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Biomedical subjects

J A Romijn

Publications and source records attributed to J A Romijn.

At least 19 recordsLinked to original sources
PubMed1995

Truncal vagotomy does not affect postabsorptive glucose metabolism in humans.

To evaluate the effects of hepatic vagal denervation on the adaptation of glucose metabolism to short-term starvation (i.e., < 24 h), glucose metabolism was studied after 16 and again after 22 h of fasting in postsurgical patients with truncal vagotomy (n = 9; radical resection of esophageal carcinoma) and without truncal vagotomy (n = 5; partial resection of the large bowel for carcinoma). Glucose metabolism was studied 3-7.5 mo postoperatively by [3-3H]glucose turnover and by indirect calorimetry. Basal glucose production, plasma glucose concentration, glucose oxidation, serum free fatty acid concentration, and fat oxidation were not different between groups; neither were plasma concentrations of glucoregulatory hormones. The adaptation to prolongation of the fast by 6 h was not different for any of these parameters between both groups. In conclusion, truncal vagotomy does not affect the adaptation of glucose metabolism to the postabsorptive state (16-22 h of fasting).

Aged↗
PubMed1995

Acute effects of interferon-alpha administration on thyroid hormone metabolism in healthy men.

Both hyper- and hypothyroidism have been reported during prolonged recombinant human interferon-alpha (rhIFN alpha) therapy. To assess the short term effects of IFN alpha therapy on thyroid hormone metabolism, we measured thyroid hormone concentrations in eight healthy volunteers for 24 h after sc administration of rhIFN alpha and, on another occasion, after sc administration of saline (control study). There were no effects of rhIFN alpha on plasma T4 and free T4 or on thyroid hormone binding index. However, rhIFN alpha induced a significant decrease in the plasma concentrations of TSH (P < 0.03) and T3 (P < 0.02) compared with those in the control study, associated with an increase in rT3 concentrations (P < 0.02). IFN alpha induced a moderate increase in interleukin-6 (IL-6) concentrations (P < 0.02 vs. control study), whereas IL-1 and tumor necrosis factor concentrations remained below the detection limit in all subjects. It is concluded that IFN alpha administration induces major changes in thyroid hormone metabolism, possibly mediated in part by IL-6. The acute effects of rhIFN alpha mimic the euthyroid sick syndrome and appear to be different from the effects of chronic rhIFN alpha treatment on thyroid hormone metabolism.

Adult↗
PubMed1995

Increased basal glucose production in type 1 Gaucher's disease.

To evaluate the metabolic effects of Gaucher's disease, glucose metabolism and parameters of fat metabolism were studied by indirect calorimetry and primed continuous infusion of [3-3H]glucose in seven clinically stable untreated patients with type 1 Gaucher's disease and in seven healthy matched control subjects. Studies were performed in the postabsorptive state. In Gaucher patients, resting energy expenditure was increased by approximately 24% (29.4 +/- 0.7 vs. 23.7 +/- 0.8 kcal/kg.day; P < 0.01). Glucose production was increased by approximately 30% in patients compared to controls (14.00 +/- 0.51 vs. 10.77 +/- 0.26; P < 0.01), although plasma glucose concentrations and net glucose oxidation were not different. Although C peptide concentrations were not different, insulin concentrations were slightly increased in Gaucher patients (P < 0.05). The differences in basal glucose production were not related to differences in plasma concentrations of insulin or other glucoregulatory hormones. In conclusion, the increase in basal glucose production is a remarkable feature of type 1 Gaucher's disease, which cannot merely be explained by endocrine mechanisms. Because Gaucher's disease is manifested within the liver in macrophages, but not in hepatocytes, altered intrahepatic regulatory mechanisms might be involved in this increase in glucose production.

Adaptation, Physiological↗
PubMed1992

Comparison of indirect calorimetry and a new breath 13C/12C ratio method during strenuous exercise.

