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Whether bad doc’s are working on new drugs is controversial, about a few thousand pages of medical journal articles are already written on the consequences of when the drugs go bad.Atypical antipsychotics are clearly a group of drugs that fit that latter category, since hyperglycemia and diabetes along with cardiovascular complications are a part of their unwanted side effects.And thus, I thought I would pass on some information, medical journal findings that is, that hopefully could be helpful in furthering favorable research for treating AAP induced hyperglycemia.
The Proceedings of the National Academy of Sciences (PNAS) in February 2007, conveyed research from Johns Hopkins, Solomon Snyder being the researcher, that AAP blockading of the Histamine receptor 1 most likely will account for the metabolic dysreguation features encountered in AAP induced conditions.In December
2006,Toronto Sick Children’s Hospital, cured diabetes 1 and diabetes 2 in mice, by injecting the compound capsaicin in pancreatic islet nerves, targeting specifically the TRPV1 Neuron.
Researchers across the country believe the favorable outcome from the Toronto trials will eventually translate into a sweeping diabetes cure, or near cure effective treatment, with the capsaicin treatments. In regards to AAP H 1 receptor blockading, (PIP)2 pathway is activated via the PLC entity, by normal H 1 activity. Since H 1 recptor activity is blockaded, and reduced substantially by AAP’s, the issue that the PLC and (PIP)2 area could be adversely affected is real. (PIP)2 and PLC play a role in glucose transport. GLucose transport diminishment is a well known recognizable initial adverse occurence for hyperglycemia and later diabetes development. And glucose transport inhibition has been well accounted for in AAP induced conditions, at least in rats, (Vestri, June 28, 2006, journal Neuropsychopharmacology, University Alabama Birmingham study.). H 1 receptor blockading thus could create glucose transport diminishment by adversely affecting the (PIP)2 and PLC pathway, as well as adversely affecting both the entities themselves. The following article entitled: “A Modular (PIP)2 Binding Site as a Determinant of Capsaicin Receptor Sensitivity” Elizabeth D. Prescott and David Julius, authors, wrote the initial abstract sentence quote: “The capsiacin receptor (TRPV1), a heat activated ion channel of the pain pathway, is sensitized by phosphatidylinositol 4-5 biphosphate (PIP)2 hydrolysis after phospholipase C activation. It is fascinating that (TRPV1) receptor, the capsaicin one at that, and also this being the same receptor the Toronto study successfully centered on to cure diabetes in mice, has to be properly sensitized by PLC and (PIP)2, once normal PLC activation occurs. In AAP cases, H 1 blockading could adversely affect such PLC activation normalcy in function, resulting in (PIP)2 hydrolysis dysfunction. This fact could lead to an insufficent senstization of TRPV 1 receptor and could play a potential substantial role in the few cases of diabetes 1 development in AAP induced conditions. And also in enhancing diabetes II insulin resistance.Toronto researcher’s successful treating of TRPV1 in their study mentioned above ( a study found in its scientific form in the Journal ‘Cell” December 16 2006) eradicated insulin resistance in diabetic mice. Since AAP H1 receptor blockading, resulting potentially in fairly low histamine metabolism functions, could affect the glucose transport function, diminishing it and further, if hydrolysis is either increased or decreased for (PIP)2, (PIP)2 metabolism in turn is adversely affected. Hence hyperglycemia could develop along with eventual insulin resistance development from all of these deleterious alterations.Oliver D. Howes Study, entitled something as- “A Prospective Study on impairment of Glucose Control with Olanzapine without insulin resistance changes” found heightened insulin resistance in the upper quintile of the healthy insulin sensitivity range for people that developed glucose dysregulation via olanzapine use. Highly importantly concerning this previous fact, the heightened insulin resistance as such depicted by Howes, is indicative of a mitochondrial energy deficit potentially. The author Richard Fiddian Green wrote in a study “Schizophrenia, and adverse effects of its treatments on mitochondrial metabolism” noted mitochondrial energy deficits that could account for neuropsychiatric disorder’s essence.ATP hydrolysis ‘increased activity’ R.F. Green noted was a component of such mitochondrial energy deficits. And likewise (PIP)2 hydrolysis dysfunction could already be adversely affected by the natural energy deficit ATP hydrolysis abnormal activity that exists in pre drug activation. Adding a H 1 receptor blcokading AAP agent could further aggravate this (PIP)2 hydrolysis situation. In any case, a lot more can be said along these lines, too much to go into here. But all in all, PLC and (PIP)2 interactive activity is a region to look into more closely in AAP H 1 receptor blockading situations, since the H 1 receptor is well documented to be biologically interactive with PLC and (PIP)2 cellular entities.