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Biomedical subjects

J Møller

Publications and source records attributed to J Møller.

At least 19 recordsLinked to original sources
PubMed1992

[Hepatocellular adenoma after oral contraception].

Raised serum basic phosphatase was found incidentally in a woman aged 43 years. Investigation with biopsy revealed a hepatocellular adenoma. The tumour regressed after withdrawal of Neogentrol oral contraception which the patient had consumed for 17 years. The patient did not desire invasive treatment. Employment of oral contraceptive steroids for more than two years is associated with increased occurrence of hepatocellular adenomata. The hepatocellular adenoma is a clearly delimited, most frequently solitary, benign tumour with limited malignant potential but with a considerable risk of rupture with haemorrhage even after withdrawal of oral contraception. The hepatocellular adenoma has no malignant tumour vessels (in contrast to hepatocellular carcinoma) and it appears as a cold region on scintigraphy (in contrast to focal nodular hyperplasia), but the diagnosis can only be established with certainty by histological examination. The hepatocellular adenoma consists most frequently of large pale hepatocytes in trabeculae surrounded by a net of reticulin and separated by sinusoids. Biliary passage and portal spaces do not occur. The best treatment consists of excision of the tumour or embolisation. If invasive treatment is postponed, regular scanning should be performed to observe regression or progression of the tumour and oral contraception and pregnancy should be advised against on account of the risk of growth of the tumour.

Adult↗
PubMed1992

Dose-response studies on the metabolic effects of a growth hormone pulse in humans.

Whereas the lipolytic and diabetogenic consequences of sustained growth hormone (GH) exposure are well described, the metabolic effects of a short-lived physiological GH pulse have only recently been reported. To assess the possible dose-response of such short-term bolus administration of GH, six healthy, male subjects were each studied thrice for 4 1/2 hours after an intravenous (IV) bolus of either 70, 140, or 350 micrograms GH, resulting in peak GH concentrations of 10, 15, and 34 micrograms/L. Observed results include: (1) Time- (but not dose-) dependent changes (P less than .05) in plasma glucose and an acute (from 10 minutes onward), persistent, 40% decrease in forearm glucose uptake. Total glucose turnover decreased steadily with time on all occasions. (2) Time- and dose-dependent increases (P less than .05) in the concentrations of circulating lipid intermediates, with an increase of 3-hydroxybutyrate (3-OHB) from a basal of 35 mumol/L to peak values of 108 +/- 34 (70 micrograms), 176 +/- 46 (140 micrograms), and 232 +/- 51 mumol/L (350 micrograms), forearm uptake of 3-OHB changed in parallel. (3) Respiratory exchange ratio decreased (P less than .05) with increasing GH doses (indicating increased lipid and decreased glucose oxidation), and energy expenditure remained unaffected. (4) Concentrations of insulin, C-peptide, and glucagon were unchanged throughout all studies. We conclude that the stimulating effects of a modest GH bolus on circulating lipid intermediates and lipid oxidation are dose-dependent. This finding underlines the potential role of GH as a principal physiological regulator of fuel consumption in the maintenance of metabolic homeostasis.

3-Hydroxybutyric Acid↗
PubMed1992

Effects of growth hormone administration on fuel oxidation and thyroid function in normal man.

In a randomized, double-blind, placebo-controlled, cross-over study, we examined the effects of 14 days of growth hormone (GH) administration (12 IU/d subcutaneously) on energy expenditure (EE), respiratory exchange ratio (RER), and thyroid function in 14 normal adults of normal weight (eight men and six women). EE (kcal/24 h) was significantly elevated after GH administration (2,073 +/- 392, [GH], 1,900 +/- 310, [placebo], P = .01). RER was significantly lowered during GH administration (0.73 +/- 0.04 v 0.78 +/- 0.06, P = .02), reflecting increased oxidation of lipids. Total triiodothyronine (TT3) (nmol/L) and free T3 (FT3) (pmol/L) increased significantly during GH (TT3: 1.73 +/- 0.06 [GH], 1.48 +/- 0.08 [placebo], P = .01; FT3: 6.19 +/- 0.56 [GH], 5.49 +/- 0.56 [placebo], P = .01). Concomitantly, an insignificant decrease in reverse T3 (rT3) (nmol/L) was observed (0.07 +/- 0.01 [GH], 0.15 +/- 0.01 [placebo], P = .08). GH caused a highly significant increase in T3/thyroxine (T4) (x 100) ratio (1.84 +/- 0.12 [GH], 1.37 +/- 0.06 [placebo]). Serum thyrotropin (TSH) was not significantly changed by GH. No changes in total thyroxine (TT4) (nmol/L) (98 +/- 6 [GH], 111 +/- 8 [placebo], P = .40) and free thyroxine (FT4) (pmol/L) (17.4 +/- 1.3 [GH], 18.6 +/- 1.1 [placebo], P = .37) after 14 days of GH administration were observed. In conclusion, 2 weeks of GH administration increases EE and lipidoxidation. This finding may partly be mediated by an increase in peripheral T4 to T3 conversion.

