Hypoglycemia insulin-induced

Griffond B., Risold P Jacquemard C., Colard C., Fellmann D. (1999). Insulin-induced hypoglycemia increases preprohypocretin (orexin) nrRNA in the rat lateral hypothalamic area. Neurosci Lett. 262(2), 77-80. 

Horinaka, N., Kuang, T. Y., Pak, H. etal. Blockade of cerebral blood flow response to insulin-induced hypoglycemia by caffeine and glibenclamide in conscious rats. /. Cereb. Blood Flow Metab. 17 1309-1318,1997. 

Hypoglycemia Pramlintide alone does not cause hypoglycemia. However, pramlintide is indicated to be coadministered with insulin therapy, and, in this setting, pramlintide increases the risk of insulin-induced severe hypoglycemia, particularly in patients with type 1 diabetes. Severe hypoglycemia associated with pramlintide occurs within the first 3 hours following a pramlintide injection. 

Glucagon Insulin-induced hypoglycemia, beta-blockers... 

Diabetes/Hypoglycemia -adrenergic blockade may blunt premonitory signs and symptoms (eg, tachycardia, blood pressure changes) of acute hypoglycemia. Nonselective -blockers may potentiate insulin-induced hypoglycemia. 

Esmolol administration maypotentiate insulin-induced hypoglycemia in diabetic patients. 

Reversal of insulin-induced hypoglycemia by admistration of subcutaneous glucagon. 

Hypoglycemia may be divided into three groups 1) insulin-induced ... 

Three major types of hypoglycemia Hypoglycemia may be divided into three groups 1) insulin-induced, 2) postprandial (sometimes called reactive hypoglycemia), and 3) fasting hypoglycemia. 

Similar to the effect on restraint stress, RmHA (10 mg/kg x 2 ip) inhibited the ACTH and P-END response to insulin-induced hypoglycemia, which increases neuronal HA turnover [30-31]. This inhibitory effect was completely or partly reversed by THIOP. Likewise, the responses of the POMC-derived peptides and corticosterone to immune stimulation with the E.coli lipopolysaccharide (LPS) endotoxin, which augmented neuronal HA turnover, were reduced by RmHA pretreatment [39]. The effect of RmHA was equal to that of HA synthesis inhibition by a-FMH [39]. In lactating female rats suckling-induced ACTH secretion was reduced by pretreatment with RmHA (Fig. 6) as well as by a-FMH [32],... 

Figure 1. Effect of the H3 receptor agonists R(a)methylHA (RHA 10 mg/kg), BP 2-94 (BP 25 mg/kg) or imetit (Imt 2 mg/kg) administered ip at -180 and -60 minutes in combination with saline (Sa) or the H3 receptor antagonist thioperamide (Th 5 mg/kg ip at -180 min) on the ACTH response to restraint stress (5 minutes), insulin-induced hypoglycemia (3 IU/kg ip -45 minutes) or LPS endotoxin (10 pg/kg ip at -120 minutes). The rats were decapitated at 0 minutes. p<0.01 vs. saline control or p<0.05 or p<0.01 vs. stimulus alone and H or nn p<0.05 or p<0.01 vs. stimulus and H3 receptor agonist.

Figure 2. Effect of the H3 receptor agonists R(a)methylHA (RHA) or BP 2-94 (BP) administered in combination with saline (Sa) or the H3 receptor antagonist thioperamide (Th) on the P-END response to restraint stress or insulin-induced hypoglycemia. Further informations are given in legend to figure 1.

Pohl J, Frohnau G, Kerner W, Fehm-Wolfsdorf G. Symptom awareness is affected by the subjects expectations during insulin-induced hypoglycemia. Diabetes Care 1997 20(5) 796-802. 

Galloway PJ, Thomson GA, Fisher BM, Semple CG. Insulin-induced hypoglycemia induces a rise in C-reactive protein. Diabetes Care 2000 23(6) 861-2. 

In human subjects, deltorphin inhibits the secretion of growth hormone and ACTH induced by insulin-induced hypoglycemia and modulates the secretion of pituitary luteinizing hormone in women [88-91]. 

Raable, W.A. (1981). Ammonia and disinhibition in cat motor cortex by ammonium acetate, monofluoroacetate and insulin-induced hypoglycemia. Brain Res. 210 311-22. 

Engler D, Pham T, Fullerton MJ, Ooi G, Funder JW, Clarke IJ (1989) Studies of the secretion of corticotropin-releasing factor and arginine vasopressin into the hypophysial-portal circulation of the conscious sheep. I. Effect of an audiovisual stimulus and insulin-induced hypoglycemia. Neuroendocrinology 49 367-381. 

Bolli, C-, DeFeo, P, I eirielJo, C Cosmo, S. D., Compagnucci, P, Santeusanio, F Brunetti, P, and Unget R. H. (1984). Mechanisms of glucagon secretion during insulin-induced hypoglycemia in man, J, CHu. invest. 73,917-922. 

BOX Sb-3 Protocol for the Insulin-Induced Hypoglycemia Stimulation T t -(Insulin Tolerance Test)... 

Rationale The stress of insulin-induced hypoglycemia triggers the release of GH and ACTH from the pituitary gland in normal subjects. GH response is measured directly cortisol is measured as the indication of ACTH response. 

Measurement of ACTH in blood collected either at baseline or after stimulation with insulin adds httle to the utility of the above tests and is not generally recommended. In fact, in patients who have undergone pituitary surgery, it takes some time before the cortisol negative feedback loop to ACTH secretion is normalized. ACTH and cortisol measurements after administration of CRH are potentially a direct test of pituitary ACTH reserve. However, the insulin-induced hypoglycemia test is currently the definitive test of ACTH and/or cortisol reserve. Tliis test, however, is contraindicated in patients with a history of coronary heart disease, seizure disorder, and general debility. 

Watabe T, Tanaka K, Kumagae M, Itoh S, Takeda F, Morio K, et al. Hormonal responses to insulin-induced hypoglycemia m man.) Clin Endocrinol Metab 1987 65 1187-91. 

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