La diabetes es un desorden metabolico producto de los malos habitos alimenticios, que con el tiempo van intoxicando los organos del cuerpo a tal grado que sus funciones (como la eliminacion de toxinas, la produccion de enzimas, asi como la de insulina para la asimilacion de la glucosa) se van deteriorando.
El Pancreas porduce insulina, pero tambien porduce enzimas para digerir los alimentos, Estas encimas incluyen LIPASA, AMILASA, PTROTEASA, TRYPTASA y muchas otras mas.
Las toxinas mas comunes que se acumulan en el higado, son residuos de medicamentos, metales pesados (tales como aluminio, mercurio, plomo, etc) residuos de pesticidas, quimicos de productos caseros e industriales (tintes, perfumes, shampoos, detergentes, aditivos y saborizantes artificiales) asi como residuos hormonales producto del consumo de carnes rojas y blancas. Muchas personas han comprobado una gran mejoria en los niveles de glucosa en la sangre al cosumir pasto de trigo. En La Huerta del Sol estan pormoviendo una serie de talleres impartidos por la Nutriologa Isabelle Gagnon, en los que se revisan a detalle los beneficios del Pasto de Trigo y una dieta verde para revertir la Diabetes. Es muy importante, pero necesito saber cual es el valor de la Juguera manual marca Lexen, si es en moneda mexicana cual es el valor en dolares, porque soy diabetico y necesito combatirla, espero pronta respuesta, por su atencion gracias.
Jose Lima me dijo, hace bastante tiempo, que chequeara la pagina que dice EXTRACTORES, que los precios estan nen pesos mexicanos, ya que preguntaba a cuanto se traduce en dolares, para comprarlo y hasta esta fecha 22 de diciembre no he podido comprar la Juguera Manual marca Lexen, yo vivo en El Salvador, cuanto me costara por todo con el envio hacia El mSalvador, espero respuesta inmediata, por su atenion gracias. In what could be the biggest breakthrough in years toward a cure for type 1 diabetes, researchers at Harvard University say they have developed a way of transforming stem cells to help diabetics produce their own insulin. The researchers say the stem cells can create hundreds of millions of beta cells, which produce insulin.
While in 15 years of testing the group has been able to develop insulin-producing cells from cadavers, they weren’t able to generate the quantity needed. Melton had a personal interest in the project because both of his children were diagnosed with the disease as youngsters.
The next steps include moving to clinical trials in humans, possibly in as few as three years. Science, Technology and Medicine open access publisher.Publish, read and share novel research.
Targeting AMPK for Therapeutic Intervention in Type 2 DiabetesMohamed Kodiha1 and Ursula Stochaj1[1] McGill University, Canada1.
For patients eating substantial amounts of food, you can use that calculated amount as the total daily dose.
Approximately 40-50% of the total daily insulin dose is to replace insulin overnight, when you are fasting and between meals. This is called background or basal insulin replacement. The other 50-60% of the total daily insulin dose is for carbohydrate coverage (food) and high blood sugar correction. The bolus dose for food coverage is prescribed as an insulin to carbohydrate ratio.The insulin to carbohydrate ratio represents how many grams of carbohydrate are covered or disposed of by 1 unit of insulin. The bolus dose for high blood sugar correction is defined as how much one unit of rapid-acting insulin will drop the blood sugar. Read some examples and therapeutic principles on how to calculate the carbohydrate coverage dose, high blood sugar correction dose and the total mealtime insulin dose. CHO insulin dose =     Total grams of CHO in the meal ? grams of CHO disposed by 1 unit of insulin (the grams of CHO disposed of by 1 unit of insulin is the bottom number or denominator of the Insulin:CHO ratio). High blood sugar correction dose =      Difference between actual blood sugar and target blood sugar*? correction factor. This example above assumes that you have a constant response to insulin throughout the day.