Adult↗
PubMed1992

Growth hormone secretory capacity and serum insulin-like growth factor I levels in primary infertile, anovulatory women with regular menses.

OBJECTIVE: To test the hypothesis that anovulation and infertility in women is associated with an impaired secretory capacity for growth hormone (GH). DESIGN: Comparison of the hormonal and metabolic response to two GH stimulation tests in a patient group and in a control group. SETTING: Outpatients and healthy volunteers studied at a clinical research unit of a university hospital. PATIENTS, PARTICIPANTS: Eight infertile, anovulatory women (luteal phase serum progesterone [P] less than 25 nmol/L) with regular cyclic bleeding. Eight age- and body mass index-matched healthy volunteers with luteal phase serum P levels greater than 25 nmol/L. INTERVENTIONS: After an overnight fast, each subject underwent a standardized GH stimulation test composed of sequential arginine infusion and heat exposure on days 5 to 8 of the menstrual cycle. MAIN OUTCOME MEASURES: Serum GH, insulin-like growth factor I (IGF-I), insulin and non-esterified fatty acids (NEFA). RESULTS: Serum GH increased in both groups but was significantly lower in the study group (P less than 0.03). No difference was found in the circulating levels of IGF-I, insulin, and NEFA. CONCLUSIONS: Relative GH insufficiency seems to be present in these patients, but the clinical significance of this finding remains to be elucidated.

Adult↗
PubMed1992

Effect of piroxicam in addition to continuous thoracic epidural bupivacaine and morphine on postoperative pain and lung function after thoracotomy.

Twenty-eight patients scheduled for lung resection with lateral thoracotomy and postoperative chest drains during combined thoracic epidural bupivacaine plus morphine and general anaesthesia were studied. Postoperative pain treatment was continuous epidural infusion of bupivacaine 0.25% 5 ml h-1 plus morphine 0.2 mg h-1 for 48 h and, in addition, the patients received rectal piroxicam 40 mg randomly and double-blind 12 h and 1 h before surgery and 20 mg 24 h-1 postoperatively or placebo. Pain was evaluated at rest, during cough and mobilisation, together with pulmonary function (FEV1, FVC, PEFR) and sensory level of analgesia repeatedly for 48 h. The results showed efficient pain relief, but without differences in pain scores or need for supplementary analgesics between the two groups. Pulmonary function decreased similarly in the two groups. Thus we were unable to show enhanced analgesia by supplementing an otherwise effective low-dose epidural bupivacaine and morphine treatment with piroxicam after thoracic surgery with chest drains.

Administration, Rectal↗
PubMed1992

Assessment of glucose turnover rates in euglycaemic clamp studies using primed-constant [3-3H]-glucose infusion and labelled or unlabelled glucose infusates.

Underestimation of glucose turnover rates has been a problem in clamp studies using primed-constant [3-3H]-glucose infusion technique. Due to slow mixing in interstitial compartments concealed specific activity gradients may arise between plasma and interstitial compartments during intravenous unlabelled glucose infusion. Such specific activity gradients, however, can be prevented if plasma specific activity is maintained constant. Two euglycaemic clamp studies (insulin infusion 40 mU m-2 min-1) were performed in six lean normal subjects. Using conventional unlabelled glucose infusates plasma specific activity declined by 74%, tracer determined glucose appearance was smaller than actual glucose infusion rates (317 +/- 11 vs 366 +/- 15 mg m-2 min-1, p < 0.001), and erroneous negative values were calculated for glucose production (- 49 +/- 7 mg m-2 min-1). Average underestimation during the first 2 h correlated with glucose infusion rates (r = 0.88, p < 0.02). In contrast, when plasma specific activity was maintained constant, using appropriately labelled glucose infusates, tracer determined glucose appearance and glucose infusion rates were similar (385 +/- 16 vs 385 +/- 17 mg m-2 min-1), and negative errors for glucose production were avoided. In conclusion, using unlabelled glucose infusates, as in previous studies, suppression of glucose production is overestimated and stimulation of glucose utilization is underestimated. As errors were greater with larger glucose infusions, the mistakes may have been greatest in insulin sensitive control subjects, and smaller in insulin resistant subjects. Therefore, re-evaluation of hepatic insulin sensitivity seems appropriate in diabetes, obesity, and other insulin resistant states.