A new stable isotope method for the determination of substrate oxidation rates in vivo is described and compared with indirect calorimetry at rest and during high-intensity exercise (30 min at 80-85% maximal O2 uptake capacity) in six well-trained cyclists. This method uses the absolute ratios of 13C/12C in expired air, endogenous glucose, fat, and protein in addition to O2 consumption and is independent of CO2 production (VCO2). Carbohydrate and fat oxidation rates at rest, calculated by both methods, were not significantly different. During exercise the breath 13C/12C ratio increased and reached a steady state after 15-20 min. Carbohydrate oxidation rates during exercise were 39.4 +/- 5.2 and 41.7 +/- 5.7 mg.kg-1.min-1 [not significant (NS)], and fat oxidation rates were 7.3 +/- 1.3 and 6.9 +/- 1.2 mg.kg-1.min-1 (NS), using indirect calorimetry, and the breath ratio method, respectively. We conclude that the breath 13C/12C ratio method can be used to calculate substrate oxidation under different conditions, such as the basal state and exercise. In addition, the results obtained by this new method support the validity of the underlying assumption that indirect calorimetry regards VCO2 as a reflection of tissue CO2 production, during exercise in trained subjects, even up to 80-85% maximal O2 uptake.

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

Erythropoietin.

Explore the source record for details and available documents.

Blood Transfusion, Autologous↗
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

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

Tumor necrosis factor mimics the metabolic response to acute infection in healthy humans.

To evaluate the role of tumor necrosis factor (TNF) in the initiation of the metabolic response to acute infection, we performed a crossover saline-controlled study in six healthy postabsorptive men, investigating the metabolic effects of a bolus intravenous injection of recombinant human TNF (50 micrograms/m2). TNF induced a transient stress hormone response, associated with an early and sustained rise in plasma glucose concentrations (percentage increase at 2 h 23 +/- 7; P less than 0.05). Glucose turnover, measured 7.5 h postinjection, was 10 +/- 3% higher after TNF administration (P less than 0.05). Plasma free fatty acids (FFA) and glycerol concentrations increased transiently after TNF injection, peaking after 4 h (percentage increase 363 +/- 83 and 67 +/- 14, respectively; both P less than 0.05). FFA turnover, determined 6.5 h postinjection, increased in five subjects to a variable extent (percentage increase 126 +/- 55; P less than 0.05). Finally, resting energy expenditure showed a transient rise after TNF injection (34 +/- 2% at 4 h; P less than 0.05). We conclude that intravenous TNF reproduces many of the metabolic changes observed in septicemia, suggesting that TNF may be an initiating factor in the development of the metabolic response to acute infection.

Acute Disease↗
PubMed1990

[Multi-organ failure caused by colchicine poisoning].

A 61-year-old woman was admitted because of colchicine intoxication. After a period with gastrointestinal symptoms multiple organ failure and secondary septicaemia developed. The patient died of irreversible shock. The pharmacology of colchicine and the clinical manifestations and therapy of colchicine intoxication are discussed.

Colchicine↗
PubMed1990

Hypoglycemia, hormones and cytokines in fatal meningococcal septicemia.

A unique case report with sequential measurements of the plasma concentrations of glucoregulatory hormones, interleukin-6 and tumor necrosis factor during development of hypoglycemia in fatal meningococcemia is presented. Hormonal explanations for hypoglycemia like hyperinsulinemia or defective hypoglycemic counter-regulation were excluded. Plasma concentrations of interleukin-6 and tumor necrosis factor were skyhigh. The putative relation between cytokines and hypoglycemia in sepsis is discussed.

Adult↗
PubMed1990

Decreased glucose oxidation during short-term starvation.