Please keep in mind, the estimated insulin regimen is an initial “best guess” and the dose may need to be modified to keep your blood sugar on target.
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One can develop a diabetic neuropathic condition where the person becomes unaware of the feelings in his legs and feet.
As a normal person would have become aware of the bruises or cuts on the legs, a diabetic person cannot sense the same. The condition of gangrene is a serious one, primarily marked by loss of adequate supply of blood to the tissues of the body, ultimately resulting in its necrosis or death.
Injury to the tissues, infection (mostly of bacterial origin) and presence of any underlying health ailment that inflicts damage to the blood carrying vessel structure form the three key underlying mechanisms that are responsible for initiation and development of irreversible tissue damage and life threatening condition of gangrene. As already explained, one of the causes of gangrene in the toes and fingers is linked with damaged blood vessels. High level of blood glucose associated with diabetes mellitus also damages the nerves (known as peripheral neuropathy), especially the nerves in the lower extremities. The dullness or lack of sensation puts diabetic individuals at an increased risk of injuring the skin of their fingers or feet without having any realization (it mostly goes unnoticed in the feet region). The sore or foot ulcer formed takes an extended time to heal because of both, poor circulation of blood through the injured area as well as lesser number of defence cells.
Bacterial infection also forms another causative factor that makes the diabetic individual more prone to developing gangrene.
Such type of infection is marked by noticeable skin discolouration and dryness along with the formation of skin blisters. The weakened immune system (seen in diabetes) further raises the risk of incurring serious infection, which later develops, into gangrene. Insulin is a 51 amino acid protein and needs to be injected into the body rather than taken orally to avoid being broken down in the digestive system.
Early insulin treatments used the hormone isolated from cow (bovine) and pig (porcine) pancreas. Modern insulin is now obtained from bacteria that have been genetically modified to produce human insulin.
Injecting insulin on a regular basis can cause problems and researchers are constantly working to develop better ways to take insulin. Skin patches are being developed that allow the insulin to be directly absorbed into the body and implants under the skin may also be a treatment of the future.
Small pumps which inject insulin under the skin in a controlled way throughout the day are now available. Inhaled insulin-powders have been developed to enable the hormone to be absorbed directly into the blood from the nose and mouth mucosa.
Transplants of the pancreas and islet cells from donors are becoming more common treatments. In the future it may be possible to grow large numbers of beta cells from stem cells in the laboratory. Lifestyle changes play a key role in the management of type 2 diabetes, and initial steps include regular physical activity, a balanced diet and loss of any excess weight.
Acarbose Inhibits the enzyme that breaks down polysaccharides in the diet and so slows the absorption of glucose in the small intestine to prevent the glucose peak after a meal.
Type 1 diabetes is characterised by the lack of insulin production, so insulin injections will be used to replace this lost insulin.
Type 2 diabetes - balanced diet and change in lifestyle to reduce body fat may be sufficient treatment to control the condition. Type 2 diabetes - insulin production may continue, so medicines to sensitise cells to insulin may be taken. Large molecule consisting of a carboxylic acid (RCOOH) with the 'R' being a long unbranched hydrocarbon chain.


