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Biomedical subjects

U Adamson

Publications and source records attributed to U Adamson.

At least 55 records · Page 3Linked to original sources
PubMed1990

Exogenous somatostatin raises plasma insulin levels in patients with insulin-dependent diabetes mellitus.

The effect of cyclic somatostatin on circulating insulin levels was studied in eight patients with insulin-dependent diabetes mellitus (IDDM). The study was performed after an overnight fast when their subcutaneous depots of insulin had been depleted during i.v. insulin substitution for 18 hours. A constant rate i.v. insulin infusion (0.4 mU/kg/min) was given for 240 min and somatostatin was co-infused between 60-120 min (100 micrograms/h) and 180-240 min (250 micrograms/h) respectively. Plasma insulin, blood glucose and hematocrit were measured at 15 min intervals. Hematocrit fell from 41.7 to 38.3% during the study period. Somatostatin increased the plasma insulin levels, corrected for the changes of hematocrit, by approximately 8% in the low dose (P less than 0.05) as well as in the high dose (P less than 0.05) period. It is concluded that somatostatin interferes with the clearance of insulin thereby increasing the circulating plasma insulin levels in IDDM patients without residual insulin secretion.

Adult↗
PubMed1990

Prevalence of anti-insulin antibodies and its relation to severe hypoglycaemia in insulin-treated diabetic patients.

The prevalence of anti-insulin antibodies (AIABs) and their association with clinical parameters, metabolic control and severe hypoglycaemia were investigated in a geographically defined population of insulin-treated diabetic patients. Eighty per cent of the patients (479) delivered venous blood samples and answered a questionnaire on severe hypoglycaemic problems during a 12-month period. Circulating AIABs were demonstrable in 78% of the patients, being more common among those with type 1 diabetes and in long-duration patients. High levels of AIABs were also more frequent in patients in whom insulin treatment had been initiated prior to the era of highly purified insulins. The AIABs did not correlate to metabolic control, insulin dose or severe hypoglycaemia. It is concluded that AIABs is not a risk factor for severe hypoglycaemia in insulin-treated diabetic patients.

Adult↗
PubMed1990

A comparative study on the hormonal responses to insulin-induced hypoglycaemia using semisynthetic human insulin and pork insulin in patients with type 1 diabetes mellitus.

In order to enlighten the controversy on whether human and pork insulin result in different hormonal responses to insulin-induced hypoglycaemia, eight C-peptide negative, diabetic patients without measurable circulating insulin-binding antibodies were exposed to insulin-induced hypoglycaemia in random order with highly purified pork insulin (Actrapid) and semisynthetic human insulin (Actrapid Human). Hypoglycaemia was provoked by a constant rate IV infusion of insulin (0.034 U kg-1 h-1) for 3 h after which the blood glucose recovery was assessed for an additional period of 60 min. Both insulin preparations gave close to identical responses for glucose, glucagon, growth hormone, adrenaline, and somatostatin. The circulating noradrenaline levels were higher during the infusion of pork insulin which also yielded a more prominent response of pancreatic polypeptide and, after cessation of the insulin infusion, plasma cortisol was also higher following pork insulin. It is concluded that human and pork insulin induce close to identical responses of the important counter-regulatory hormones during hypoglycaemia in Type 1 diabetic patients.

Adult↗
PubMed1990

Muscle strength in hyperthyroid patients before and after medical treatment.

Ten hyperthyroid patients were assessed for muscle strength before and after a period of medical treatment that averaged 12 months. The subjects did not change their habitual level of physical activity between the two test occasions. Maximal voluntary isokinetic knee extensor muscle strength was determined during various concentric, eccentric and isometric conditions. Average increases in strength from before to termination of treatment ranged from 25 to 41% for the concentric and isometric tests (P less than 0.01, n = 10), and from 19 to 35% for the eccentric tests (P less than 0.01, n = 6). The present study demonstrates that medical treatment of hyperthyroid patients results in a marked increase in muscle strength.

Adult↗
PubMed1990

Combined insulin-glibenclamide therapy of NIDDM patients in primary health care. A follow-up study of its compliance and efficacy and a review of the literature.

