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Biomedical subjects

S Attvall

Publications and source records attributed to S Attvall.

At least 37 records · Page 2Linked to original sources
PubMed1995

Influence of the sympathetic nervous system on insulin sensitivity and adipose tissue metabolism: a study in spinal cord-injured subjects.

To evaluate insulin sensitivity and adipose tissue metabolism, seven spinal cord-injured (SCI) subjects (age, 43 +/- 6 years; body mass index, 22.8 +/- 1.4; mean +/- SE) and their seven siblings (age, 45 +/- 6 years; body mass index, 24.8 +/- 0.8) were studied using oral glucose (100-g) tolerance tests (OGTTs), euglycemic insulin clamps (insulin infusion, 1 mU/kg.min), and microdialysis of the subcutaneous tissue. Blood glucose and insulin after oral glucose were significantly increased in SCI subjects as compared with their siblings. During insulin clamping, plasma adrenaline increased significantly in controls, but not in SCI subjects. However, the rates of glucose production (2.02 +/- 0.36 v 1.59 +/- 0.09 mg/kg.min) and utilization (5.13 +/- 0.71 v 5.78 +/- 0.34) were similar in the two groups. Furthermore, interstitial subcutaneous glycerol and lactate concentrations before and after oral glucose were similar in the two groups, even in neurally decentralized tissue with broken connection between the central nervous system and peripheral sympathetic nerves. The data suggest that (1) well-mobilized SCI subjects show minor insulin resistance, and (2) sympathetic nervous activity has a minor influence on adipose tissue metabolism in the postabsorptive state, but may affect insulin sensitivity during euglycemic clamping.

Adipose Tissue↗
PubMed1995

Microalbuminuria, insulin sensitivity and haemostatic factors in non-diabetic treated hypertensive men. Risk Factor Intervention Study Group.

OBJECTIVE: To examine whether microalbuminuria in non-diabetic, treated hypertensive men is associated with insulin resistance and measures of endothelial function, thrombogenesis and fibrinolysis. DESIGN: Cross-sectional study. SETTING: Outpatient clinic in city hospital. PATIENTS: Ninety-two treated hypertensive men, aged 57-77 years, either with a serum cholesterol of > or = 6.5 mmol L-1 or smokers, or both. Patients with diabetes mellitus or overnight urinary albumin excretion of > 100 mg 12 h-1 were excluded. MAIN OUTCOME MEASURES: Overnight urinary albumin excretion, insulin-mediated glucose disposal (hyperinsulinaemic euglycaemic clamp), blood glucose and plasma insulin during oral glucose tolerance test, fibrinogen, von Willebrand factor and plasminogen activator inhibitor activity. RESULTS: Microalbuminuric patients had increased blood glucose concentrations during the oral glucose tolerance test and higher plasma fibrinogen levels compared with the normoalbuminuric patients. In a randomly selected subgroup (n = 36), insulin-mediated glucose disposal was lower in microalbuminuric than in normoalbuminuric patients, and an inverse relationship between insulin sensitivity and albuminuria (r = -0.37; P = 0.028) was found. This relationship was not significant after adjustment for body-mass index (P = 0.098). In the univariate analyses including all patients, albuminuria was associated with blood glucose, serum creatinine, body-mass index, systolic blood pressure, fibrinogen, von Willebrand factor and cholesterol (negatively). In a multiple regression analysis, only the body-mass index was independently related to urinary albumin excretion. CONCLUSIONS: Microalbuminuria was associated with insulin resistance but obesity was a confounding factor. Relationships between microalbuminuria and fibrinogen as well as von Willebrand factor were found, but only in univariate analysis.

Aged↗
PubMed1995

Characterization of the insulin-antagonistic effect of growth hormone in insulin-dependent diabetes mellitus.