Adult↗
PubMed1992

Thyroid function during growth hormone therapy.

Administration of growth hormone (GH) in GH-deficient patients has been reported to cause a variety of perturbations in thyroid function. Reports range from decreased sensitivity of thyrotropin (TSH) to thyrotropin-releasing hormone (TRH) stimulation and induction of hypothyroidism to increased energy expenditure and enhanced peripheral thyroxine (T4) to triiodothyronine (T3) conversion. Some of the diversities may relate to the fact that earlier studies were uncontrolled case reports, which furthermore employed pituitary GH preparations, which may have been contaminated with TSH. A confounding variable in terms of incipient TSH insufficiency in some patients may also have been present. Data from a placebo-controlled crossover study of 4-months GH therapy in GH-deficient adults, some of whom were on ongoing T4 substitution, revealed that the most prominent effect on thyroid function was increased peripheral T4 to T3 conversion without significantly affecting TSH levels or secretion from the thyroid gland. It was furthermore observed that T3 levels during placebo were significantly decreased compared to an untreated healthy control group. Comparable findings have been made in a controlled study of 6-months GH therapy in adult-onset GH-deficient patients. More recent data suggest that these effects prevail after long-term (16 months) therapy. Similar findings have also been reported in healthy subjects receiving pharmacological GH doses. It is likely that this effect is not caused by GH per se inasmuch as reduced T4 to T3 conversion is a common observation in catabolic states with concomitant GH hypersecretion. It remains to be shown whether insulin-like growth factor I (IGF-I) stimulates peripheral deiodination.

Adult↗
PubMed1992

Effects of a physiological growth hormone pulse on substrate metabolism in insulin-dependent (type 1) diabetic subjects.

When present in inappropriate amounts GH induces substantial insulin resistance and it has furthermore been suggested that modest nocturnal surges of GH may precipitate the emergence of the dawn phenomenon. To characterize the metabolic effects of physiologically relevant, small-scale GH exposure, six type 1 diabetic subjects were studied for 5 h in the postabsorptive state after an iv pulse of either 210 micrograms GH or saline. Identical amounts of insulin were infused on both occasions to maintain a prevailing blood glucose concentration of 125 +/- 12 mg/100 ml. The GH bolus caused an increase in serum GH levels to a peak value of 22 +/- 2 micrograms/L after 10 min, a 70% increase in serum FFA (from 570 +/- 80 to 980 +/- 60 mumol/L) and a 400% increase in blood 3-hydroxybutyrate (3-OHB) (from 100 +/- 15 to 420 +/- 35 mumol/l) concentrations after 180 and 240 min respectively (P less than 0.05). Blood glycerol and forearm uptake of 3-OHB rose in parallel (P less than 0.01). Plasma glucose, isotopically measured glucose turnover and forearm glucose uptake was not affected by GH. Blood lactate concentrations increased (P less than 0.05) and nonoxidative glucose use and lipid oxidation tended to increase with GH. Energy expenditure remained unaffected. These results suggest that under everyday conditions GH acts as an important regulator of fuel fluxes in type 1 diabetic subjects, the main effect being a transient stimulation of lipolysis. Since no significant effect on glucose metabolism was recorded, we do not presently find evidence to support a primary role for small surges of GH in the pathogenesis of the dawn phenomenon.

Adult↗
PubMed1992

Lack of effects of hypoglycemia on glucose absorption in healthy men.

