Search PubMed⌕ Search

Biomedical subjects

M Kollind

Publications and source records attributed to M Kollind.

28 records · Page 2Linked to original sources
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

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↗
PubMed1988

Studies on posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus.

Altogether 54 male patients with insulin-dependent diabetes mellitus participated in the studies. The impact of insulin-induced hypoglycemia on posthypoglycemic insulin sensitivity was evaluated for up to 12 hours following nadir hypoglycemia. The effect on glucose homeostasis following transient elevation of counterregulatory hormones was studied by exogenous administration of adrenaline, adreno-corticotropic hormone and growth hormone and by suppression of the endogenous release of growth hormone in connection with hypoglycemia. The studies were performed in the fasting state preceded by a 24 hour intravenous insulin infusion in order to avoid interference of subcutaneous insulin. Insulin resistance was determined by a constant rate intravenous infusion of somatostatin, insulin and glucose. This test seemed appropriate for the evaluation of total insulin resistance, and its reproducibility was acceptable. By using this method it was demonstrated that insulin resistance occurred for at least 12 hours after a hypoglycemic event in patients with IDDM, and that adrenaline caused immediate insulin resistance which, however, faded out within four to six hours, while GH exerted no immediate effect on insulin sensitivity but caused marked and sustained insulin resistance after a lag period of about four hours. Cortisol had no apparent effect within six hours but enhanced the effect of GH. The magnitude of these diabetogenic effects of hypoglycemia and GH was less pronounced in patients who already were more insulin resistant. These results are compatible with the idea that adrenaline is of major importance for the counterregulation and restoration of blood glucose during the first few hours following hypoglycemia, while GH is responsible for the induction of a long-lasting state of insulin resistance. It is possible that such prolonged insulin resistance may cause posthypoglycemic hyperglycemia in patients with IDDM. These studies therefore indicate that the GH suppressing hormone somatostatin may be of clinical value as an adjunct to insulin in the treatment of patients with insulin-dependent diabetes mellitus and labile blood glucose control.

Adolescent↗
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

Insulin resistance following nocturnal hypoglycaemia in insulin-dependent diabetes mellitus.

Glucose metabolism was studied by a somatostatin-insulin-glucose infusion test (SIGIT) for 8 h in 7 male patients with insulin-dependent diabetes mellitus. They were investigated on two occasions in random order, with and without preceding hypoglycaemia induced between 3.00 and 4.00 h. SIGIT was started at 7.00 h when blood glucose was restored to normal and the counterregulatory hormones had returned to basal values. As expected, hypoglycaemia evoked an enhancement of the plasma levels of GH (43.7 +/- 10.1 vs 4.4 +/- 1.8 micrograms/l), cortisol (690 +/- 59 vs 140 +/- 32 nmol/l), glucagon (225 +/- 35 vs 143 +/- 25 ng/l), and epinephrine (3.80 +/- 1.00 vs 0.10 +/- 0.03 nmol/l). During the SIGIT, the levels of circulating free insulin and counterregulatory hormones were similar in the two tests notwithstanding that excessive hyperglycaemia appeared when SIGIT was preceded by hypoglycaemia. The present study thus demonstrates that nocturnal hypoglycaemia induces insulin resistance in insulin-dependent diabetic patients not deprived of insulin.

Adult↗
PubMed1986

Glipizide does not affect absorption of glucose and xylose in diabetics without residual beta-cell function.

We have previously demonstrated that oral glipizide suppresses the absorption of xylose in diabetics treated with diet alone. We suggested that glipizide might influence postprandial glucose levels by interfering with absorptive mechanisms. In the present study we have extended our observations to insulin-dependent diabetics (IDDM). Nine non-obese diabetics without residual beta-cell function and with normal respiratory sinus arrhythmia and Valsalva ratio were studied on two occasions. Their ordinary insulin treatment was discontinued 24 hours before the study and glucose control was maintained by i.v. insulin infusion. The experiments began at 8 a.m. after an overnight fast. Insulin was given as a continuous i.v. infusion of 0.01 U/kg/h at 8-11 a.m. and 0.005 U/kg/h at 11 a.m. -2 p.m. At 8 a.m. the patients ingested 25 g of xylose and 15 g of glucose in 300 ml of water. Glipizide (5 mg) or placebo were given 30 min prior to the glucose-xylose load in random order, each patient serving as his own control. Blood samples were taken every 60 min for analysis of glucose, xylose, C-peptide and glipizide. The rise in blood glucose in the control experiment was similar to that previously seen in non-insulin-dependent diabetics (NIDDM) given the same xylose-glucose load. Glipizide did not exert any effects on either blood C-peptide, glucose or xylose levels. We conclude that oral glipizide administered in a therapeutic dose does not reduce xylose absorption in IDDM, in contrast to its previously demonstrated effect in NIDDM.

Adult↗
PubMed1985

Effect of improved glycemic control by continuous subcutaneous insulin infusion on hormonal responses to insulin-induced hypoglycemia in type 1 diabetics.

Glucose counter-regulatory capacity and the hormonal responses to insulin-induced hypoglycemia were studied in eight type 1 diabetics before and after improvement of metabolic control by continuous subcutaneous insulin infusion (CSII). The intensified treatment resulted in a decrease in mean glycosylated hemoglobin from 11.6 +/- 0.5 to 9.3 +/- 0.4% within a mean period of 14 weeks. During a constant rate infusion of insulin (2.4 U/h), steady state levels of glucose appeared in all subjects. The steady state glucose level was identical before and after CSII. The counter-regulatory hormonal responses showed significantly higher epinephrine levels, while glucagon, growth hormone, and cortisol were not influenced. In parallel with the heightened epinephrine response the pulse rate response was significantly enhanced. The restitution of blood glucose after insulin hypoglycemia was not modified. It is concluded that a more vigorous catecholaminergic response to hypoglycemia is achieved after improved metabolic control by CSII.

Adult↗
PubMed1985

Genetics and clinical significance of thyroxine binding globulin deficiency, an analysis of seven families.

Seven families, ascertained through probands with undetectable levels of thyroxine binding globulin (TBG) were studied from clinical and genetic points of view. The blood levels of TBG, thyroxine binding prealbumin (TBPA), thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were determined in altogether 128 family members. The concentration of free thyroxine (FT4) was calculated from the concentrations of T4, TBG and TBPA. Only men (n = 15) were found to have total TBG deficiency. Their TSH levels were within normal range and they did not show any clinical symptoms of thyroid dysfunction. The mothers and daughters of the affected men had significantly lower TBG levels than control women. Segregation analysis performed on 46 nuclear families showed significant evidence for an X-linked additive mode of transmission and an additional multifactorial component with heritability 0.47.

Adolescent↗
PubMed1984

Extrapancreatic effects of a sulphonylurea. Decrease in xylose absorption by glipizide in type II diabetics.

The effects of glipizide on the absorption of glucose and d-xylose were studied in six type II diabetics on diet treatment alone. Glipizide was given intravenously (12 micrograms/kg at 0 min) or orally (5 mg at -30 min). Oral glucose (15 g) and xylose (25 g) loads were given at zero time. Glipizide stimulated insulin secretion and reduced glucose and xylose levels significantly with both routes of administration. The suppression of xylose levels lasted longer after oral than after intravenous administration of the drug. It is suggested that part of the influence of glipizide on postprandial glucose levels may represent interference with absorptive mechanisms.

Administration, Oral↗