To characterize its insulin-antagonistic effect, growth hormone (GH) was infused at variable rates (24, 12 or 6 mU kg-1 min-1) for 1 h in 7 IDDM patients. Saline infusion was used as control (C) and all patients participated in all studies. The effect of insulin was measured with the euglycaemic clamp technique for 6 h combined with d-(3-3H)-glucose to evaluate glucose turnover. The insulin levels during the clamps were similar in all studies (23 +/- 3 mU l-1). The infusions produced peak GH levels of (24 rate = 24) 157 +/- 11, (12 rate = 12) 76 +/- 7, and (6 rate = 6) 45 +/- 8 mU l-1 (mean +/- SEM). The insulin-antagonistic effect of GH on glucose uptake was seen after 2 h and was at a maximum 4 to 5 h after the start of the GH infusion (difference in glucose infusion rate between C and 24 was 1.7 +/- 0.4 mg kg-1 min-1, p < 0.01). The resistance was due to a less pronounced effect of insulin to both inhibit rate of appearance and to stimulate rate of disappearance. Infusion of GH at 12 mU kg-1 min-1 induced a less pronounced insulin resistance both with regards to maximal effect (glucose infusion rate C - GH 1.4 +/- 0.5 mg kg-1 min-1, p < 0.05) and duration (3 h). At 6 mU kg-1 min-1, a clear GH-induced insulin-antagonistic effect was only seen during the third hour of the clamp (glucose infusion rate C-GH 1.3 +/- 0.5 mg kg-1 min-1, p < 0.05). GH infusion impaired the effect of insulin to lower both the levels of free fatty acids (NEFA) and glycerol between 2 and 5 h after the start of the infusion (NEFA, C:110 +/- 29, 24:303 +/- 95, p < 0.05: glycerol, C:32 +/- 4, 24:50 +/- 7 mumol l-1, p < 0.05). The present study therefore demonstrates that the insulin-antagonistic effect of GH in IDDM is related to the plasma levels both with regard to duration and response. The results also indicate that GH impairs the effect of insulin on lipolysis in IDDM after physiological peaks.

Adult↗
PubMed1995

Carotid artery wall intima-media thickness is associated with insulin-mediated glucose disposal in men at high and low coronary risk.

BACKGROUND AND PURPOSE: The aim of this investigation was to examine the relationship between insulin sensitivity and intima-media thickness in the common carotid artery. METHODS: Ultrasound examinations of the common carotid artery and hyperinsulinemic euglycemic clamp examinations were performed in a group (n = 25) of men aged 57 to 77 years at high risk for atherosclerotic disease (hypertension and at least one of the following factors: hypercholesterolemia and/or smoking) and in an age-matched low-risk group (n = 23) with no cardiovascular risk factors. Subjects with cardiovascular disease or diabetes mellitus were excluded. RESULTS: A significant negative relationship between insulin sensitivity index and common carotid maximum intima-media thickness was observed in both the high-risk group (r = -.45, P < .05) and in the low-risk group (r = -.59, P < .01). CONCLUSIONS: Our results suggest that an increase in intimamedia thickness, as a possible expression of early atherosclerosis, is negatively related to insulin sensitivity.

Aged↗
PubMed1995

Effects of insulin and beta-adrenergic blockade on the migrating motor complex in humans.

BACKGROUND: Interdigestive small-intestinal motility is suppressed by hyperglycemia and also by hyperinsulinemia per se. Since hyperinsulinemia may increase sympathetic activity, the present study was undertaken to ascertain to what extent insulin affects phase III of the migrating motor complex (MMC) and MMC-related duodenal retroperistalsis and whether beta-adrenergic receptors may mediate the effects of insulin. METHODS: Fasting motility was studied in eight healthy volunteers on three occasions with an eight-lumen perfused pressure catheter, with closely spaced recording points in the proximal duodenum. On the control day 5-h antroduodenojejunal manometry was performed. On another study day euglycemic hyperinsulinemic clamping was performed for 2 h after an initial basal recording. On a 3rd day motility was recorded during propranolol infusion, combined with a period of euglycemic hyperinsulinemia. RESULTS: During hyperinsulinemia complete absence of phase III of the MMC in the gastric antrum was observed, whereas 55% of the MMC had a gastric phase-III component on the control day. The duration of phase III in the proximal duodenum was decreased during hyperinsulinemia compared with the control period (p < 0.05). This inhibitory effect of insulin on the activity front was not prevented by beta blockade. Under control conditions the proportion of retroperistaltic pressure waves in the proximal duodenum was 13 +/- 8% in early phase III, increasing in late phase III to 79 +/- 15% (p < 0.01). Duodenal phase III during hyperinsulinemia showed a similar increase in retroperistalsis, from 4 +/- 4% in early phase III to 67 +/- 21% in late phase III (p < 0.01). The corresponding proportions during beta blockade were 16 +/- 10% and 86 +/- 14%, respectively. CONCLUSIONS: Hyperinsulinemia per se abolishes antral phase III and makes the duodenal phase III shorter but does not interrupt the distinct pattern of retroperistalsis in late phase III. Beta-adrenergic receptors seem not to be important for these effects of insulin or for the retroperistalsis in duodenal phase III.