OBJECTIVE: To assess the effects of hypoglycemia on glucose absorption by examining the systemic appearance of 3-OMG (a glucose analogue that is transported by the same mechanism as glucose) after oral administration. RESEARCH DESIGN AND METHODS: Six healthy males 22-31 yr of age were studied during a hypoglycemic (50 mg [2.7 mM]/100 ml) and a euglycemic (90 mg [5.0 mM]/100 ml) glucose clamp. At 50 min after exposure to insulin, an oral glucose load containing 20 g of glucose and 4.5 g of 3-OMG dissolved in 300 ml of tap water was administered. Insulin administration was interrupted 30 min after oral glucose administration. RESULTS: Plasma glucose was clamped at 88 +/- 1.3 mg (4.9 +/- 0.1 mM)/100 ml during euglycemia and at 50 +/- 1.9 mg (2.7 +/- 0.1 mM)/100 ml during hypoglycemia. Concentrations of glucagon, growth hormone, cortisol, and epinephrine were significantly elevated during hypoglycemia. After 60 min, circulating 3-OMG concentrations increased to zeniths of 11.4 +/- 0.2 mg (585 +/- 10.0 mM)/100 ml (hypoglycemia) and 11.6 +/- 1.1 mg (585 +/- 56.0 microM)/100 ml (euglycemia; P = 0.95). Absorption of 3-OMG was evident between 15 and 20 min after administrations in both situations. Serum insulin was significantly lower during hypoglycemia compared with the control situation (345 +/- 50 microM [hypoglycemia], 445 +/- 50 microM [euglycemia], P = 0.03). CONCLUSIONS: We conclude that hypoglycemia does not seem to affect intestinal absorption of glucose as judged by systemic appearance of 3-OMG.

3-O-Methylglucose↗
PubMed1991

[Screening for neuroblastoma in infants aged 6 months. A method of testing].

In a number of cases, neuroblastoma (NB) may be diagnosed by routine screening of the urine for vanillinic-mandelic acid (VMA) and homovanillinic acid (HVA) in symptomfree infants at the age of six months. Early diagnosis of this disease may possibly improve the prognosis. The object of this project was to establish a method of measuring VMA and HVA concentrations in urine collected on filter paper and to assess participation by the parents as regards three different methods of collecting urine with the object of establishing a population screening programme for NB in Denmark. A total of 1,111 infants aged 6-8 months participated in the investigation. The equipment for testing the urine was given in three different was: 1) By the health nurses (County of Arhus), 2) By the general practitioner at the 6-month vaccination (County of Ringkøbing) and 3) By post (County of Viborg). In Arhus, the health nurses delivered the equipment to 96.7% of the age group concerned. Altogether, urine samples were obtained from 673 infants (61%). Participation was greatest in the County of Arhus (66%) and the County of Ringkøbing (62%) and lowest in the County of Viborg (54%). Two infants were found with marginally raised VMA or HVA but these values were found to be normal on repeated examinations. No cases of neuroblastoma were found in the material nor in the screened group in the course of 1 1/2 years after the conclusion of the investigation. In just over 3% of the cases, renewed urine samples had to be sent on account of too little urine on the filter paper. If current population investigations reveal that screening for neuroblastoma can alter the course of the disease in children, the method described here may form the basis for introduction of population investigations in Denmark.

Denmark↗
PubMed1991

Increased frequencies of the CD29 and CD57 markers and decreased frequency of CD45RA within CD4+ and CD8+ subsets after allogeneic bone marrow transplantation in man.

Two monoclonal antibodies, anti-CD45RA and anti-CD29, reciprocally divide the CD4+ and CD8+ lymphocytes into CD4+ CD45RA+, CD4+ CD29+, CD8+ CD45RA+ and CD8+ CD29+ subsets. The CD4+ CD45RA+, CD4+ CD29+ and CD8+ CD45RA+ possess suppressor-inducer, helper-inducer and suppressor-effector functions respectively. Since the role of these subsets has not been established after allogenic bone marrow transplantation we studied lymphocyte subpopulations in 12 patients 45-227 days after the procedure. The fraction of CD4+ lymphocytes was significantly (P = 0.0005) decreased to 20 +/- 9% versus 43 +/- 3% in controls. Within the CD4+ compartment, we found an increase in the fraction of CD4+ cells that co-expressed CD29 (CD29+/CD4+) to 92 +/- 10% versus 48 +/- 15% (P = 0.008) in controls and a concomitant decrease in CD45RA+/CD4+ to 16 +/- 12% versus 56 +/- 25% (P = 0.008). Patients were also noted to have an increase in the percentage of CD8+ lymphocytes to 41 +/- 5% compared to 23 +/- 4% in controls (P = 0.0004). Examination of the CD8+ subsets revealed a significant increase in the CD29+/CD8+ fraction to 97 +/- 3% versus 64 +/- 2% in controls (P = 0.008) and a decrease in the CD45RA+/CD8+ fraction to 36 +/- 11% versus 70 +/- 21% (P = 0.008). The number of cells co-expressing CD57 were also determined within the CD4+ and CD8+ subsets. In patients CD57+/CD4+ were increased to 29 +/- 7% versus 1 +/- 1% in controls (P = 0.04), and CD57+/CD8+ to 49 +/- 12% versus 23 +/- 9% (P = 0.02). Since CD29+ and CD57+ cells have a poor capability for IL-2 production and proliferation this shift in subset distribution may account for some of the defects in cellular immunity seen within the first year after allogeneic bone marrow transplantation.

