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Biomedical subjects

J Hilsted

Publications and source records attributed to J Hilsted.

At least 109 records · Page 6Linked to original sources
PubMed1983

Response of pancreatic polypeptide to hypoglycaemia in insulin-dependent diabetics with and without residual beta-cell function.

To investigate a possible association between the beta-cells and the cells secreting pancreatic polypeptide (PP), the response of PP to insulin-induced hypoglycaemia was investigated in seven insulin-dependent diabetics with and seven without residual beta-cell function, all without signs of autonomic neuropathy. The mean concentrations of PP was significantly greater from 15 to 60 min after symptoms of hypoglycaemia in patients with residual beta-cell function than in patients without (P less than 0.05) despite similar blood glucose concentrations in the two groups. Also the total integrated areas beneath the response curves as well as the incremental integrated areas were significantly greater in patients with beta-cell function (216 +/- 36 pmol/l x min and 188 +/- 34 pmol/l x min, respectively) than in patients without beta-cell function (125 +/- 26 pmol/l x min and 102 +/- 26 pmol/l x min) (P less than 0.05 for both). The mean maximal concentrations of adrenaline (1.53 +/- 0.28 ng/ml v. 1.29 +/- 0.12 ng/ml) and noradrenaline (0.56 +/- 0.16 ng/ml v. 0.45 +/- 0.04 ng/ml) were not statistically different in the two groups. No well established explanation for an association between residual insulin secretion and capacity for PP-response to hypoglycaemia in type 1 diabetics exists.

Adult↗
PubMed1983

Autonomic neuropathy: the diagnosis.

The diagnosis of autonomic neuropathy is often difficult to establish, since clinical symptoms generally appear late in the course of the disease, and may be non-specific. A number of recently developed quantifiable and reproducible autonomic nerve function tests are reviewed, with emphasis on the physiological basis of the tests and on practical applicability. Finally, diagnostic criteria, based on autonomic nerve function tests, are suggested.

Amphetamine↗
PubMed1983

Whole body clearance of norepinephrine. The significance of arterial sampling and of surgical stress.

The whole body clearance of norepinephrine (NE) was measured in seven patients pre- and postoperatively. L[(3)H]NE was infused intravenously for 90 min and steady-state concentrations of L[(3)H]NE were measured at 75 and 90 min in both arterial and peripheral venous blood. Preoperatively, in the resting supine position, the clearance values based on arterial and venous sampling averaged 1.4 and 2.5 liter/min, respectively (P < 0.02). The difference in clearance values was due to a peripheral uptake of NE averaging 45%. The mean plasma NE increased from 1.70 nmol/liter preoperatively to 5.20 nmol/liter postoperatively (P < 0.02). The plasma appearance rate of NE averaged 2.4 nmol/min before surgery and it increased to 9.5 nmol/min postoperatively (P < 0.02). The plasma clearance of NE averaged 1.4 and 1.6 liter/min pre- and postoperatively, respectively (not significantly different). Our study demonstrates that the calculation of plasma NE clearance based on venous sampling results in values that are too high. Furthermore, such values may be influenced by individual variations in the peripheral uptake of NE, since we found no correlation between clearance values based on venous and arterial sampling. The increase in plasma NE postoperatively was due to an increase in the plasma appearance rate of NE because the clearance rate did not change.

Adult↗
PubMed1983

Discrepancy between plasma C-peptide and insulin response to oral and intravenous glucose.

Plasma insulin, proinsulin, and C-peptide responses to 25 g glucose orally and intravenously administered were measured in 10 healthy males. Plasma insulin response was higher during the oral load in accordance with the "incretin" concept. However, the actual amount of insulin secreted, as measured by the plasma C-peptide response, was similar during the two glucose loads. The higher plasma insulin response after oral glucose was not due to crossreactivity with proinsulin in the insulin assay. These results suggest that the higher plasma insulin response during an oral glucose load is due at least partially to a lower hepatic extraction of insulin.

Administration, Oral↗
PubMed1982

Changes in platelet function, blood coagulation and fibrinolysis during insulin-induced hypoglycaemia in juvenile diabetics and normal subjects.

