Diabetes mellitus type 2 fatty liver wiki,mantra for curing diabetes permanently,articles of january 2015 - Downloads 2016


In the insulin-resistant state, availability of FFA is increased, which raises triglyceride storage and intracellular concentrations of lipid metabolites (DAG, ceramides, LCA-CoA). Insulin is an anabolic hormone (a hormone causing storage and growth) secreted by the ? cells of the islets of Langerhans of the pancreas. As mentioned above, the pathophysiology of diabetes mellitus is lack of insulin and therefore one of the best methods of management of diabetes is to replace insulin. In history until 1980’s insulin was manufactured from pancreas of cattle and pigs called bovine and porcine insulin respectively.
Secondary diabetes mellitus, also known as type 2 diabetes or adult onset diabetes, is a form of disease which leads to high levels of blood glucose by adversely affecting the insulin production in the body. This disease hampers the insulin resistance of the body by weakening the cells and gradually starts to show in the functioning of muscles, liver and tissues.
There are a number of contributing factors related to one’s lifestyle that lead to the onset of type 2 diabetes. Mainly the people from America and other European countries, and also of African, Chinese and Japanese descent are more prone to type 2 diabetes because of the unhealthy lifestyle they lead.
Because of the high intake of fast food items which these people have incorporated as a normal and regular part of their diets, they suffer from this and various other diseases.This diet contains too much of trans fatty acids, artificial flavors,  and saturated fats and thus increase the risk.
Genetic disorders, although constituting a small risk percentage (10%), is another cause of the development of type 1 and type 2 diabetes. In twins, the probability of one twin contracting diabetes is about 90% if the other twin has it; in siblings the same percentage is decreased to 25-30%. Many already existing health conditions can also lead to the development of diabetes in the patients.
Science, Technology and Medicine open access publisher.Publish, read and share novel research. Pro-Inflammatory Cytokines, Lipid Metabolism and Inflammation in Gestational Diabetes Mellitus as Cause of Insulin ResistanceAlexander E.
Arends NJT, Boostra VH, Duivenvoorden HJ, Hofman PL, Cutfield WS, Hokken- Koelega ACS 2005 Reduced insulin sensitivity and the presence of cardiovascular risk factors in short prepubertal children born small for gestational age (SGA). Barker DJ, Martyn CN, Osmond C, Hales CN, Fall CH (1993) Growth in utero and serum cholesterol concentration in adult life.
Bray GA, Jablonski KA, Fujimoto WY, Barrett-Connor E, Haffner S, Hanson RL, Hill JO, Hubbard V, Kriska A, Stamm E, Pi-Sunyer FK (2008). Canadian Diabetes Association (2003) Clinical practice guidelines for the prevention and management of diabetes in Canada.
Cigolini M, Tonoli M, Borgato L, Frigotto L, Manzato F, Zeminian S, Cardinale C, Camin M, Chiaramonte E, DeSandre G, and Lunardi C (1999). Cnop M, Havel PJ, Utzschneider KM, Carr DB, Sinha MK, Boyko EJ, Retzlaff BM, Knopp RH, Brunzell JD, Kahn SE (2003). Diabetic Ketoacidosis - What is Diabetic Ketoacidosis?Diabetic ketoacidosis (DKA) is a potentially life-threatening complication in patients with diabetes mellitus. What is Insulin Resistance?Insulin resistance (IR) is the condition in which normal amounts of insulin are inadequate to produce a normal insulin response from fat, muscle and liver cells. DAG and ceramides induce impairment of the insulin signaling pathway via activation of inflammatory messengers (for example, PKCδ), which leads to inhibitory serine phosphorylation of IRS.
Lack of insulin secretion or its action in the target tissue is the pathophysiology of diabetes mellitus and replacement of insulin as a drug is one of the commonest and standard treatments of diabetes. Being a hexamer secreted in response to glucose or other stimuli like amino acids it has a normal basal level with peaks after each meal. Being an anabolic hormone it increases glucose uptake, particularly in muscle, liver and adipose tissue (Here the brain is not under the control of insulin dependent glucose uptake). Thus, the uses of insulin are multiple with regard to diabetes.• In Type 1 diabetes it is essential for survival since the synthesis of hormone is reduced• In Type 2 diabetes it may be necessary for control in certain individuals where the response to oral hypoglycaemic agents is poor and at later stage when production of insulin is also law apart from the peripheral resistance to insulin• In gestational diabetes to optimize the outcome insulin is used• Women with diabetes mellitus become pregnant since oral hypoglycaemic agents cannot be used• Rapid-acting insulin is used in hyperglycemic emergencies like diabetic ketoacidosis and hyperosmolar non ketotic coma (HONK)• In late onset autoimmune diabetes mellitus of adult (LADA)• Transiently in type 2 diabetes in special situations such as surgery or infectionWhat are the types of insulin? However, in the present days human insulin, known as insulin analogues is produced by recombinant DNA technology; examples are rapid –acting insulins like Aspart and Lispro and long-acting insulin like Glargine.