Adult↗
PubMed1994

Regulation of insulin-like growth factor binding protein-1 (IGFBP-1) in insulin-dependent diabetes mellitus. Effects of hyperglycaemia and insulin.

The aim of the present study was to characterize the effect of 44 h of hyperglycaemia on diurnal levels of insulin-like growth factor binding protein-1 (IGFBP-1), insulin-like growth factor-1 (IGF-1), growth hormone (GH) and glucagon in 7 well-controlled subjects with insulin-dependent diabetes mellitus (IDDM). Hyperglycaemia (approximately 15 mmol/l) was induced by a glucose infusion, while the degree of insulinisation was similar to that of a corresponding period with near normoglycaemia (approximately 6.9 mmol/l). Hyperglycaemia for 44 h did not alter the normal diurnal IGFBP-1 levels when the degree of insulinisation was unchanged. The diurnal secretion pattern of IGFBP-1 was preserved in both genders and without any difference between the control and hyperglycaemic periods. However, the IGFBP-1 levels were increased in these IDDM subjects despite a peripheral hyperinsulinemia. An inverse correlation was found between IGFBP-1 and peripheral insulin levels both during periods of rapid changes in IGFBP-1 and insulin concentrations (i.e. morning hours) as well as during the total 24-h sampling period. Total IGF-1 levels were low, but no further decrease was seen after 24 h of hyperglycaemia in the presence of unchanged insulin levels. In conclusion, the present study clearly shows that the increased IGFBP-1 level seen during poor metabolic control in IDDM is not caused by hyperglycaemia. Glucose levels per se do not influence either total IGF-1 or IGFBP-1 concentrations in well-insulinised diabetic patients.

Adult↗
PubMed1994

Insulin sensitivity is more related to fat distribution than to heredity for hypertension in normotensive men.

The insulin-mediated glucose disposal rate was assessed during a euglycemic hyperinsulinemic clamp in 16 normotensive men (mean age, 41 +/- 5 years) with positive family histories of hypertension and mild overweight (PFHO) and in 25 men with negative family histories of hypertension (NFH). The control group was divided into one group with normal body weight ([NFHN] n = 11) and a second group with a similar degree of overweight ([NFHO] n = 14) as in the group with PFHO. Systolic and diastolic blood pressures were significantly greater in subjects with PFHO as compared with the NFHN group. Blood glucose and plasma insulin at baseline and during the insulin clamp did not differ between the three groups. Insulin sensitivity, expressed as the glucose disposal rate per total body weight, was significantly (P < .01) decreased in PFHO subjects (7.7 +/- 3.0 mg/kg/min) and in NFHO subjects (7.1 +/- 3.5 mg/kg/min) as compared with NFHN subjects (11.1 +/- 4.0 mg/kg/min). In multivariate analysis using body mass index, waist to hip ratio, and blood pressure as predictor variables, the waist to hip ratio was significantly related to both baseline plasma insulin (r = .70, P < .0001) and insulin sensitivity (r = -.71, P < .0001). In the present study, insulin sensitivity was related to body weight and fat distribution, whereas no difference was found regarding insulin sensitivity in subjects with or without positive family histories of hypertension.

Adipose Tissue↗
PubMed1994

The insulin resistance syndrome in smokers is related to smoking habits.

The relationship between smoking habits, insulin resistance, and related risk factors for cardiovascular disease was examined in 57 middle-aged male smokers whose degree of insulin resistance was quantified by using the euglycemic clamp technique. Smoking habits correlated with degree of insulin resistance and consequently with various manifestations of the insulin resistance syndrome including levels of insulin, high-density lipoprotein cholesterol, triglycerides, and plasminogen activator inhibitor-1 (PAI-1) activity. Smoking habits, independent of degree of insulin resistance, were also related to levels of total cholesterol and low-density lipoprotein cholesterol as well as triglycerides. Stepwise regression analyses considering the effects of age, lean body mass, body fat, body mass index, waist/hip ratio, and alcohol consumption showed that only smoking habits and percent body fat were independently related to degree of insulin resistance. This study shows that insulin resistance and the insulin resistance syndrome are important but not unique contributors to the strong risk profile for cardiovascular disease in middle-aged men who smoke.