Prolonged fasting (for days or weeks) decreases glucose production and oxidation. The effects of short-term starvation (ie, less than 24 hours) on glucose metabolism are not known. To evaluate this issue, glucose oxidation and glucose turnover were measured after 16-hour and subsequently after 22-hour fasting. Glucose oxidation was calculated by indirect calorimetry in 12 healthy men (age 22 to 44 years); glucose turnover was measured by primed, continuous infusion of 3-3H-glucose in eight of these 12 volunteers. After 16-hour fasting net glucose oxidation was 0.59 +/- 0.17 mg x kg-1 x min-1 and glucose tissue uptake 2.34 +/- 0.12 mg x kg-1 x min-1. No correlation was found between net glucose oxidation and glucose tissue uptake. Prolonging fasting with an additional 6 hours resulted in decreases of respiratory quotient (0.77 +/- 0.01 v 0.72 +/- 0.01) (P less than .005), plasma glucose concentration (4.7 +/- 0.1 v 4.6 +/- 0.1 mmol/L) (P less than .05), glucose tissue uptake (2.10 +/- 0.12 mg x kg-1 x min-1) (P less than .05), net glucose oxidation (0.09 +/- 0.04 mg x kg-1 x min-1) (P less than .005), and plasma insulin concentration (8 +/- 1 v6 +/- 1 mU/L) (P less than .005). Net glucose oxidation expressed as a percentage of glucose tissue uptake decreased from 22% +/- 8% to 2% +/- 1% (P less than .05). There was no net glucose oxidation in seven of 12 controls after 22-hour fasting.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Increased resting energy expenditure in human immunodeficiency virus-infected men.

Even in the absence of anorexia and malabsorption, weight loss is frequently observed in patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC). To investigate whether increased resting energy expenditure (REE) might be responsible for this weight loss, indirect calorimetry was performed in 18 human immunodeficiency virus (HIV)-infected men free of clinically active opportunistic infections for at least 2 months. Patients with AIDS (n = 11) or ARC (n = 7) had 9% higher rates of REE when compared with 11 healthy volunteers (P less than .05) with similar food intake and of the same body composition. The results obtained from patients with AIDS or ARC were identical. As no differences were found between patients and controls in plasma concentrations of catecholamines, thyroid hormones, cortisol, or tumor necrosis factor, except for lower concentrations of norepinephrine in the patients (mean +/- SD, 233 +/- 111 v 367 +/- 125 ng/L, patients v controls, P less than .01), this hypermetabolism is not explained by higher levels of these catabolic hormones. The results indicate that even in the absence of acute concomitant infections, increased REE may contribute to the weight loss in patients with AIDS or ARC.

AIDS-Related Complex↗
PubMed1990

Decreased nocturnal surge of thyrotropin in nonthyroidal illness.

To evaluate the regulation of TSH secretion in nonthyroidal illness (NTI) we studied the nocturnal TSH surge in 11 healthy controls and 26 NTI patients; none of the patients was on medication known to interfere with TSH secretion. The presence of a nocturnal TSH surge was defined as a mean nighttime TSH (the mean of 5 samples taken hourly from 0000-0400 h) significantly greater than the mean daytime TSH (the mean of 5 samples taken from 1500-1900 h). A nocturnal TSH surge was present in 11 of 26 NTI patients and in 11 of 11 controls (P less than 0.01). Both the absolute (0.3 +/- 0.1 vs. 1.0 +/- 0.2 mU/L; P less than 0.01) and relative (11 +/- 6% vs. 71 +/- 12%; P less than 0.001) nocturnal TSH surges were lower in NTI patients than in controls. NTI patients had lower plasma T3 (1.11 +/- 0.08 vs. 1.84 +/- 0.11 nmol/L; P less than 0.001) and higher plasma rT3 (0.81 +/- 0.24 vs. 0.23 +/- 0.01 nmol/L; P less than 0.001) concentrations than controls, but T4, FT4, and TSH values were similar in both groups. No differences were found between the 15 NTI patients without nocturnal TSH surge and the 11 patients with a nocturnal TSH surge in sex distribution, age, caloric intake, or plasma T4 and T3, but hospital mortality was slightly, although not significantly, higher in those with an absent nocturnal TSH surge. An absent nocturnal TSH surge occurred in 2 of 2 patients with a low TSH (less than 0.4 mU/L), in 11 of 20 patients with a normal TSH (0.4-4.0 mU/L), and in 2 of 4 patients with a high TSH (greater than 4.0 mU/L). Pituitary TSH responsiveness to TRH was similar in patients with or without a nocturnal TSH surge. We conclude that NTI is frequently associated with a decreased nocturnal TSH surge. This phenomenon is not related to ambient plasma T4, T3, or TSH concentrations or pituitary TSH responsiveness to TRH. A decreased nocturnal TSH surge appears to be one of the features of the sick euthyroid syndrome and is probably related to hypothalamic dysregulation.

Age Factors↗