Unlike type 1 diabetes, secondary diabetes mellitus doesn’t destroy the insulin producing beta cells but makes them less efficient in tackling the sugar content of the body. Almost about 95% of the diabetes cases in the US have lifestyle issues as the core reason behind them. Also, one can’t do anything to avoid a faulty genetic development inside the body, which makes it an important cause of this disease.
Most of the times, these genetic complications are found to be related to the beta cell structure. Medical conditions like hyperthyroidism, glucagonomas (a form of cancer), testosterone deficiency, etc. Improving one’s lifestyle at once, including the diet, is the only way of avoiding this disease.


Impact of Hyperlipidemia on Plasma Protein Binding and Hepatic Drug Transporter and Metabolic Enzyme Regulation in a Rat Model of Gestational Diabetes. Metabolic Syndrome in Childhood: Association With Birth Weight, Maternal Obesity, and Gestational Diabetes Mellitus. Relation of central adiposity and body mass index to the development of diabetes in the Diabetes Prevention Program.
Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus.
Down-regulated IRS-1 and PPARgamma in obese women with gestational diabetes: relationship to FFA during pregnancy.
Combined treatment with vitamins E and C decrease oxidative stress and improves fetal outcome in experimental diabetic pregnancy.
Oxidant regulation of gene expression and neural tube development: Insights gained from diabetic pregnancy on molecular causes of neural of neural tube defects.
Insulin resistance in fat cells reduces the effects of insulin and results in elevated hydrolysis of stored triglycerides in the absence of measures which either increase insulin sensitivity or which provide additional insulin. Lack of insulin secretion or its action in the target tissue is the pathophysiology of diabetes mellitus and replacement of insulin as a drug is one of the commonest and standard treatments of diabetes (particularly type I). At the same time insulin suppresses glucose output from liver, glycogenolysis (break down of glycogen in the liver and muscle), gluconeogenesis (synthesis of glucose from amino acids and glycerol). All the fat that accumulates in arteries and tissues affects the body by clogging the blood flow and making the person obese over a prolonged period of time. If the body mass index gets greater than 30, it is a case of obesity. Various diabetic conditions such as maturity onset diabetes of the young (MODY) and Rabson-Mendenhall syndrome are the results of monogenic type of diabetes, which arises out of a single gene malfunction, hence the name. This inhibits IRS-1 binding and activation of PI 3-kinase and insulin signalling with resultant reduced insulin-stimulated glucose transport. Increased mobilization of stored lipids in these cells elevates free fatty acids in the blood plasma. Therefore, a thorough knowledge on insulin is crucial for health care professionals to offer a better management to the increasing number of patients suffering from diabetes mellitus. Intermediate acting insulin is made by adding substances to the unmodified insulin thereby slowing the breakdown of the molecule; which has a slower onset, peak and longer duration of action. Medications too, like atypical antipsychotics, thiazides and others, are responsible for triggering diabetes in the patients.
Obesity-associated changes in secretion of adipokines and inflammatory IKK? and NF-k? and JNK pathways through ligands for TNF-?, IL-1, Toll and AGE receptors, intracellular stresses like Reactive oxygen species,Ceramide and PKC isoforms.
Insulin resistance in muscle cells reduces glucose uptake (and so local storage of glucose as glycogen), whereas insulin resistance in liver cells results in impaired glycogen synthesis and a failure to suppress glucose production.
Though this hub is mainly aimed at educating the healthcare professionals and medical students the medical terms have been clarified as much as possible for the interest of the lay community.How does insulin act? The uptake of amino acids into muscles is promoted and breakdown of muscle (protein catabolism) is reduced.
Long acting insulin has longer duration of action and it is used to maintain the basal levels of insulin. So these medicines must be avoided, or not taken without the proper guidance of your doctor. These factors modulate insulin signalling, through activation of NF-k? and cause insulin Resistance( Shoelson et al 2006, Qatanani et al 2007, Savage et al 2007,)8.3. Elevated blood fatty-acid concentrations (associated with insulin resistance and diabetes mellitus Type 2), reduced muscle glucose uptake, and increased liver glucose production all contribute to elevated blood glucose concentration.
Stimulation of oxidative capacity, mitochondrial biogenesis and mitochondrial lipid uptake is impaired in the insulin-resistant state. Thus, whole-body lipid oxidation decreases in humans with obesity and insulin resistance as a result of impaired mitochondrial plasticity.
However, prior to the use of insulin as a drug, the dose has to be determined and the type of insulin suitable for each individual should be decided. The individual should become aware of the technique of injection and the common adverse effects.
In an ''insulin-resistant'' person, normal levels of insulin do not have the same effect on muscle and adipose cells, with the result that glucose levels stay higher than normal.