Twenty non-insulin-dependent diabetic (NIDDM) patients with secondary failure to sulphonylureas were given combined insulin-glibenclamide therapy. After discharge they were followed for the following 12 months at different primary care centres. In the 19 patients who completed the combined therapy, the mean glycosylated haemoglobin A1c (HbA1c) level decreased from 11.2 +/- 0.5% to 9.1 +/- 0.3% at 2 months (p less than 0.001), and remained at 9.1 +/- 0.4% at 12 months. The reduction of HbA1c was positively correlated with the HbA1c value and inversely with the initial body weight (both p less than 0.05). There was a slight rise in the body mass index (BMI) from 26.9 +/- 0.9 to 28.2 +/- 0.7 at 12 months (p less than 0.001), which was inversely correlated with the BMI value at 0 month (p less than 0.05). The insulin doses were similar at 2 and 12 months. A review of the literature since 1985 identified ten double-blind, controlled studies on combined insulin-sulphonylurea therapy, comprising 156 NIDDM patients followed for 8-52 weeks. Improved glycaemic control and endogenous insulin secretion were documented in nine of these studies in parallel with a decrease of insulin requirement in six studies. We conclude from our own experience and the literature that combined insulin-glibenclamide therapy is an efficient and compliant therapeutic regimen.

Aged↗
PubMed1989

The prevalence of impaired glucose counter-regulation during an insulin-infusion test in insulin-treated diabetic patients prone to severe hypoglycaemia.

Among 603 patients over the age of 18, with insulin-treated diabetes mellitus, a questionnaire identified 98 patients who during a 12-month period had experienced severe hypoglycaemia, defined as an event which required the help of another person. Twenty of these patients had repeatedly suffered from such episodes, without any obvious reason, for a period of at least three years. The capacity to counter-regulate a standardized, insulin-infusion test (0.034 U.kg-1.h-1 given for 3 h unless severe neuroglucopenia developed) was evaluated in 14 of these patients. In 12, an impaired glucose counter-regulation was registered, defined as blood-glucose values below -2 SD of healthy subjects. In all but one of these patients, a combined deficiency of glucagon and adrenaline was documented, and was believed to be the likely cause of their inclination towards hypoglycaemia. In patients with severe hypoglycaemia, but not in diabetic patients without severe hypoglycaemia or in healthy subjects, a significant relationship between insulin disappearance and glucose rise was found. It is concluded that in insulin-treated diabetic patients, the prevalence of recurrent attacks of severe hypoglycaemia amounts to about 4%. In such patients, a combined deficiency of adrenaline and glucagon responses to hypoglycaemia is the predominant finding and the disappearance rate of insulin becomes critical for recovery of blood glucose after hypoglycaemia.

Blood Glucose↗
PubMed1989

Fasting for 72 h decreases the responses of counterregulatory hormones to insulin-induced hypoglycaemia in normal man.

We have evaluated the influence of fasting on the response of counterregulatory hormones to insulin-induced hypoglycaemia. Eight healthy, non-obese volunteers were studied after an overnight fast and again after a 72-h fast period. Levels of blood glucose were higher after overnight fasting (4.59 +/- 0.10 mmol/l) than after 72 h of fasting (3.38 +/- 0.12 mmol/l). Hypoglycaemia was induced by a constant insulin infusion (2.4 mU/kg/min) and clamped between 2.1 and 2.3 mmol/l of glucose by a variable glucose infusion. Hypoglycaemia evoked stimulation of glucagon release after the overnight fast but did not alter release after 72 h of fasting. The response of other counterregulatory hormones were also influenced by the longer fasting period: the normal rise in adrenaline levels during hypoglycaemia was delayed and attenuated and the normal rise in cortisol levels was absent; paradoxically, cortisol levels decreased during hypoglycaemia. Seventy-two hours of fasting, therefore, profoundly alters hormonal responses to hypoglycaemia.

Adult↗
PubMed1988

Transient insulin resistance following infusion of adrenaline in type 1 (insulin-dependent) diabetes mellitus.