Haemostatic parameters were assessed before insulin induced hypoglycaemia and 0, 1 and 2 hr after discontinuation of insulin infusion in 7 non-diabetics, aged 28 (22-31) years (mean and range), and 8 juvenile diabetics, aged 31 (27-35) years, with a mean duration of diabetes of 4 years. The patients were normoglycaemic for at least 10 hr before the study. Platelet aggregation in vitro was induced by lower adenosine diphosphate (ADP) concentrations in the diabetics than in the controls before hypoglycaemia and 0 and 60 min after insulin infusion. Platelet counts decreased significantly in the diabetics after hypoglycaemia, whereas no changes were seen in the control group. The activated partial thromboplastin time (APTT) was reduced in both groups and significantly lower in the diabetics than in the controls 120 min after insulin infusion. Fibrinogen and factor VIII R:Ag increased after insulin infusion; highest values were seen in the diabetics. The euglobulin clot lysis time (ELT) was reduced in both groups during insulin infusion; 120 min after end of insulin infusion ELT was significantly longer in the diabetics than in the control group.

Adult↗
PubMed1982

Hormonal, metabolic and cardiovascular responses to hypoglycaemia in Type 1 (insulin-dependent) diabetes with and without residual B cell function.

Hormonal, metabolic and cardiovascular responses to insulin induced hypoglycaemia were investigated in seven Type 1 (insulin-dependent) diabetic patients with residual B cell function, eight Type 1 diabetic patients without B cell function and six healthy subjects. No differences were found between the diabetic groups regarding nadir of glucose and rate of recovery to normoglycaemia. The patients with residual B cell function had a glucagon response to hypoglycaemia which was close to that of normal subjects. In patients without B cell function, the glucagon response to hypoglycaemia was present, albeit significantly smaller than in the patients with preserved B cell function (0.025 ng/ml, range 0.007-0.042 versus 0.054 ng/ml, range 0.029-0.087). The group without B cell function had signs of an exaggerated rate of lipolysis and ketogenesis compared with the patients with B cell function and the normal subjects.

Adult↗
PubMed1982

Subcutaneous blood flow during insulin-induced hypoglycaemia: studies in juvenile diabetics with and without autonomic neuropathy and in normal subjects.

Subcutaneous blood flow was measured preceding insulin-induced hypoglycaemia, at the onset of hypoglycaemic symptoms and 2 h later in juvenile diabetics with and without autonomic neuropathy and in normal males. In all groups subcutaneous blood flow decreased at the onset of hypoglycaemic symptoms compared with pre-hypoglycaemic flow. Two hours after onset of hypoglycaemic symptoms, subcutaneous blood flow was still significantly decreased compared with pre-hypoglycaemic flow. In normal subjects local nerve blockade had no effect on blood flow changes during hypoglycaemia, whereas local alpha-receptor blockade abolished the vasoconstrictor response. We suggest that circulating catecholamines stimulating vascular alpha-receptors are probably responsible for flow reduction in the subcutaneous tissue during hypoglycaemia.

Adult↗
PubMed1982

No response of pancreatic hormones to hypoglycemia in diabetic autonomic neuropathy.

The responses of pancreatic hormones (i.e. glucagon, pancreatic polypeptide, and somatostatin) to insulin-induced hypoglycemia were investigated in 18 insulin-dependent diabetics without residual beta-cell function and in 6 normal subjects. Nine of the diabetics had autonomic neuropathy, and 9 had no neuropathy. After hypoglycemia, no significant increase in any of the 3 pancreatic hormones was found in the diabetics with autonomic neuropathy, whereas significant increments were found in the diabetics without neuropathy and in the normal subjects. These results suggest that autonomic nervous activity is of major importance for pancreatic hormone release during hypoglycemia in man.

Adult↗
PubMed1981

Prevalence of diabetic autonomic neuropathy measured by simple bedside tests.

To investigate the prevalence of diabetic autonomic neuropathy, five simple bedside tests, beat-to-beat variation during quiet respiration, beat-to-beat variation during forced respiration, heart rate and blood pressure response to standing, heart rate response to exercise, and heart rate response to Valsalva's manoeuvre were applied to 75 male insulin-dependent diabetics, mean age 40 years, (range 30-49 years). The subjects were subdivided into three groups according to duration of diabetes, which was between 0 and 40 years. Twenty-eight healthy age-matched male controls were also studied. The prevalence of diabetic autonomic neuropathy in the whole diabetic population indicated by abnormal response in beat-to-beat variation during forced respiration was 27%. Diabetic autonimic neuropathy increased in frequency with duration of disease. Patients with nephropathy or proliferative retinopathy had a significantly higher prevalence of diabetic autonomic neuropathy as indicated by abnormal beat-to-beat variation during forced respirations (p less than 0.01) than patients without these complications.

Adult↗
PubMed1981

Hemodynamics in diabetic orthostatic hypotension.