Protein molecules attached to cells that only bind to specific molecules with a particular structure. En enfermos de Diabetes ll, el higado y el pancreas se encuentran saturados de toxinas y sus funciones estan vitales estan comprometidas. Mientras mas comidas procesadas comen los diabeticos, mas enzimas tiene que producir el pancreas, con la consecuente sobrecarga a un organo ya de por si debilitado.
Esto se debe a la enorme cantidad de enzimas, aminoacidos, vitaminas, minerales y nutrientes faciles de asimilar, ademas, como contiene el 80% de clorofila, limpia y desintoxica el cuerpo entero. When the cells are transferred to diabetic mice, they behaved as healthy cells do and regulated blood sugar. Organization of AMPK and regulation of kinase activity by phosphorylation.AMPK is a heterotrimeric enzyme that is activated by phosphorylation on Thr172 of the ? subunit. AMPK? concentrates in nuclei when cells are exposed to oxidative stress or depleted for energy. IntroductionThis chapter begins with general information on the role of 5’-AMP activated kinase (AMPK) in human physiology and the molecular mechanisms that control this kinase. Between 40% and 50% of that total dose should be administered as basal, with the rest dosed out in nutritional boluses. You should give 50% of that total dose as basal insulin about four hours before patients’ IV insulin is turned off.
This range can vary from 4-30 grams or more of carbohydrate depending on an individual’s sensitivity to insulin.
Bear in mind, this may be too much insulin if you are newly diagnosed or still making a lot of insulin on your own. You will need to work out your specific insulin requirements and dose regimen with your medical provider and diabetes team. You can get them over the counter and are specially designed for people suffering from diabetes.
As you do not get any sensation of the hurt, it is possible that there could be redness or pain. Death of cell and tissue may target any part of the body, however, it has been typically observed in the extremities, such as the toes, fingers and hands.
In both, type 1 and type 2 diabetes, the raised level of sugar is capable of causing damage to the blood vessels and reducing blood supply. Owing to the nerve damage, the transmission of sensation, particularly those of pain to the brain gets impaired. A notorious bacterial organism, Clostridium perfringes is often linked with gas gangrene; after it attacks the site of injury or sometimes, surgical wound.
This needed a great deal of purification to isolate the insulin and even then, there were contaminants.
The amino acid sequence of porcine insulin is different to human insulin by one amino acid. By further manipulating the insulin, it has been possible to develop a range of medications that have different properties. People with diabetes, particularly if they have associated kidney disease that requires a kidney transplant, may be given a whole pancreas from a donor. This would be a much more readily available supply of insulin-producing beta cells which can then be used for islet cell embolisation.
For a large proportion of people with type 2 diabetes changes to their lifestyle will reduce their blood glucose levels sufficiently. Type 1 diabetics monitor glucose levels throughout the day; blood glucose levels in type 2 diabetics are monitored during clinic appointments.
Other medications reduce the production of glucose by the liver and reduce cardiovascular damage.
There are twenty amino acids used, in different combinations, to make every protein required by the human body. It is active in controlling blood glucose levels as it allows cells in the body to take in and store glucose.
In certain areas, such as the nose and mouth, this membrane absorbs substances and secretes mucus. The amino acids present and the order in which they occur vary from one protein to another.
Un beneficio casi inmediato al consumir Pasto de Trigo, es el aumento de globulos rojos en la sangre, con el consecuente incremento de oxigeno disponible a nivel celular. AMPK controls the physiology of multiple organs which are critical to type 2 diabetes, obesity and other metabolic diseases. HeLa cells were treated with diethyl maleate to induce oxidative stress or with a combination of sodium azide and 2-deoxyglucose for energy depletion.
The possible changes induced by the compartment-specific alteration of AMPK activity are depicted. We discuss the functions of AMPK in different tissues and their relationship to type 2 diabetes. Once patients start eating, add the rest in bolus amounts.You should also take into account how well the patient’s glucose was controlled in the ICU on the preceding day.
Insulin sensitivity can vary according to the time of day, from person to person, and is affected by physical activity and stress. Someone who is resistant in the morning, but sensitive at mid-day, will need to adjust the insulin-to-carbohydrate ratio at different meal times.
With a professional advice behind you, you may most probably need to make your next visit to the podiatrist.
This means, the footwear you use should be wide enough so that the tips of the toe do have enough space to move in its vicinity. A podiatrist can make such footwear available that are specially designed for the diabetics. In the absence of a continuous supply of nutrient and oxygen rich blood, the cells within the body begin to fail in carrying out their normal function and finally give up.
As a result of restricted blood circulation to the extremities, such as the feet, the area becomes deprived of those cells (white blood cells) which aid in fighting off any infection.
For example, adding zinc causes the insulin molecules to form hexamers (six insulin molecules loosely attached to each other). As such, AMPK regulates both anabolic and catabolic pathways as well as the function and biogenesis of organelles. Some of the tissue-specific reactions regulated by AMPK and relevant to type 2 diabetes are listed. AMPK substrates in different subcellular organelles and compartments are described, and we speculate how the localized action of AMPK could help to control type 2 diabetes. For patients with poor control, consider factoring in another 10% to your total daily dose. Talk to your provider about the best insulin dose for you as this is a general formula and may not meet your individual needs.