Insulin resistance was assessed after an intravenous infusion of adrenaline (50 ng.kg-1.min-1) or saline (control study) given between 08.00 and 08.30 hours in nine patients with Type 1 (insulin-dependent) diabetes mellitus. The blood glucose level during a somatostatin (100 micrograms/h)-insulin (0.4 mU.kg-1.min-1)-glucose (4.5 mg.kg-1.min-1)-infusion-test performed between 10.30 and 14.30 hours served as an indicator of the total body insulin resistance. Blood glucose was maintained around 7 mmol/l between 08.00 and 10.30 hours by a constant infusion of regular insulin (0.57 mU.kg-1.min-1) and a variable infusion of a 20% glucose solution. The infusion of adrenaline raised plasma adrenaline to 2.7 +/- 0.3 nmol/l (mean +/- SEM) at the end of the infusion; thereafter it returned to its basal level within 30 min. The plasma levels of free insulin, glucagon, cortisol and growth hormone were similar in the adrenaline and the control studies from 08.00 to 14.30 hours. In comparison with the control study the infusion of adrenaline decreased the need for intravenous glucose significantly over the initial 2 h. Furthermore, during the somatostatin-insulin-glucose infusion test the blood glucose rose significantly (p less than 0.05) over the initial 2 h; thereafter no significant differences between the two studies were seen. It is concluded that a short term infusion of adrenaline, resembling the adrenergic hormone response to hypoglycaemia, induces a diabetogenic effect which subsides within 6 h after omission of the adrenaline infusion.

Adult↗
PubMed1988

Studies of insulin resistance following hypoglycemia in insulin-dependent diabetes mellitus.

Insulin resistance was assessed after a hypoglycemia induced by insulin (1.5 mU X kg-1 X min-1) between 7 and 8 a.m. in 10 well-insulinized patients with insulin-dependent diabetes mellitus (IDDM). Blood glucose levels during a somatostatin (100 micrograms X h-1)-insulin (0.4 mU X kg-1 X min-1)-glucose (4.5 mg X kg-1)-infusion test (SIGIT) performed between 11 a.m. and 3 p.m. served as an indicator of total body insulin resistance. Plasma epinephrine, growth hormone, and cortisol increased in response to hypoglycemia, while blunted responses of glucagon were simultaneously registered. At the start of the subsequent SIGIT, blood glucose and plasma-free insulin concentrations were similar to those obtained in the control study without preceding hypoglycemia, and at this point all counter-regulatory hormones had returned to basal. During the SIGIT close to identical levels of plasma-free insulin and counter-regulatory hormones were registered, despite which a significant hyperglycemia was seen 2 hours after the start of the SIGIT when preceded by hypoglycemia. In a separate study, the SIGIT was shown to have a good reproducibility in IDDM patients. We conclude that hypoglycemia evokes a state of insulin resistance for several hours, as demonstrated by elevated blood glucose levels during a somatostatin-insulin-glucose-infusion test.

Adult↗
PubMed1988

Importance of growth hormone for blood glucose regulation following insulin-induced nocturnal hypoglycemia in insulin-dependent diabetes mellitus.

The effect of growth hormone (GH) on the glucose homeostasis following nocturnal hypoglycemia was studied between 4 a.m. and noon in eight male patients with insulin-dependent diabetes mellitus (IDDM) by a somatostatin (250 micrograms/h)-insulin (0.4 mU/kg/min)-glucose (6 mg/kg/min)-infusion test (SIGIT). The patients participated in two experiments in which hypoglycemia at 4 a.m. was induced by i.v. insulin (1.5 mU/kg/min). In both experiments the endogenous secretion of GH was suppressed by somatostatin (250 micrograms/h) and glucagon (0.5 ng/kg/min) was given as substitute for the somatostatin-induced suppression of endogenous glucagon secretion. GH (20 mU/kg/h) or saline was given for 60 min from nadir blood glucose in random order. Mean nadir glucose values were the same in both studies (1.7 +/- 0.2 vs. 1.7 +/- 0.1 mmol/l) and no differences were registered in plasma-free insulin, glucagon and the responses of adrenaline and cortisol to hypoglycemia. The infusion of GH resulted in plasma GH levels of about 50 micrograms/l at the end of the infusion, thereafter decreasing to low or immeasurable levels within 2 hours. Infusion of GH evoked a marked hyperglycemia within 4 hours. It is concluded that when hypoglycemia is accompanied by a transient increase in plasma GH, insulin resistance occurs after a lag period of approximately 4 hours and that this effect persists for at least another 4 hours.

