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Biomedical subjects

K Lundbaek

Publications and source records attributed to K Lundbaek.

At least 37 records · Page 2Linked to original sources
PubMed1977

[Diabetic angiopathy. A new concept of pathogenesis (author's transl)].

In juvenile diabetes there is a renal hypertrophy: glomerular volume and capillary lumen of the individual glomeruli are about twice the size of healthy ones. The hypertrophy is associated with a hyperfunction (increased glomerular filtration and tubular reabsorption). If the diabetes is strictly controlled these changes may regress, which suggests a metabolically induced hypertrophy. Long-standing diabetes is characterized by a phase of intermittent proteinuria which gradually becomes permanent. Diabetic angiopathy is the result of many years of abnormal metabolism, presumably with involvement of the growth hormone and glucose. Whereas microangiopathy is considered specific for diabetes, it is still a matter for discussion whether a diabetic macroangiopathy exists. The results of numerous investigations suggest that it does.

Animals↗
PubMed1976

Neuropathy in experimental diabetes: an animal model.

A morphometric study of the common peroneal nerve in early experimental diabetes in rats showed that fibre size was diminished. The reduction in the size of the axon was twice that of the myelin sheath. This may contribute to the understanding of the impaired motor conduction velocity found in diabetics shortly after the onset of their disease.

Animals↗
PubMed1976

Failure of somatostatin to correct manifest diabetic ketoacidosis.

Juvenile diabetic patients were studied 60-72 hours after insulin withdrawal when moderate ketoacidosis had developed. Somatostatin infusion for 4 hours in five patients resulted in almost complete suppression of plasma pancreatic glucagon and growth hormone, a fall in plasma-cyclic-adenosine-monophosphate (A.M.P.) concentrations, and a large fall in plasma-glucose concentration. After infusion plasma concentrations of these substances rose again. Blood-ketone-bodies, plasma-free-fatty-acids (F.F.A.), and plasma glycerol concentrations, however, did not decrease appreciably with somatostatin administration. In three patients 2 to 3 h somatostatin infusions were twice superimposed upon a continuous 9-5 h insulin infusion (1 unit/h). An insulin effect was noticeable within 30 minutes, with pronounced falls in the concentrations of plasma glucose, pancreatic glucagon, F.F.A., and blood-ketone-bodies. There was no significant change in these patterns when somatostatin was administered or withdrawn. These results do not indicate that somatostatin infusion would be useful in the treatment of manifest diabetic ketoacidosis.

Adult↗
PubMed1976

Effects of somatostatin on basal levels of plasma growth hormone and insulin in acromegalics: dose-response studies and attempted total growth hormone suppression.

Somatostatin 5, 10, and 25 mug and saline were given as a 2 min bolus injection to 6 acromegalic patients in basal conditions. A significant dose-response relationship could be demonstrated between somatostatin and the suppressions of plasma growth hormone and insulin. The lowest somatostatin dose tested exerted a significant suppression of both hormones. Insulin suppression after the bolus injection lasted for 15 minutes, while the suppression of growth hormone was maintained for 30-50 minutes. In order to obtain total suppression of the elevated plasma growth hormone levels in acromegalics, 3 patients received 50, 250, and 500 mug of somatostatin as bolus injections at time 0, 90, and 180 minutes, 2 patients received 50 mug of somatostatin as bolus injections 4 times with an interval of 20 minutes between each injection, and finally 3 patients received a large dose of somatostatin, 3000 mug given as an infusion over 2 hours. The single injections of somatostatin were not followed by a satisfactory growth hormone suppression. In the infusion experiments, the average plasma growth hormone level was suppressed only 65%, resulting in individual plasma growth hormone plateaus of 20, 14, and 3.6 ng/ml. Only the lowest of these plateaus would be acceptable from a clinical point of view.

Acromegaly↗
PubMed1976

Somatostatin: a review of its effects especially in human beings.

A review is given of the early 1976 situation in somatostatin research: the effects on pituitary hormones and the effects outside the pituitary gland, the production of somatostatin outside the hypothalamus, the artificial analogues, the problem of "side effects", and the mode of action. The possible clinical applications of somatostatin and somatostatin analogues are discussed.

Acromegaly↗
PubMed1976

Growth hormone's role in diabetic microangiopathy.

The state of the blood vessels is normal at the clinical onset of juvenile diabetes. Vascular changes develop slowly and progressively. According to the growth hormone hypothesis, elevated serum growth hormone is one casual factor in the development of diabetic angiopathy. The hypothesis proposes an effect of growth hormone not on blood glucose but directly on blood vessels. This hypothesis is based on serum growth hormone studies and on a controlled clinical trial of the effect of hypophysectomy on small blood vessels. An animal model of large-vessel disease in diabetes is briefly described. There is a large molecule in diabetic serum causing proliferation of aortic myomedial cells in culture. Growth hormone causes a similar proliferation. A short summary is given of the present situation in somatostatin research relating to diabetes mellitus.

Adolescent↗
PubMed1975

Twenty-four-hour serum growth hormone levels in maturity-onset diabetics.

Serum growth hormone, glucose, and insulin were studied every half hour during a twenty-four-hour period of "daily life" in four groups of subjects: nonobese normal subjects, obese normal subjects, nonobese maturity-onset diabetics, and obese maturity-onset diabetics. It was found that (1) serum growth horomone was uniformly low without meal- and sleep-related peaks in obese normals and diabetics. The twenty-four-hour serum growth hormone level was significantly higher in nonobese subjects than in obese subjects, in both diabetics and normals; (2) the twenty-four-hour serum growth hormone level was more fluctuating and significantly higher in nonobese diabetics than in nonobese normals; (3) there was no difference in the twenty-four-hour serum growth hormone level between obese diabetics and obese normals.

Adult↗
PubMed1975

The effect of somatostatin on the rise of growth hormone and glucagon secretion induced by arginine and L-dopa in diabetic patients.

The growth-hormone-release-inhibiting hormone somatostatin was infused in seven juvenile diabetic subjects during an arginine infusion test and in six juvenile diabetic subjects during an L-dopa stimulation test. The plasma growth hormone response to arginine and L-dopa was completely inhibited by somatostatin. The plasma pancreatic glucagon response to arginine was also inhibited by somatostatin. The plasma pancreatic glucagon level was not changed by L-dopa, but somatostatin induced a significant fall in this level. The plasma glucose increase after arginine and L-dopa administration was slightly inhibited by somatostatin. The arginine-induced fall in free fatty acids was prevented by somatostatin, and the L-dopa-induced rise in free fatty acids was enhanced by somatostatin. The growth hormone- and glucagon-surppressive effect of somatostatin may prove useful in controlling the metabolic state and in preventing the development of angiopathy in diabetic patients. A somatostatin preparation with prolonged activity is needed for lifelong administration, but the presently available compound may be of value as an adjunct in the standard treatment of diabetic ketoacidosis and coma.

Arginine↗