Swelling and inflammation resulting from the infection causes the local temperature of the area involved to be slightly elevated, and also leads to pain. This form of insulin is absorbed into the body more slowly than regular insulin, thus reducing the need for more frequent insulin injections. These donor cells are isolated from the several donors and then injected into the hepatic vein. How does the compartment-specific action of AMPK impact cellular functions that are relevant to type 2 diabetes?
As a result of these contributions, AMPK is vital to the function of several organs and tissues in metazoans (Fig.
It should be noted that although in most cases a correlation between treatment and changes in AMPK activity has been demonstrated, the molecular mechanisms are not always fully understood. In particular, the low activation state of AMPK could contribute to the increase in type 2 diabetes and obesity (Hardie et al., 2006). For some of the treatments, it has yet to be established whether AMPK is essential for the downstream physiological effect.
Moreover, as essential regulator of glucose homeostasis and lipid metabolism, AMPK has become an important therapeutic target in type 2 diabetes and obesity. More recent experiments with knockout cells and animal models will help to fill these gaps (Viollet et al., 2009a).
Organization and activation of AMPKAMPK senses a drop in cellular energy as it is induced by a reduction in glucose availability or other metabolic stresses. As a result of AMPK activation, the cellular metabolism switches from anabolic to catabolic processes. This metabolic shift is accomplished by the AMPK-dependent phosphorylation of multiple targets which are located in different cellular organelles and compartments (see below).The heterotrimeric enzyme AMPK (Fig. The regulatory ? and ? subunits are encoded by two and three genes, respectively (Hardie et al., 2006). The ? subunits (?1, ?2, ?3) bind AMP and ATP in a mutually exclusive fashion, this AMP binding is important to the activation of the enzyme. Control of AMPK activity by phosphorylation and changes in AMPK concentrationThe importance of AMPK as a key regulator in cellular metabolism requires a tight control of the enzyme. Under these conditions, AMP binding to the regulatory ? subunit promotes the subsequent Thr172 phosphorylation.
By contrast, a relative small change is observed for the ?3 subunit which is mostly synthesized in glycolytic skeletal muscle. It was proposed that ? subunit myristoylation provides a switch that is a prerequisite for Thr172 phosphorylation (Oakhill et al., 2010). This modification is mediated by CaMKK? and particularly important in tissues where LKB1 is not the predominant kinase for Thr172. The tissue-specific regulation of AMPK activity is likely achieved by the combined effects of upstream activating kinases, inactivating phosphatases as well as the synthesis and degradation of AMPK subunits. For example, LKB1 is particularly important to activate AMPK in skeletal muscle, whereas CaMKK? is crucial in the brain (Ronnett et al., 2009).
Indeed, in a clinical setting AMPK activity is altered with the anti-diabetic drug metformin and other biguanides. Phenphormin promotes the LKB1-dependent activation of AMPK by inhibiting mitochondrial complex I (Hawley et al., 2010). AICAR generates the AMP mimetic 5-amino-4-imidazolecarboxamide ribotide (ZMP) and causes a drop in cellular ATP and ADP, which leads to AMPK activation (Hawley et al., 2010). Aside from drugs that activate AMPK, compound C serves as an ATP-competitive inhibitor of AMPK that has been used widely. All of the compounds discussed here are established pharmacological tools that alter AMPK activation or enzymatic activity; they have been useful for the analysis of AMPK in vitro, in growing cells and in whole animals. Of particular importance at the cellular, organ and organismal level is the ability of AMPK to switch from anabolic to catabolic processes when energy supplies are low.
AMPK regulates metabolism and other aspects of cell physiology both under normal and disease conditions; studies with different cells or tissues emphasize the significance of AMPK for cellular metabolism and the response to various forms of stress. Notably, this signaling in the central nervous system contributes to the regulation of food uptake. Research with hepatic, skeletal muscle, adipose, pancreatic and kidney cells is particularly important to our understanding of type 2 diabetes as these cell types are crucial to the etiology or pathophysiology of the disease (Fig.
Whereas the phosphorylation of key enzymes produces a fast downregulation of ATP-consuming metabolic pathways, long-term effects involve changes in the expression of target genes that control metabolism. Since several recently published excellent reviews covered these topics extensively, Table 2 only summarizes the impact of AMPK activation on tissues that are critical to type 2 diabetes.
Subcellular distribution of AMPK substratesThe combination and integration of different subcellular events regulated by AMPK enables cells, tissues and organs to coordinate different metabolic pathways in order to achieve and maintain the proper energy balance of the whole organism. 3 depicts established AMPK substrates according to their presence in different subcellular compartments.
Table 3 expands this information and specifies how the AMPK-dependent phosphorylation of individual substrates alters their functions.It is obvious from Fig. 3 that AMPK phosphorylates a large number of proteins that are associated with distinct organelles or subcellular compartments.
Cytoplasmic and mitochondrial substrates of the kinase include enzymes that are involved in fat, protein, glucose and glycogen metabolism.
Kinase targets in the plasma membrane consist of ion channels, carriers and receptors, whereas other substrates are linked to the function or trafficking of intracellular membranes. This includes the transport of vesicles containing the glucose transporter GLUT4, because GLUT4 translocation to the plasma membrane is a pre-requisite for efficient glucose uptake in skeletal muscle and other tissues. In the nucleus, the AMPK-mediated modification of transcription factors, transcriptional regulators and a subunit of RNA-polymerase I control the expression of genes that are implicated in specific anabolic and catabolic reactions. The phosphorylation of several of these targets is also critical to the biogenesis of mitochondria and the assembly of ribosomes.
See text and Table 3 for details.Given the diverse types of AMPK substrates and their presence in different cellular locations, it is helpful to recapitulate their functions (Table 3a). This knowledge is a prerequisite to understand how the dynamic association and action of AMPK in different compartments will impact downstream events.Substrates that have been established for AMPK heterotrimers that contain the ?1 or ?2 subunit are shown. For different AMPK substrates the function, effect of AMPK-dependent phosphorylation and the major subcellular localization are depicted. For some substrates, there are cell-type specific differences, and the effect of AMPK-dependent phosphorylation may not be fully understood or controversial.



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Comments

  1. KOR_ZABIT

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    27.11.2014

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    27.11.2014

  3. Roni_013

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    27.11.2014

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    27.11.2014