| Name |
Views and Comments | Date |
| Harry Horton |
As of May 2007, gastric bypass surgery is being considered as potential cure for diabetes II patients with normal body weight composition. That is, non obese and a normal weight with these individuals. In the past two months if not longer, the surgery has been performed in Italy, possibly if I have my facts right on that. I could be wrong though. But reachievement of normal glucose levels and evidently good insulin sensitivity has occured with gastric bypass surgery for diabetics of the type II.
Other news related to diabetic conditions that I have, is a team of Canadian, French and British scientists supposedly have discovered 70% of the underlying genes that give rise to diabetes. Montreal Canada was where these discoveries were reported from and the google " Diabetes News " web site carries several media reports on the discovery in their February 2007 archives. Zinc transporter functions, that is the genes that encode the body's zinc transport functions, was one particular area that was determined to go awry and dysfunctional in the onsetting diabetic condition. Even more interestingly, the journal "daibetes" April 2007 edition carried an article where the following finding was made: Zinc, not insulin is responsible for the islet switching mechanism in the pancreas for glucagon secretion in rats experiencing imminent development of hypoglycemia. The zinc thus switches the mechanism to the alpha islets that are responsible for glucagon secretion. and as result bringing up the glucose levels from dangerously low points. Personally, I wonder if zinc could be responsible for overall general glucagon secretion and as such this fact could play an important role in developing fasting hyperglycemia found in diabetic patients and hyperglycemia cases of other disease types. That is when such glucagon secretory processes go dysfunctional for some reason or the other. Previously, insulin was believed to be the major biochemical entity for conducting the switch to glucagon secretion in impending hypoglycemic states. So this article from "journal" Diabetes, is a novel discovery. For diabetics that suffer hypoglycemic conditions from atypical antipsychotic usage, diabetes de novo included in that category of people, in February 2007, the Proceedings of the National Academy of Sciences reported the blocking of the histamine receptor 1 plays a major role in the development of weight gain in atypical antipsychotic (AAP) treated individuals. AMPK activity was found to be quadrupled in mice hypothalamic areas via AAP blockading of the histamine receptor 1. Thus glucose homeostasis and insulin sensitivity could be adversely affected by abnormal AMPK activity since AMPK is the master metabolic switch for many metabolic functions in the body. This fact though has not been medically confirmed. What this PNAS discovery could mean is that its findings can be combined with the zinc transporter findings from Cananda. Zinc transporter metabolism is substantially comprised of histidine amino acids, and histidine amino acids are the precursor for histamine and the histamine metabolism. For example their is a function known as zinc fingers. Two cysteine amino acids and two histidine amino acids form as a structural biochemical entitiy that acts like a catcher's mit to catch zinc atoms passing through the body. And such action comprises an important biological process in the body. If the AAP's lower histamine levels by blockading the H1 receptor over lengthy periods of time, the histamine compolex could be adversely affected. Lowering of histamine could occur and the adverse effects could extend back further to histidine amino acids not getting adequately expressed. This action could potentially leave a deficit of histidine amino acids in the internal body's anatomical and physiologicalol strucutres. And if that is the case, zinc transporter functions could be ill developed and thus dysfunctional. Sustained lowered histamine levels resulting from AAP blockading of the H1 receptor could result in lowered histidine amino acids and thus faulty zinc transporter functions and possibly ill developed zinc fingers functions. If the zinc transporter system occurs, fasting hyperglycemia could develop in AAP users. It is well documented a central glucose disorder in AAP users is fasting hyperglycemia. Dysfunctional glucagon secretion plays a role in fasting hyperglycemia. And this fact brings us back to the first area of facts of this report concerning zinc as the switching mechanism to glucagon secretion with rat hypoglycemia. Zinc plays thus a major role in determining potentially whether fasting hyperlgycemia develops or not. Could this be true? This is a fact that could be true but needs to be validated scientifically, if zinc did play such a role. Perhaps zinc does not. But zinc in this context is a major issue for AAP hyperglycemic conditions to be clarified, potentially, in the months and years ahead, if zinc has anything to do with fasting hyperglycemia in AAP diabetic cases. Or fasting hyperglycemia in other cases of diabetes for that matter. Trying to get these high glucose levels down is imperative for individuals who suffered adversely from the effects of the AAP's. Since complications can develop from their elevated status of glucose amounts in the blood stream. And thus the AAP users who develop hyperglycemic condtions and de novo diabetes thus become, sadly enough ,another candidate group for future gastric bypass surgery, whether obese or not. |
5/5/2007 |
| Pat |
How do you find a surgeon in your area? |
8/20/2006 |
| Dinsh Baker |
Hello I am a 29yr. old disabled woman. I suffer with being overweight due to some of the medication that I had to take due to an MVA that I was in. I so desperately want to have gastric surgery. The weight gains affects my physiclolgical well being as well as my personal and environmental life. I have gone to therapy to talk to someone because of my depressive state. I just want to be able to go out and not feel ashamed of myself. I have high blood pressure and I know that after my car wreck alot of complications have come about but this weight is the biggest burden on me yet. I have low-self esteem and I'm always at home. I don't attend activites with my family or friends. I have no social life because of it and I feel that if I don't like myself why should I expect other people to like me as well. I'm reaching out for your help and support to help me in getting a doctor in the Memphis TN. area to perform the surgery on me. I have insurances. |
4/30/2006 | |