Adult↗
PubMed1988

Glibenclamide improves the response to insulin treatment in non-insulin-dependent diabetics with second failure to sulfonylurea therapy.

The effect of combined insulin-glibenclamide therapy on glucose control was evaluated in a double-blind placebo controlled study of 20 patients with non-insulin-dependent diabetes mellitus (NIDDM) and second failure to oral antidiabetic therapy with glibenclamide or glipizide. After an observation period of 1-3 months, insulin treatment was initiated which resulted in rapid improvement of the glycemic control within 6 weeks. Thereafter glibenclamide or placebo was added to insulin for a further 12 weeks. Glibenclamide improved the glycemic control as expressed by a diminution of blood glucose and HbA1c. This was observed in spite of the fact that the daily insulin dose was reduced by approximately 30% in the glibenclamide-treated group of patients. It is concluded that in NIDDM patients with second failure to glibenclamide ot glipizide therapy, the responsiveness to glibenclamide may be at least partially restored by a short period of insulin treatment. It is suggested that therapy with insulin and glibenclamide is an appropriate treatment regimen for NIDDM patients with second failure to sulfonylurea therapy.

Adult↗
PubMed1988

Somatostatin reduces posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus.

In order to study whether somatostatin reduces posthypoglycemic insulin resistance, hypoglycemia was induced between 7.00 and 8.00 h by an iv infusion of insulin with and without somatostatin (250 micrograms/h) in 6 male patients with insulin-dependent diabetes mellitus (IDDM). Exogenous glucagon was infused to substitute for the suppression of its endogenous release (1.0-1.5 ng.kg-1.min-1). Insulin resistance was assessed by a somatostatin-insulin-infusion test (SIGIT) between 11.00 and 15.00 h. In the study without hypoglycemia, blood glucose was kept close to 6 mmol/l from 8.00 h until start of the SIGIT. In both hypoglycemic studies similar nadir blood glucose levels were achieved and hypoglycemia evoked the same increase of plasma epinephrine and cortisol, whereas plasma glucagon remained at its basal level. The growth hormone response to hypoglycemia was suppressed by somatostatin. At the onset of the SIGIT, the plasma levels of the counterregulatory hormones had returned to basal, and blood glucose and plasma free insulin concentrations were almost identical. During the SIGIT there were no differences in plasma free insulin or counterregulatory hormone levels. Insulin resistance, as seen following hypoglycemia, was not demonstrable in the study with somatostatin. It is concluded that somatostatin reduces insulin resistance following hypoglycemia in patients with IDDM. It is therefore suggested that an analogue with a specific GH release inhibiting property may be useful in reducing glycemic instability when given as adjunct therapy to insulin in patients with labile glycemic control.

Adult↗
PubMed1987

Diabetogenic action of GH and cortisol in insulin-dependent diabetes mellitus. Aspects of the mechanisms behind the Somogyi phenomenon.

The effect on glucose homeostasis of a transient elevation of plasma growth hormone (GH) and cortisol was studied over 6 h in 14 male patients with insulin-dependent diabetes mellitus (IDDM) by using an i.v. somatostatin (100 micrograms/h) - insulin (0.4 mU/kg/min) glucose (3 mg/kg/min) - infusion test (SIGIT). GH (20 mU/kg) was given as a 60 min i.v. infusion during the initial SIGIT period raising the plasma GH level to about 40 micrograms/l, and returning to low basal within 3 h. ACTH (0.1 mg) was given as an i.v. bolus injection at the start of the SIGIT, resulting in plasma cortisol peak values of about 900 nmol/l within 2-3 h. GH raised blood glucose after a lag of 4 h while ACTH alone had no effect. However, ACTH added to GH enhanced the diabetogenic effect of GH. It is concluded that an episodic increase in circulating GH-cortisol, resembling the responses of these hormones to an insulin-induced hypoglycemia, exerts a diabetogenic effect in IDDM-patients not deprived of insulin. While GH is essential in this respect the diabetogenic effect of cortisol is evident only in conjunction with GH.