Adult↗
PubMed1994

Carbohydrate-deficient transferrin is associated with insulin sensitivity in hypertensive men.

An elevated concentration of carbohydrate-deficient transferrin in serum (CDT) has been reported to indicate excessive ethanol consumption. However, in hypertensive men, we found low values for diagnostic sensitivity and specificity. Furthermore, in the individuals with high CDT values, the concentrations of serum triglycerides and blood glucose were low rather than high, indicating that factors related to insulin/glucose metabolism may be operative. The current study addresses this issue by examining 48 patients with treated hypertension and at least 1 of following: hypercholesterolemia, history of smoking, and diabetes mellitus. We determined serum CDT, fasting plasma insulin, and glucose disposal rate during hyperinsulinemic euglycemic clamp. Seven patients had elevated CDT concentrations. This group of patients had higher glucose disposal rates than the others (mean difference, 19 mumol/min.kg lean body mass; 95% confidence interval, 5-33 mumol/min.kg lean body mass; P = 0.0096), but did not differ in body mass index or alcohol intake. Serum CDT correlated positively with glucose disposal rate (r = 0.55; P = 0.0004) and negatively with fasting plasma insulin (r = -0.43; P = 0.0039). These relationships remained after exclusion of 8 patients with diabetes mellitus and adjustment for potentially confounding factors. We conclude that the serum CDT concentrations in our patients were associated with insulin sensitivity.

Aged↗
PubMed1994

Effects of hyperglycemia on interdigestive gastrointestinal motility in humans.

BACKGROUND: Gastrointestinal motility disorders are common in patients with diabetes mellitus. Recent studies indicate that hyperglycemia can affect gastric emptying and gastric motility in healthy subjects and diabetics. METHODS: The effect of acute hyperglycemia on gastrointestinal motility was studied with a manometric technique in healthy subjects. Seven individuals, four men and three women, 23-34 years old, were studied on 2 different days. On 1 of the days a 5-h registration was performed after an overnight fast. On another day and after an initial basal period, acute steady-state hyperglycemia was induced by intravenous glucose infusion for 90 min. Motility variables were evaluated in four segments: in the gastric antrum, the proximal duodenum, the distal duodenum, and the proximal jejunum. RESULTS: Fasting migrating motor complex rhythm including migration of phase III prevailed during hyperglycemia. Compared with euglycemia, the motility index in phase II was lower during hyperglycemia in all segments studied. In the antrum the difference was 62% (p < 0.01); in the proximal duodenum, 37% (p < 0.01); in the distal duodenum, 44% (p < 0.05); and in the jejunum, 58% (p < 0.01). During hyperglycemia the prevalence of propagated contractions in phase II was significantly lower than during euglycemia both in the antrum and the proximal duodenum. In the last part of phase III in proximal duodenum most individual contractions were propagated in orad direction compared with early phase III, and this difference persisted during hyperglycemia. The number of long clusters was significantly increased during hyperglycemia as compared with euglycemia: 2.0 +/- 0.6 per hour versus 0.4 +/- 0.14 (p < 0.01). In late phase II plasma levels of motilin and pancreatic polypeptide were significantly decreased during hyperglycemia. CONCLUSION: Hyperglycemia not only reduces the motility in the stomach but also inhibits motility in both the duodenum and the jejunum. The results show that acute hyperglycemia has an important impact on small-intestinal motility.

Adult↗
PubMed1994

The effect of metformin and insulin on sympathetic nerve activity, norepinephrine spillover and blood pressure in obese, insulin resistant, normoglycemic, hypertensive men.

