Responses of glucose and glucoregulatory hormones to exercise in thyrotoxic and myxoedematous patients before and after 3 months of treatment

1991 ◽  
Vol 81 (1) ◽  
pp. 91-99 ◽  
Author(s):  
Leif Sestoft ◽  
Niels Juel Christensen ◽  
Bengt Saltin

1. The effect of moderate endurance exercise on blood glucose concentration and on glucoregulatory hormones was studied in nine thyrotoxic and five myxoedematous humans before and 3 months after anti-thyroid and substitution therapy, respectively. 2. At rest, the fasting concentrations of insulin and pro-insulin correlated positively with the prevailing total tri-iodothyronine concentration, whereas the concentrations of noradrenaline and cortisol correlated inversely with the tri-iodothyronine concentration. 3. During exercise the plasma insulin, pro-insulin and C-peptide concentrations decreased. The plasma glucagon concentration increased slightly in thyrotoxic patients before and after treatment and was largely unchanged in myxoedematous patients in either state. 4. The plasma noradrenaline concentration increased before and after treatment in both groups, with concentrations two times higher in the myxoedematous than in the thyrotoxic patients. Treatment for 3 months did not change this pattern. The plasma adrenaline concentration increased in both groups, but in the untreated thyrotoxic patients the increase was two to three times greater than that after treatment or that in the myxoedematous group. 5. The blood glucose concentration decreased in eight of nine untreated thyrotoxic patients, but was largely unchanged after treatment or in the myxoedematous patients. A strong negative correlation was found between the decline in blood glucose concentration and the increase in plasma adrenaline concentration in the thyrotoxic group. 6. Thus, during exercise untreated thyrotoxic patients are prone to hypoglycaemia, show an inadequate glucagon response, and exhibit a large counter-regulatory increase in plasma adrenaline concentration.

1981 ◽  
Vol 98 (3) ◽  
pp. 402-406 ◽  
Author(s):  
Johannes Järhult ◽  
Lars-Ove Farnebo ◽  
Bertil Hamberger ◽  
Jens Holst ◽  
Thue W. Schwartz

Abstract. The effects of insulin hypoglycaemia (0.15 IU/kg) on plasma adrenaline, noradrenaline, dopamine, glucagon and pancreatic polypeptide (PP) concentrations were investigated in 6 adrenalectomized subjects and 6 healthy controls. Both the rise in mean plasma insulin and the fall in mean blood glucose concentration were closely similar in the two groups. Mean plasma adrenaline concentration rose by about 3 nmol/l in the normal subjects, but remained unchanged in adrenalectomized subjects. Mean plasma noradrenaline concentration increased by about 2 nmol/l in both groups. Despite the large difference in adrenaline concentrations during hypoglycaemia, there was no significant difference between the responses of the endocrine pancreas of the normal and adrenalectomized subjects. Thus, mean plasma glucagon concentration rose by about 30 pmol/l and mean plasma PP concentration by about 150 pmol/l in each group. We conclude that the release of glucagon and PP during hypoglycaemia does not depend upon changes in plasma adrenaline concentration in man.


Author(s):  
Katherine Gregory ◽  
Daria Turner ◽  
Charis Nicole Benjamin ◽  
Carmen Monthe-Dreze ◽  
Lise Johnson ◽  
...  

ObjectivesTo determine the impact of incorporating dextrose gel in the treatment of neonatal hypoglycaemia (NH) and the role of feeding type in NH outcomes.Study designWe conducted a retrospective analysis of 2688 infants >35 weeks’ gestation who were screened for NH before and after implementation of a clinical guideline for NH evaluation and treatment. We analysed the proportion of infants who required intravenous dextrose for NH before and after guideline implementation, the change in blood glucose concentrations with gel by feeding type and the odds of successful NH treatment with gel and feeding by feeding type.ResultsFollowing implementation of the guideline, a lower proportion of infants required intravenous dextrose for NH treatment (8.6% (60 infants) before guideline vs. 5.6% (112 infants) after guideline (p=0.007)). The median rise in blood glucose concentration with gel administration in the entire cohort was 0.61 mmol/L (11 mg/dL) (IQR 0.28–1.06 mmol/L (5–19 mg/dL)). Blood glucose concentration of formula-fed infants rose more in response to feeding and gel than breastfed infants (p≤0.0001). Formula feeding was associated with a lower odds of recurrent hypoglycaemia, as defined by requiring a second gel, in a fully adjusted model. Specifically, in infants with a pregel blood glucose of 2.00–2.17 mmol/L (36–39 mg/dL), formula feeding with gel was associated with a lower odds of recurrent hypoglycaemia.ConclusionsDextrose gel is an effective tool in the treatment of NH. An infant’s pregel blood glucose concentration may be helpful in guiding decisions around type of feeding provided.


2014 ◽  
Vol 307 (4) ◽  
pp. H587-H597 ◽  
Author(s):  
Mark W. Sims ◽  
James Winter ◽  
Sean Brennan ◽  
Robert I. Norman ◽  
G. André Ng ◽  
...  

While it is well established that mortality risk after myocardial infarction (MI) increases in proportion to blood glucose concentration at the time of admission, it is unclear whether there is a direct, causal relationship. We investigated potential mechanisms by which increased blood glucose may exert cardiotoxicity. Using a Wistar rat or guinea-pig isolated cardiomyocyte model, we investigated the effects on cardiomyocyte function and electrical stability of alterations in extracellular glucose concentration. Contractile function studies using electric field stimulation (EFS), patch-clamp recording, and Ca2+ imaging were used to determine the effects of increased extracellular glucose concentration on cardiomyocyte function. Increasing glucose from 5 to 20 mM caused prolongation of the action potential and increased both basal Ca2+ and variability of the Ca2+ transient amplitude. Elevated extracellular glucose concentration also attenuated the protection afforded by ischemic preconditioning (IPC), as assessed using a simulated ischemia and reperfusion model. Inhibition of PKCα and β, using Gö6976 or specific inhibitor peptides, attenuated the detrimental effects of glucose and restored the cardioprotected phenotype to IPC cells. Increased glucose concentration did not attenuate the cardioprotective role of PKCε, but rather activation of PKCα and β masked its beneficial effect. Elevated extracellular glucose concentration exerts acute cardiotoxicity mediated via PKCα and β. Inhibition of these PKC isoenzymes abolishes the cardiotoxic effects and restores IPC-mediated cardioprotection. These data support a direct link between hyperglycemia and adverse outcome after MI. Cardiac-specific PKCα and β inhibition may be of clinical benefit in this setting.


2014 ◽  
Vol 19 (3) ◽  
pp. 527-533 ◽  
Author(s):  
Miho Senda ◽  
Susumu Ogawa ◽  
Kazuhiro Nako ◽  
Masashi Okamura ◽  
Takuya Sakamoto ◽  
...  

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