Adolescent↗
PubMed1991

Immunohistological demonstration of intermediate trophoblast in the diagnosis of uterine versus ectopic pregnancy: a retrospective survey and results of a prospective trial.

Immunohistological demonstration of human placental lactogen (hPL) in non-villous, mononuclear intermediate trophoblastic cells may be of routine diagnostic value, when chorionic villi are absent in endometrial curettings from patients suspected of miscarriage of an intrauterine pregnancy. The histological presence and distribution of hPL was investigated in endometrial curettings from 90 patients studied retrospectively (47 had ectopic pregnancies, 14 miscarriages, and 29 legal abortions), and a consecutive, prospective series of 50 patients (40 had miscarriages and 10 had ectopic pregnancies) without chorionic villi in their endometrial curettings. Non-specific background staining was not a problem. The retrospective survey disclosed that hPL was a highly sensitive marker of intrauterine pregnancy (sensitivity = 0.98). In the prospective series, the predictive value of positive staining for hPL for intrauterine pregnancy was 1.00, and the sensitivity of hPL, as an indicator of uterine gestation, was 0.62. In absence of specific hPL-staining, the risk of ectopic pregnancy was about 50%. The immunohistochemical demonstration of hPL is a useful tool for identifying patients who are suspected of having had a miscarriage, but for whom evidence in the form of chorionic villi in endometrial curettings is lacking.

Abortion, Spontaneous↗
PubMed1991

GH-replacement therapy in adults.

Growth hormone (GH) deficiency in adults, whether GH deficient since childhood or patients rendered GH deficient in adult life, is associated with psychosocial maladjustment, reduced muscle strength and reduced exercise capacity. Body composition is significantly altered with increased fat and decreased muscle volume as compared to healthy subjects. Kidney function is subnormal, and so is sweat secretion. Epidemiological data suggest premature mortality due to cardiovascular disease in hypopituitary patients. Short-term GH treatment trials have shown improved psychosocial performance, normalization of body composition, increased muscle strength, improved exercise capacity, increased cardiac performance and increase in bone mineral mass as well as in serum markers of bone turnover, and normalization of kidney function. Thus GH replacement therapy in GH-deficient adults exhibits potential long-term beneficial effects. A number of important questions has to be addressed before long-term GH replacement therapy in GH-deficient adults can be considered on a routine basis.

Adult↗
PubMed1991

Expansion of extracellular volume and suppression of atrial natriuretic peptide after growth hormone administration in normal man.

Sodium retention and symptoms and signs of fluid retention are commonly recorded during GH administration in both GH-deficient patients and normal subjects. Most reports have however, been casuistic or uncontrolled. In a randomized double blind placebo-controlled cross-over study we therefore examined the effect of 14-day GH administration (12 IU sc at 2000 h) on plasma volume, extracellular volume (ECV), atrial natriuretic peptide (ANP), arginine vasopressin, and the renin angiotensin system in eight healthy adult men. A significant GH induced increase in serum insulin growth factor I was observed. GH caused a significant increase in ECV (L): 20.45 +/- 0.45 (GH), 19.53 +/- 0.48 (placebo) (P less than 0.01), whereas plasma volume (L) remained unchanged 3.92 +/- 0.16 (GH), 4.02 +/- 0.13 (placebo). A significant decrease in plasma ANP (pmol/L) after GH administration was observed: 2.28 +/- 0.54 (GH), 3.16 +/- 0.53 (placebo) P less than 0.01. Plasma aldosterone (pmol/L): 129 +/- 14 (GH), 89 +/- 17 (placebo), P = 0.08, and plasma angiotensin II (pmol/L) levels: 18 +/- 12 (GH), 14 +/- 7 (placebo), P = 0.21, were not significantly elevated. No changes in plasma arginine vasopressin occurred (1.86 +/- 0.05 pmol/L vs. 1.90 +/- 0.05, P = 0.33). Serum sodium and blood pressure remained unaffected. Moderate complaints, which could be ascribed to water retention, were recorded in four subjects [periorbital edema (n = 3), acral paraesthesia (n = 2) and light articular pain (n = 1)]. The symptoms were most pronounced after 2-3 days of treatment and diminished at the end of the period. In summary, 14 days of high dose GH administration caused a significant increase in ECV and a significant suppression of ANP.