To evaluate the effect of metformin on insulin sensitivity and to further examine the relationship between insulin resistance, sympathetic nerve activity and blood pressure, 6 obese insulin resistant, normoglycemic hypertensive men were investigated (age 49 +/- 2 years, BMI 27.6 +/- 1.2, mean +/- SEM). The study had a placebo controlled, double blind, cross over design with 6 weeks' metformin treatment (850 mg b.i.d) vs placebo. Blood pressure was measured weekly. At the end of each treatment period, glucose infusion rate (GIR), muscle sympathetic nerve activity (MSA) and renal and total body norepinephrine (NE) kinetics (radioisotope dilution) were examined during euglycemic hyperinsulinemic clamp. Fasting insulin was 13 +/- 3 and 10 +/- 2 mU/l and fasting glucose 5.3 +/- 0.2 and 5.1 +/- 0.1 mmol/l after placebo and metformin treatment, respectively (ns). GIR during the last hour of the insulin clamp was 3.7 +/- 0.6 vs 3.6 +/- 0.6 mg/kg x min (ns). Resting MSA, total body and right renal NE spillover did not differ significantly after placebo and metformin treatment. Systolic and diastolic blood pressures were 151 +/- 10/95 +/- 5 mmHg after placebo and 146 +/- 5/94 +/- 5 mmHg after metformin treatment (ns). Thus metformin treatment did not have any significant effect on insulin sensitivity, blood pressure or sympathetic activity in this small group of patients. Renal plasma flow and MSA increased significantly during the insulin clamp, whereas renal NE and total body NE spillover remained unchanged, suggesting nonuniform regional sympathetic nerve responses to acute hyperinsulinemia.

Antihypertensive Agents↗
PubMed1993

Effect of prolonged hyperglycemia on growth hormone levels and insulin sensitivity in insulin-dependent diabetes mellitus.

The aim of the present study was to characterize the effect of a hyperglycemic period (44 hours) on the levels of insulin-antagonistic hormones and insulin sensitivity in seven subjects with well-controlled insulin-dependent diabetes mellitus (IDDM). Hyperglycemia (approximately 15 mmol.L-1) was induced by a glucose infusion while the degree of insulinization was similar to that of the period with near normoglycemia (approximately 6.9 mmol.L-1). Insulin sensitivity was measured with hyperinsulinemic euglycemic clamps performed 4 hours before and after the periods of normoglycemia (control) and hyperglycemia. D-[3-3H]glucose was infused in the second clamp in each study to evaluate glucose production and utilization. Since growth hormone (GH) levels frequently are elevated during poor diabetic control, diurnal GH secretion was measured in blood samples continuously drawn for 24 hours during the euglycemic and hyperglycemic periods. Levels of epinephrine, norepinephrine, cortisol, and nonesterified free fatty acids (NEFA) were similar during the control and hyperglycemic periods and during the clamps. GH levels were also similar, but an abnormal diurnal secretion pattern was present with increased numbers of daytime peaks. Hyperglycemia did not reduce GH secretion in IDDM. Hyperglycemia for 44 hours induced insulin resistance (32% reduction of glucose infusion rate, P < .02). In the control study, a 21% reduction (P = .064, NS) of the glucose disposal rate (Rd) was seen, suggesting that the hospitalization period per se may also reduce insulin sensitivity. In conclusion, a period of hyperglycemia leads to insulin resistance in IDDM patients. This insulin resistance cannot be attributable to increased levels of insulin-antagonistic hormones, although an abnormal secretion pattern for GH was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of treatment with recombinant human growth hormone on insulin sensitivity and glucose metabolism in adults with growth hormone deficiency.

In a double-blind, cross-over, placebo-controlled trial, the effect of 26 weeks of replacement therapy with recombinant human growth hormone (rhGH) on insulin sensitivity and glucose metabolism in nine patients with adult-onset growth hormone deficiency was studied with a euglycemic clamp. Glucose production and utilization were studied with D-(3-3H)-glucose infusions. Comparisons were made with placebo treatment for 6 and 26 weeks, respectively. GH therapy for 6 weeks increased fasting plasma concentrations of glucose and insulin. However, after 26 weeks of GH treatment, no significant changes in glucose or insulin concentrations were recorded. GH treatment induced a marked change in insulin action evident after 6 weeks of therapy as shown by lower glucose infusion rates (GIRs) during the clamp compared with placebo treatment (2.6 +/- 0.4 v 4.1 +/- 0.7 mg.kg-1.min-1). This change in insulin action was due to a decreased insulin effect on glucose utilization. After 26 weeks of GH therapy, there was no significant difference in GIRs. During placebo treatment, insulin sensitivity and insulin, glucose, and nonesterified fatty acid (NEFA) concentrations were unchanged compared with concentrations measured before the study. Thus GH replacement therapy induces a change in insulin action in GH-deficient individuals. Whether this change represents a decrease in insulin action (ie, insulin resistance) or a restoration of action to normal is presently unclear, since a healthy control group was not included in the study. During long-term treatment, the present study suggests that the change in insulin action can be reversed, probably secondarily to changes in body composition.

