Glucagon response to hypoglycemia in sympathectomized man.

Palmer, Jerry P.; Henry, David P.; Benson, James W.; Johnson, David G.; Ensinck, John W.

doi:10.1172/jci108305

Cited by 109 publications

(40 citation statements)

References 26 publications

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“…In accordance with this, we have also found no glucagon response to hypoglycaemia in 10 Type 1 diabetic patients with autonomic neuropathy [24]. Several reports have demonstrated that the sympathetic nervous system is of minor or no importance for the glucagon response to hypoglycaemia [25,26]. Parasympathetic activity has been held responsible for glucagon release [24].…”

Section: Discussionsupporting

confidence: 88%

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

et al. 1982

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Summary. 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 0.054ng/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.

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Section: Discussionsupporting

confidence: 88%

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

et al. 1982

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“…21 Spinal cord injury results in varying degrees of autonomic disturbances with eects also on metabolic regulation. Hypoglycaemia among subjects with high paraplegia and tetraplegia is accompanied by a reduction in blood pressure, absent increase of padrenaline 22 and noradrenaline 23 and lack of neuroglycopenic symptoms. In tetraplegic patients, mental arousal, cold or pain stimuli above lesion level do not cause any signi®cant cardiovascular response.…”

Section: Introductionmentioning

confidence: 99%

Insulin resistance and sympathetic function in high spinal cord injury

Karlsson

1999

Spinal Cord

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Objective: Cardiovascular disease (CVD) is today one of the main causes of death and aects spinal cord injured (SCI) earlier than able-bodied. Risk factors for CVD, such as decreased glucose tolerance, insulin resistance and increased fat mass, are all reported among SCI subjects and may be related to changes in sympathetic nervous system (SNS) function. Methods: In order to test our hypothesis of a relationship between metabolic disturbances and alterations in SNS function, glucose and adipose tissue metabolism was investigated by the hyperinsulinaemic normoglycaemic clamp and microdialysis. Body composition was determined by DEXA-scanning. The SNS function was evaluated in total body as well as above and below lesion level by radiolabelled noradrenaline (NA) isotope dilution technique. A 24 h continuous plasma-NA monitoring was performed in seven SCI subjects. Results: Following an oral glucose load the SCI group demonstrated normal glucose tolerance but impaired insulin sensitivity with a maximum insulin value of 83 mU.1 71 in SCI compared to 50 in siblings, while adipose tissue metabolism was normal compared to siblings. Fat tissue mass constituted 34% of body mass in SCI group compared to 21% in weightmatched controls. Peripheral aerent activation resulted in increased blood pressure, decreased heart rate and reduction in muscle and skin blood¯ow. Furthermore, lipolysis below lesion level was activated by peripheral stimulation (89 ± 135 mmol.l 71 ). The 24 h continuous monitoring revealed p-NA levels 41.40 nmol.l 71 sucient to induce lipolysis in 20% of the registrations. NA spillover below lesion level increased substantially following peripheral aerent stimulation (0.06 ± 0.90 pmol.min.71 .100 g 71 ), whereas spillover above lesion level increased during central activation. Conclusions: We found signs of decreased insulin sensitivity and increased fat tissue mass. Peripheral activation of SNS was visualised in the SCI group by increased transmitter spillover as well as increased lipolysis and vasoconstriction. The diurnal registration of NA levels indicated frequent episodes of peripheral sympathetic activation in the group. This may compensate for the inability of central activation of SNS and may contribute to maintain lipolysis activity as well as to generate insulin resistance in the group

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“…However, factors other than catecholamines must be capable of restoring normoglycemiiia because apparently normal glucose counterregulation has been observed in catecholamine-deficient patients with spinal cord transections (10,11), epinephrine-deficient adrenalectomized patients (11)(12)(13)(14), and normal subjects during the infusioIn of a-or ,-adrenergic blocking agents (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

Role of Glucagon, Catecholamines, and Growth Hormone in Human Glucose Counterregulation

1979

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A B S T R A C T To further characterize mechanisms of glucose counterregulation in man, the effects of pharmacologically inducd deficiencies of glucagon, growth hormone, and catecholamines (alone and in combination) on recovery of plasma glucose from insulin-induced hypoglycemia and attendant changes in isotopically ([3-3H]glucose) determined glucose fluxes were studied in 13 normal subjects. In control studies, recovery of plasma glucose from hypoglycemia was primarily due to a compensatory increase in glucose production; the temporal relationship of glucagon, epinephrine, cortisol, and growth hormone responses with the compensatory increase in glucose appearance was compatible with potential participation ofall these hormones in acute glucose counterregulation. Infusion of somatostatin (combined deficiency of glucagon and growth hormone) accentuated insulin-induced hypoglycemia (plasma glucose nadir: 36±2 ng/dl during infusion ofsomatostatin vs. 47±2 mg/dl in control studies, P < 0.01) and impaired restoration of normoglycemia (plasma glucose at min 90: 73±3 mg/dl at end ofsomatostatin infusion vs. 92±3 mg/dl in control studies, P < 0.01). This impaired recovery of plasma glucose was due to blunting of the compensatory increase in glucose appearance since glucose disappearance was not augmented, and was attributable to suppression of 62 glucagon secretion rather than growth hormone secretion since these effects of somatostatin were not observed during simultaneous infusion of somatostatin and glucagon whereas infusion of growth hormone along with somatostatin did not prevent the effects of somatostatin. The attenuated recovery of plasma glucose from hypoglycemia observed during somatostatininduced glucagon deficiency was associated with plasma epinephrine levels twice those observed in control studies. Infusion of phentolamine plus propranolol (combined a-and,8-adrenergic blockade) had no effect on plasma glucose or glucose fluxes after insulin administration. However, infusion of somatostatin along with both phentolamine and propranolol further impaired recovery ofplasma glucose from hypoglycemia compared to that observed with somatostatin alone (plasma glucose at end of infusions: 52+6 mg/dl for somatostatin-phentolamine-propranolol vs. 72+±5 mg/dl for somatostatin alone, P < 0.01); this was due to further suppression of the compensatory increase in glucose appearance (maximal values: 1.93±0.41 mg/kg per min for somatostatin-phentolamine-propranolol vs. 2.86+0.32 mg/kg per min for somatostatin alone, P < 0.05). These results indicate that in man (a) restoration of normoglycemia after insulin-induced hypoglycemia is primarily due to a compensatory increase in glucose production; (b) intact glucagon secretion, but not growth hormone secretion, is necessary for normal glucose counterregulation, and (c) adrenergic mechanisms do not normally play an essential role in this process but become critical to recovery from hypoglycemia when glucagon secretion is impaired.J. Clin. Invest.

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Glucagon response to hypoglycemia in sympathectomized man.

Cited by 109 publications

References 26 publications

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 hypoglycaemia in Type 1 (insulin-dependent) diabetes with and without residual B cell function

Insulin resistance and sympathetic function in high spinal cord injury

Role of Glucagon, Catecholamines, and Growth Hormone in Human Glucose Counterregulation

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