Hormonal Control of Haemostasis During Hypoglycaemia in Diabetes Mellitus

1987 ◽  
Vol 57 (03) ◽  
pp. 341-344 ◽  
Author(s):  
P J Grant ◽  
M H Stickland ◽  
P G Wiles ◽  
J A Davies ◽  
J K Wales ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Plasma Insulin ◽  
Vascular Complications ◽  
Hormonal Control ◽  
Diabetic Patients ◽  
Coagulant Activity ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryFactor VIII (FVIII) and plasminogen activator activity (PAA) rise during hypoglycaemia, and this might contribute to the vascular complications of diabetes. Similar changes in haemostasis accompany raised plasma levels of vasopressin (aVP) and adrenaline. To investigate the effects of these hormones on haemostasis during hypoglycaemia and the role of plasma insulin concentrations, eight insulin-dependent diabetic patients underwent controlled hypoglycaemia for 20 min and 13 diabetic patients were investigated during hyperinsulinaemia with blood glucose maintained at 8.0 mmol/1. During hypoglycaemia, insulin levels increased to median values of 114 mU/1, aVP rose from 0.5 to 4.4 (p <0.005) pg/ml and adrenaline from 0.4 to 4.4 nmol/l (p <0.005). FVIII coagulant activity (FVIII :C) rose from 0.75 to 1.09 iU/ml (p <0.01) and the ristocetin co-factor (FVIIIR:Co) and von Willebrand factor antigen (vWF:Ag) showed similar responses. PAA increased from 156 to 745 units (p <0.005). During hyperinsulinaemia, insulin rose following infusion from 24 to 52 and 118 mU/l, maintained for an hour at each level. Despite this, plasma aVP, FVIII :C, FVIIIR:Co, vWF:Ag and PAA remained unchanged. This study indicates that the marked changes in FVIII, vWF and PAA concentrations which accompany hypoglycaemia depend on low blood glucose and not raised plasma insulin. The response in probably mediated by increases in adrenaline and aVP, which are part of the physiological response to hypoglycaemia.

β-Adrenoceptor Blockade and Recovery from Hypoglycaemia in Diabetic Subjects: Normalization after Lactate and Glycerol Infusions

1982 ◽  
Vol 62 (2) ◽  
pp. 131-136 ◽  
Author(s):  
I. Lager ◽  
U. Smith
Keyword(s):  
Blood Glucose ◽  
Recovery Rate ◽  
Type I Diabetes ◽  
Diabetic Patients ◽  
Type I ◽  
Insulin Dependent ◽  
Propranolol Treatment ◽  
Glucose Recovery ◽  
Insulin Dependent Diabetic ◽  
Gluconeogenic Substrates

1. Previous studies have shown that non-selective β-adrenoceptor blockade attenuates the blood glucose recovery rate after hypoglycaemia in type I diabetes. Apart from possible effects on hepatic glycogenolysis propranolol also inhibits the release of the important gluconeogenic substrates lactate and glycerol. 2. To determine whether the effect of non-selective β-adrenoceptor blockade on glucose recovery could be associated with diminished availability of gluconeogenic substrates, lactate and glycerol were infused during hypoglycaemia in four insulin-dependent diabetic patients. Comparisons were made of the blood glucose recovery on placebo, propranolol and propranolol combined with the infusion. 3. The blood glucose recovery rate after hypoglycaemia was less on propranolol than with placebo but was significantly improved and not different from placebo when propranolol treatment was combined with lactate and glycerol infusions. Thus, at least for type I diabetic patients, in whom gluconeogenesis is proportionally greater than in healthy subjects, non-selective β-adrenoceptor blockade attenuates the glucose recovery rate from hypoglycaemia mainly by reducing the availability of gluconeogenic substrates.

Nocturnal versus diurnal hormonal counterregulation to hypoglycemia in Type 1 (insulin-dependent) diabetic patients

1993 ◽  
Vol 128 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Inger Bendtson ◽  
Anne Mette Rosenfalck ◽  
Christian Binder
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Insulin Infusion ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Diabetic Patients ◽  
Hormonal Responses ◽  
Nocturnal Hypoglycemia ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Asymptomatic hypoglycemia in IDDM patients seems to be more frequent during the night than during the day, with reported frequencies as high as 56%. Hormonal counterregulation to diurnal and nocturnal hypoglycemia was studied in 10 insulin-dependent diabetic patients without diabetic complications in order to test whether hormonal responses were lower at night than during daytime. A lower catecholamine response might imply less marked symptoms and therefore one reason why patients are not awakened by hypoglycemia. Blood glucose was stabilized to around 6 mmol/1 by iv insulin infusion and hypoglycemia was induced by increasing the insulin infusion rate—in the night studies at 01.30, in the day studies at 08.00. Blood glucose nadirs were 1.5±0.4 (1.2–1.9) mmol/1 at night and 1.9±0.3 (1.3–2.2) mmol/l during the day; in three patients the nadirs were identical during both the night and day. One patient had no adrenaline response to daytime hypoglycemia. In general, nocturnal hypoglycemia elicited greater catecholamine responses correlated to the duration of hypoglycemia. Glucagon responses showed a great heterogeneity independently of diabetes duration and hypoglycemic level. Growth hormone secretion was reduced during the night study; however, no refractory periods were found after sleep-related growth hormone secretion. In conclusion: counter-regulatory hormonal responses tend to be greater at night than during the day and do not explain why patients are not awakened by nocturnal hypoglycemia.

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