Adult↗
PubMed1993

Low-dose angiotensin II increases glucose disposal rate during euglycemic hyperinsulinemia.

To study the metabolic effects of angiotensin II we examined the glucose disposal rate and calf blood flow in healthy men (n = 39) during euglycemic hyperinsulinemia followed by a period with simultaneous angiotensin II infusion at a low dose (0.1 ng/kg/min). Angiotensin II infusion abruptly increased the glucose disposal rate significantly as compared with glucose disposal rate during euglycemic hyperinsulinemia only. There were no differences in blood glucose or plasma insulin between the euglycemic hyperinsulinemic and the angiotensin II infusion period. During hyperinsulinemia alone, blood pressure was unchanged while calf muscle blood flow increased significantly as compared with the baseline period, while during the angiotensin infusion the systolic blood pressure increased and calf blood flow decreased significantly as compared with the hyperinsulinemic period. We conclude that angiotensin II within physiological range stimulates insulin-mediated glucose uptake in healthy men. The mechanisms are, however, unclear, but changes in blood flow are probably not responsible for the observed effects.

Adult↗
PubMed1993

Smoking induces insulin resistance--a potential link with the insulin resistance syndrome.

OBJECTIVES: The acute effect of smoking and snuffing on insulin sensitivity was studied in a group of healthy habitual smokers. DESIGN: The euglycaemic clamp technique was combined with the subcutaneous injection of a bolus (0.1 U kg-1) of fast-acting insulin (Actrapid). Randomized subjects smoked either one cigarette per hour for 6 h, took one bag-packed snuff per hour for 6 h or refrained from nicotine for 48 h before as well as during the clamp. SUBJECTS: Seven healthy smokers, four females and three males, of normal weight (BMI, mean +/- SEM, 21 +/- 0.7 kg m-2 with a range of 18.6-23.9), aged 31 +/- 2 years (range 24-35 years), who had consumed at least 20 cigarettes per day for at least 5 years were studied. They were recruited through an advertisement in a newspaper. RESULTS: The steady-state plasma nicotine levels were similar during smoking and snuffing. The insulin and glucose levels were also similar during all three clamps. Smoking, but not snuffing, impaired insulin action (P < 0.05) mainly due to a lower peripheral glucose uptake. The mean growth hormone levels during the 6-h study were more than doubled during smoking (P < 0.01) while no significant differences were seen in the other counter-regulatory hormones. CONCLUSION: Smoking (also in habitual smokers) acutely impairs insulin action and leads to insulin resistance. Thus, smoking can be of importance for the development of the insulin resistance syndrome associated with risk for cardiovascular disease.

Adult↗
PubMed1992

Insulin-antagonistic effects of pulsatile and continuous glucagon infusions in man--a comparison with the effect of adrenaline.

The insulin-antagonistic effects of pulsatile (3 min pulses every 20 min) and continuous glucagon infusions were studied over 4 h with the euglycemic clamp technique in healthy subjects. Comparisons were made to the effect of a continuous adrenaline infusion. Glucose production and utilization were evaluated with D-3-3H-glucose and somatostatin was used in all studies to inhibit the endogenous release of insulin and glucagon. The amount of glucagon given during the pulsatile infusions (27% of that during continuous infusion) was adjusted so that the peak glucagon levels were the same as during the continuous infusion (372 +/- 22 and 365 +/- 20 ng/L, respectively). The insulin-antagonistic effects of pulsatile and continuous glucagon infusions were similar during the first hour and imparied the insulin effect with 44 +/- 8 and 47 +/- 6%, respectively. However, when infused continuously, the effect of glucagon declined rapidly, whereas the effect of a pulsatile infusion decreased more slowly and was evident for 3 h. Raising the glucagon level 4-fold restored the insulin-antagonistic effect again suggesting that the cells had become desensitized. In contrast, the insulin-antagonistic effect of adrenaline was persistent throughout the 4 h of the study and impaired insulin action with 54 +/- 2%. The effects of pulsatile and continuous glucagon infusions were entirely due to the stimulation of glucose production while that of adrenaline mainly was due to inhibition of peripheral glucose uptake. In conclusion, the acute stimulatory effect of glucagon on glucose production is transient but it is better maintained when given as intermittent pulses rather than as a continuous infusion. In contrast, the insulin-antagonistic effect of adrenaline on glucose uptake is persistent for at least 4 h.

Adult↗