheter was inserted after induction of anesthesia in the spontaneously breathing patient. The study drug was injected 30 min prior to surgery. Peak plasma bupivacaine concentrations in the respective groups were 1.30 +/- 0.78 and 1.16 +/- 0.48 micrograms.ml-1. In all patients concentrations were below suggested convulsive level. Two patients in Group 1 and two in Group 2 required intraoperative fentanyl (0.1 mg each). In contrast, eight patients in the saline group received an average of 0.21 mg (range 0.1 +/- 0.4 mg) fentanyl (P less than 0.05). Postoperatively, a second dose of the study drug was given. Subsequently, pain was assessed using a visual analog score and a verbal rating scale. Pain scores decreased significantly 30 min after the interpleural injection in both bupivacaine groups and remained unchanged in the saline group (P less than 0.05). Pain management by means of interpleural bupivacaine was successful in 17 of the 20 patients. In the saline group seven out of ten patients needed additional analgesics (P less than 0.05). Cortisol levels increased in response to surgery in all groups: maximum levels in Groups 1, 2 and 3 were: 1.09 +/- 0.29, 1.11 +/- 0.20 and 1.19 +/- 0.16 mumol.l-1, respectively. Plasma glucose concentrations increased significantly in all groups: maximum levels in Groups 1, 2 and 3 were: 7.6 +/- 1.3, 7.3 +/- 1.7 and 8.3 +/- 1.7 mmol.l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