Hemodynamic variables (blood pressure, cardiac output, heart rate, plasma volume, splanchnic blood flow, and peripheral subcutaneous blood flow) and plasma concentrations of norepinephrine, epinephrine, and renin were measured in the supine position and after 30 min of quiet standing. This was done in normal subjects (n = 7) and in juvenile-onset diabetic patients without neuropathy (n = 8), with slight neuropathy (decreased beat-to-beat variation in heart rate during hyperventilation) (n = 8), and with severe neuropathy including orthostatic hypotension (n = 7). Blood pressure decreased precipitously in the standing position in the diabetics with orthostatic hypotension, whereas moderate decreases were found in the other three groups. Upon standing, heart rate rose and cardiac output and plasma volume decreased similarly in the four groups. The increases in total peripheral resistance, splanchnic vascular resistance and subcutaneous vascular resistance were all significantly lower (P less than 0.025) in the patients with orthostatic hypotension compared with the other three groups. The increase in plasma norepinephrine concentrations in the patients with orthostatic hypotension was significantly lower (P less than 0.025) than in the patients without neuropathy, whereas plasma renin responses to standing were similar in the four groups. We conclude that in diabetic hypoadrenergic orthostatic hypotension the basic pathophysiological defect is lack of ability to increase vascular resistance, probably due to impaired sympathetic activity in the autonomic nerves innervating resistance vessels; cardiac output and plasma volume responses to standing are similar to those found in normal subjects and in diabetics without neuropathy.

Adult↗
PubMed1980

Metabolic responses to hypoglycemia in juvenile diabetics.

Glucagon and metabolic responses to insulin-induced hypoglycemia were studied in seven juvenile diabetics, age 31 +/- 2 years (mean and S.E.M.), duration of diabetes 17 +/- 3 years, with diabetic autonomic neuropathy (decreased beat-to-beat variation in heart rate during hyperventilation and/or orthostatic hypotension) and in seven control patients of similar age and duration of diabetes with out neuropathy. Before the hypoglycaemic episode, normoglycemia had been maintained for at least 10 hours. Following hypoglycemia, a slight but significant and similar increase in plasma glucagon was found in both patient groups. Metabolic responses to hypoglycemia were also similar in the two patient groups. In conclusion, diabetic autonomic neuropathy has no effect on glucagon and metabolic responses to hypoglycemia in juvenile, insulin-treated diabetics.

Adult↗
PubMed1980

Cardiovascular, hormonal and metabolic responses to graded exercise in juvenile diabetics with and without autonomic neuropathy.

Thirteen juvenile diabetics were studied in order to determine if decreased beat-to-beat variation during deep respiration, indicating abnormal autonomic nerve function, imply that cardiovascular, hormonal and metabolic responses are impaired. Patients with decreased beat-to-beat variation had to be more heavily stressed during exercise to reach a certain heart rate or catecholamine level. The relation between other metabolic and hormonal response is discussed.

Adult↗
PubMed1980

Gastroenteropancreatic hormonal changes during exercise.

Peripheral plasma concentrations of gastroenteropancreatic peptides were measured during a 3-h period of bicycle exercise at 40% of maximal oxygen uptake in six normal men. Marked increases (P < 0.02) were found in vasoactive intestinal polypeptide (VIP) [1.8 +/- 0.7 (rest) vs. 22.3 +/- 5.4 pmol x l-1 (mean +/- SE) (3 h)], secretin (0.5 +/- 0.5 vs. 11.1 +/- 2.7 pmol x l-1), pancreatic polypeptide (PP) (4.0 +/- 1.5 vs. 46.3 +/- 11.5 pmol x l-1), somatostatin (SRIF) (12.8 +/- 1.2 vs. 17.7 +/- 0.6 pmol x l-1), whereas no changes occurred in gastric inhibitory polypeptide (37.3 +/- 5.9 vs. 39.2 +/- 9.8 pmol x l-1). Immunoreactive insulin and C-peptide decreased from 0.08 +/- 0.004 and 0.39 +/- 0.03 pmol x l-1, respectively, to 0.04 +/- 0.003 (P < 0.005) and 0.13 +/- 0.02 (P < 0.001). The significant decrease in C-peptide and in the C-peptide-to-insulin molar ratio indicate decreased insulin secretion and clearance, respectively, during exercise. Plasma glucose decreased [5.0 +/- 0.1 (rest) vs. 4.2 +/- 0.3 mmol.l-1 (3 h)] (P < 0.01). During 3 h of rest, none of the measured parameters had changed. The marked exercise-induced changes in plasma concentrations of PP, secretin, VIP, and SRIF are provocative. We know in detail neither the stimuli for the release of these peptides nor their physiological role during exercise.

Adolescent↗