Adult↗
PubMed1991

Long-term growth hormone treatment in growth hormone deficient adults.

Growth hormone treatment in GH-deficient adults has proved beneficial in recent short-term trials, but long-term results have not yet been reported. Thirteen GH-deficient adults (4 females, 9 males; mean (SEM) age 26.4 (1.7) years), who had completed 4 months of GH therapy in a double-blind placebo-controlled cross-over study were followed, for further 16.1 (0.8) months of uninterrupted GH therapy in an open design. A significant mean increase of 1.3 cm in linear height was recorded, whereas body mass index remained unchanged. Mean muscle volume of the thigh, estimated by computerised tomography, increased significantly compared with that of the initial placebo period (p = 0.01), and a slight decrease was recorded in adipose tissue volume of the thigh (p = 0.10) and subscapular skinfold thickness (p = 0.10). Still, the muscle to fat ratio of the thigh was significantly lower compared with that of normal subjects (72.6/27.4 vs 77.9/22.1) (p less than 0.01). The mean isometric strength of the quadriceps muscles increased significantly during long-term GH therapy (p less than 0.01), but remained lower compared with that of normal subjects (1.66 (0.10) vs 2.13 (0.11) Nm/kg body weight). Exercise capacity performed on a bicycle ergometer increased significantly after long-term therapy (p less than 0.05), but still did not reach the values seen in normal subjects (22.5 (3.4) vs 37.4 (4.2) watt.min.kg-1. No adverse reactions were recorded during long-term therapy and hemoglobin A1c remained unchanged. These data suggest that long-term GH replacement therapy in GH-deficient adults has beneficial effects on several physiological features which are subnormal in these patients.

Adult↗
PubMed1990

Substrate metabolism during modest hyperinsulinemia in response to isolated hyperketonemia in insulin-dependent diabetic subjects.

To assess the metabolic effects of moderate hyperketonemia, six young male type 1 diabetic patients received a 200-minute intravenous (IV) infusion of (1) 0.9 mmol 3-hydroxybutyrate (3-OHB)/kg/h, and (2) saline. To ensure comparable metabolic conditions, a low-dose hyperinsulinemic euglycemic glucose clamp was performed from 5 hours before and throughout 3-OHB/saline infusions. The forearm technique was employed to estimate substrate fluxes in muscle. Infusion of 3-OHB caused: (1) increases (P less than .05) in circulating levels of 3-OHB (from 112 +/- 73 mumol/L to 825 +/- 111 mumol/L) and forearm arteriovenous differences of 3-OHB (from 19 +/- 10 mumol/L to 145 +/- 46 mumol/L), as well as an eightfold increase of plasma acetoacetate. (2) Decreased (P less than .05) levels of nonesterified fatty acids (NEFA; from 466 +/- 85 mumol/L to 201 +/- 14 mumol/L) and glycerol (from 39 +/- 7 mumol/L to 11 +/- 4 mumol/L) and decreased (P less than .05) arteriovenous differences of glycerol (from -16 +/- 8 mumol/L to -3 +/- 2 mumol/L). (3) Increased (P less than .05) levels of serum growth hormone (GH; from 4.1 +/- 1.5 micrograms/L to 15.9 +/- 8.0 micrograms/L). No change was recorded in circulating concentrations of free insulin, glucagon, glucose, lactate, or alanine. Nor were arteriovenous balances of these intermediary metabolites, isotopically determined glucose turnover or amounts of exogenously administered glucose affected. In conclusion, in type 1 diabetic man, the main regulatory effect of isolated hyperketonemia appears to be a direct negative feedback inhibition of lipolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