Adrenocorticotropic Hormone↗
PubMed1987

Pre-exposure to glucagon impairs glucose recovery after insulin-induced hypoglycemia in man.

The effect of a two hour period of hypo- and hyperglucagonemia on a subsequent insulin-induced hypoglycemia was studied in nine healthy volunteers. Hypoglucagonemia was provoked by somatostatin (50 micrograms/h) and hyperglucagonemia by glucagon infusion (3.25 ng/kg/min) together with somatostatin, while saline alone was given as control. Hypoglycemia was induced by insulin infusion (2.4 U/h) for two hours. The hyperglycemic effect of glucagon was transient and similar nadir glucose levels were obtained in the three experiments. Preinfusion with glucagon impaired glucose recovery in spite of preserved secretion of epinephrine during restitution of blood glucose in this experiment. It is concluded, that a period of elevated glucagon levels deteriorates the restitution of blood glucose following hypoglycemia. Hyperglucagonemia, commonly apparent in poorly controlled diabetics, may therefore be of importance in explaining the impaired recovery of blood glucose seen in such patients after hypoglycemia.

Adult↗
PubMed1987

Effects of metoprolol on the counter-regulation and recognition of prolonged hypoglycemia in insulin-dependent diabetics.

The effect of metoprolol on the counter-regulation of prolonged hypoglycemia was studied in eight insulin-dependent diabetics. Insulin was given as an i.v. infusion of 2.4 U/h over 180 min alone, or together with metoprolol (3.0 mg i.v. bolus followed by an i.v. infusion of 4.8 mg/h) in random order. Blood glucose, counter-regulatory hormones, hypoglycemic symptoms and the cardiovascular responses were assayed over 240 min. Metoprolol did not significantly modify the blood glucose levels. The plasma levels of free insulin, however, were elevated by approximately 20% (p less than 0.01) by metoprolol during hypoglycemia and the plasma concentrations of epinephrine, norepinephrine, growth hormone and cortisol were enhanced by the drug. Sweating was increased by metoprolol, while other symptoms were unaltered. We conclude that metoprolol administered acutely does not aggravate prolonged hypoglycemia in diabetics with blunted response of glucagon. Moreover, exaggerated responses of counter-regulatory hormones, provoked by metoprolol, may compensate for the inhibitory effect of this drug on insulin clearance.

Adult↗
PubMed1987

Microalbuminuria in long-term insulin-dependent diabetes mellitus. Prevalence and clinical characteristics in a normotensive population.

Albumin excretion rate was determined by radioimmunoassay in overnight urine from 102 normotensive patients with insulin-dependent diabetes mellitus of more than 10 year's duration. Based on two samples, 16 patients (16%) exhibited microalbuminuria, defined as a mean excretion rate greater than 20 micrograms/min. Microalbuminuric patients were significantly younger at onset of diabetes but did not differ from normoalbuminuric patients concerning age or duration of diabetes. Nonetheless, diastolic and mean arterial blood pressures were significantly higher in the microalbuminuric group. The existing glycemic control, assessed by glycosylated hemoglobin (HbA1c) was better in normoalbuminurics, but not significantly so. The albumin excretion rate in microalbuminuric patients correlated significantly (p less than 0.01) to diastolic (r = 0.69) and to mean arterial blood pressure (r = 0.69), but did not correlate to HbA1c. Thus, it is concluded that even normotensive patients with signs of early diabetic nephropathy, i.e. microalbuminuria, exhibit small, but significant increases in blood pressure.

Adolescent↗