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Biomedical subjects

K Lundbaek

Publications and source records attributed to K Lundbaek.

At least 19 recordsLinked to original sources
PubMed1980

Nervous system abnormality and nervous disease in diabetes.

Symptomatic diabetic neuropathy is present only in a few percent of the total diabetic population. In contrast abnormalities of the various parts of the nervous system can be demonstrated very early using neurophysiological techniques. These abnormalities are reversible at first, but progressive with duration of diabetes. Similar nervous abnormalities are present in experimental diabetes in the rat. The earliest structural changes have been demonstrated to be a decreased calibre of the myelinated axons. An abnormality in the axonal transport of proteins is possibly the very first change to appear. These recent results have enabled us to propose a hypothesis concerning the sequence of events in the development of the peripheral nerve abnormalities.

Animals↗
PubMed1979

The clinical diagnosis of insulinoma.

Based on the literature and on experience and on experience with 23 cases the clinical diagnosis of insulinomas is reviewed. In clinical praxis the diagnostic steps can usually be simplified to a demonstration of fasting, symptomatic hypoglycaemia. Hence, we have used the 72-hour fast as the single diagnostic test for insulinomas during the last 5 years. Pro-insulin measurements may be a valuable supplementary tool. Other diagnostic tests are probably of little importance.

Adenoma, Islet Cell↗
PubMed1978

Plasma prolactin in juvenile diabetics. 24-h studies with somatostatin.

In normal subjects during 24-hours saline infusion, plasma prolactin showed a number of small rises during day and night. The mean night-time level was significantly higher than the day-time level (8.2 +/- 0.6 ng/ml as against 4.7 +/- 0.5 ng/ml). In 12 insulin-dependent diabetics the 24 h plasma prolactin pattern was identical to that found in normals. Somatostatin infusion (4 mg/24 h in normals; 2--6 mg/24 h in diabetics) had no effect on the 24 h plasma prolactin pattern in either normals or in diabetics.

Adult↗
PubMed1978

Growth hormone enhances basement membrane thickening in experimental diabetes. A preliminary report.

Injection of porcine growth hormone (200 microgram) or saline 5 days a week for 16 to 20 weeks in streptozotocin-diabetic rats showed that compared to saline growth hormone produced a 2 1/2-fold larger increase in glomerular capillary basement membrane thickness (2p = 0.027). The possible significance of this effect of an elevated level of growth hormone for diabetic microangiopathy is discussed.

Animals↗
PubMed1978

Somatostatin in the treatment of patients with extra-pyramidal disorders and patients with EEG abnormalities.

The growth hormone release inhibiting hormone acts probably both as a true hypophysiotropic hormone and as a neuroregulatory substance. Neurophysiological studies have shown that somatostatin is a CNS depressant. Somatostatin might therefore be of therapeutic significance in neurological diseases. Sixteen patients with different extrapyramidal disorders and seven patients with various EEG abnormalities were tested with 2-hour somatostatin infusions and control infusions with saline. Somatostatin did not induce any improvement or deterioration of symptoms, signs, or EEG abnormalities in any patient.

Adult↗
PubMed1978

Somatostatin in maturity-onset diabetes.

Plasma FFA, glucagon, insulin, glucose, and growth hormone were followed every hour during 24 hours of saline infusion, 24 hours of somatostatin (4mg.) infusion, and three hours without infusion in six nonobese and six obese maturity-onset diabetic men. Somatostatin induced the same changes in the parameters of both groups of diabetic patients: A rise in plasma FFA, which gradually disappeared after some hours of infusion, a suppression of plasma glucagon and insulin, and an augmentation of plasma glucose both postprandially and during the night. Plasma growth hormone was suppressed in the nonobese patients, but somatostatin could not further suppress the low and nonfluctuating plasma growth hormone concentration in the obese maturity-onset diabetics. The results indicate that a preparation with a pattern of hormone suppression like that of somatostatin will not be useful in the control of maturity-onset diabetes, because it suppresses insulin and elevates the blood glucose concentration.

Aged↗
PubMed1978

24-hour studies of the effects of somatostatin on the levels of plasma growth hormone, glucagon, and glucose in normal subjects and juvenile diabetics.

Somatostatin was infused in various doses into normal subjects and juvenile diabetics for a 24-hour period preceded by a 24-hour control period and followed by another three-hour control period. Saline was infused during the first control period. Meals were served during the two 24-hour periods. Blood samples were taken hourly. Five normal males received a total dose of 4 mg. somatostatin. Four male diabetics received 2 mg., four received 4 mg., and four 6 mg. In the diabetics, somatostatin suppressed plasma growth hormone, glucagon, and glucose throughout the infusion. All parameters rebounded at cessation of infusion. In the normals, somatostatin suppressed plasma growth hormone, glucagon, and insulin but increased plasma glucose. It is concluded that the plasma glucose suppression in the diabetics is mainly due to the suppression of the diabetogenic hormones growth hormone and glucagon. A minor effect of decreased and/or delayed absorption of carbohydrates cannot be excluded in these experiments. The elevated plasma glucose levels in normals must be due to the suppressive effects of somatostatin on insulin secretion.

Adolescent↗