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Thursday, 12 June 2008

HYPOglucose-induced autonomic failure in IDDM is specific for stimulus of HYPOglycemia and is not attributable to prior autonomic activation ... HOW ?


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Diabetes. 1994 Jun;43(6):809-18.

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NeuroGlycoPenia - induced autonomic failure in IDDM is specific for stimulus of HYPOglycemia and is not attributable to prior autonomic activation.

Rattarasarn C, Dagogo-Jack S, Zachwieja JJ, Cryer PE.

Division of Endocrinology, Diabetes, and Metabolism, Washington University School of Medicine, St. Louis, Missouri 63110.

It has been HYPOthesized, first, that recent antecedent HYPOglycemia causes reduced autonomic responses to subsequent HYPOglycemia in patients with well-controlled insulin-dependent diabetes mellitus (IDDM) and that the reduced responses are specific for the stimulus of hypoglycemia while the responses to other stimuli are unaltered and, second, that reduced autonomic responses, specifically sympathochromaffin, so-induced are not simply the result of prior activation of the system.

To test the first HYPO-thesis, eight patients with IDDM, selected for HbA1c levels. HYPO-glucose-associated autonomic failure can be induced in patients with well-controlled IDDM and is specific for the stimulus of HYPOglycemia and, second, that this is not simply the result of prior activation of the system.


Related Articles ...

HYPOglycemia-associated autonomic failure in insulin-dependent diabetes mellitus. Recent antecedent HYPOglycemia reduces autonomic responses to, symptoms of, and defense against subsequent HYPOglycemia. [J Clin Invest. 1993]

Exaggerated epinephrine response to HYPOglucose in a physically fit, well-controlled IDDM subject. [Diabetes Res Clin Pract. 1994]

Mechanism of awareness of hypoglycemia. Perception of neurogenic (predominantly cholinergic) rather than neuroglycopenic symptoms. [Diabetes. 1993]

Contribution of autonomic neuropathy to reduced plasma adrenaline responses to hypoglycemia in IDDM: evidence for a nonselective defect. [Diabetes. 1997]

Reversal of hypoglycemia unawareness, but not defective glucose counterregulation, in IDDM. [Diabetes. 1994]


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Jacobson L, Ansari T, Potts J, McGuinness OP.
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4:
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Davis SN, Shavers C, Davis B, Costa F.
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6:
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Havel PJ, Akpan JO, Curry DL, Stern JS, Gingerich RL, Ahren B.
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8:
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Katsura M.
[Mechanism of the blunted glucagon response to insulin-induced HYPOglucose in Diabetics]
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Koyama Y, Galassetti P, Coker RH, Pencek RR, Lacy DB, Davis SN, Wasserman DH.
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PMID: 11934679 [PubMed]

10:
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Horm Metab Res. 1979 Oct;11(10):561-6.

Effect of thyroxine treatment on metabolic responses to a single insulin injection.
Kaciuba-Uścilko H, Brzezińska Z.

Metabolic responses to a single i.v. injection of cristalline insulin (0.2 i.u./kg b.w.) were compared in control and T4-treated dogs both at rest and after prolonged physical exercise. The post-insulin decrease in blood glucose was significantly correlated with the pre-insulin BG concentration. Thus, the insulin-induced fall of BG was greatest in T4-treated dogs at rest, in which significantly higher BG levels were found in comparison with controls, and smallest in the same dogs after exercise, i.e. at the lowest initial BG concentrations. The post-insulin hypoglycaemia caused marked increases in the plasma FFA level in control dogs, both at rest and after physical effort, and in T4-treated dogs at rest. They were accompanied by elevations in the plasma adrenaline levels. In T4-treated dogs given insulin after exercise decreases both in the plasma FFA and A concentrations were found. In the majority of the control and T4-treated dogs insulin injected at rest caused an increase in blood LA levels, being more pronounced in the latter. Insulin injected after physical exercise did not change blood LA level in T4 treated dogs, and it caused its decrease in the control animals. The results of these investigations show that both T4-treatment and physical exercise, performed prior to insulin injection, modify the metabolic response to insulin and post-insulin HYPOglucose.

Links
PMID: 11934679 [PubMed]


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Glucagon (GlucaGen Diagnostic Kit®) Glucagon is a hormone produced in the pancreas. Glucagon is used to raise very low blood sugar. Glucagon is also used in diagnostic testing of the stomach and other digestive organs.

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