To compensate for this, the pancreas in an insulin-resistant individual is stimulated to release more insulin. The elevated insulin levels have additional effects (see insulin) which cause further biological effects throughout the body.The most common type of insulin resistance is associated with a collection of symptoms known as metabolic syndrome. This is often seen when hyperglycemia develops after a meal, when pancreatic I?-cells are unable to produce sufficient insulin to maintain normal blood sugar levels (euglycemia).
The inability of the I?-cells to produce sufficient insulin in a condition of hyperglycemia is what characterizes the transition from insulin resistance to Type 2 diabetes mellitus.Various disease states make the body tissues more resistant to the actions of insulin.


Recent research is investigating the roles of adipokines (the cytokines produced by adipose tissue) in insulin resistance. Exercise reverses this process in muscle tissue, but if left unchecked, it can spiral into insulin resistance.Elevated blood levels of glucose a€” regardless of cause a€” leads to increased glycation of proteins with changes (only a few of which are understood in any detail) in protein function throughout the body.
With respect to visceral adiposity, a great deal of evidence suggests two strong links with insulin resistance. First, unlike subcutaneous adipose tissue, visceral adipose cells produce significant amounts of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), and Interleukins-1 and -6, etc.
In numerous experimental models, these proinfammatory cytokines profoundly disrupt normal insulin action in fat and muscle cells, and may be a major factor in causing the whole-body insulin resistance observed in patients with visceral adiposity. Second, visceral adiposity is related to an accumulation of fat in the liver, a condition known as nonalcoholic fatty liver disease (NAFLD). In this case, the production of antibodies against insulin leads to lower-than-expected glucose level reductions (glycemia) after a specific dose of insulin. In vitro and in vivo studies have demonstrated that insulin may modulate the shift of Mg from extracellular to intracellular space. Intracellular Mg concentration has also been shown to be effective in modulating insulin action (mainly oxidative glucose metabolism), offset calcium-related excitation-contraction coupling, and decrease smooth cell responsiveness to depolarizing stimuli. Poor intracellular Mg concentrations, as found in Type 2 diabetes mellitus and in hypertensive patients, may result in a defective tyrosine-kinase activity at the insulin receptor level and exaggerated intracellular calcium concentration. Both events are responsible for the impairment in insulin action and a worsening of insulin resistance in noninsulin-dependent diabetic and hypertensive patients. By contrast, in T2DM patients daily Mg administration, restoring a more appropriate intracellular Mg concentration, contributes to improve insulin-mediated glucose uptake. The benefits deriving- from daily Mg supplementation in T2DM patients are further supported by epidemiological studies showing that high daily Mg intake are predictive of a lower incidence of T2DM. An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance.Insulin resistance has also been linked to PCOS (polycystic ovary syndrome) as either causing it or being caused by it.
Insulin resistance has certainly risen in step with the increase in sugar consumption and the substantial commercial usage of HFCS since its introduction to the food trades; the effect may also be due to other parallel diet changes however. CellularAt the cellular level, excessive circulating insulin appears to be a contributor to insulin resistance via down-regulation of insulin receptors. Since the usual instances of Type 2 insulin resistance are distinct from pathological over production of insulin, this does not seem to be the typical cause of the insulin resistance leading to Type 2 diabetes mellitus, the largest clinical issue connected with insulin resistance. The presence of insulin resistance typically precedes the diagnosis of Types 2 diabetes mellitus, however, and as elevated blood glucose levels are the primary stimulus for insulin secretion and production, habitually excessive carbohydrate intake is a likely contributor. Additionally, some Type 2 cases require so much external insulin that this down-regulation contributes to total insulin resistance.Inflammation also seems to be implicated in causing insulin resistance. PKC Theta inhibits Insulin Receptor Substrate (IRS) activation and hence prevents glucose up-take in response to insulin. MolecularInsulin resistance has been proposed at a molecular level to be a reaction to excess nutrition by superoxide dismutase in cell mitochondria that acts as a antioxidant defense mechanism. It is also based on the finding that insulin resistance can be rapidly reversed by exposing cells to mitochondrial uncouplers, electron transport chain inhibitors, or mitochondrial superoxide dismutase mimetics.GeneticIndividual variability is a cause with an inherited component, as sharply increased rates of insulin resistance and Type 2 diabetes are found in those with close relatives who have developed Type 2 diabetes. DiseaseSub-clinical Cushing's syndrome and hypogonadism (low testosterone levels) seem to be the major insulin resistance causes .Recent research and experimentation has uncovered a non-obesity related connection to insulin resistance and Type 2 diabetes. It has long been observed that patients who have had some kinds of bariatric surgery have increased insulin sensitivity and even remission of Type 2 diabetes. This suggested similar surgery in humans, and early reports in prominent medical journals (January 8) are that the same effect is seen in humans, at least the small number who have participated in the experimental surgical program.
The speculation is that some substance is produced in that portion of the small intestine which signals body cells to become insulin resistant.
If the producing tissue is removed, the signal ceases and body cells revert to normal insulin sensitivity.
Both metformin and the thiazolidinediones improve insulin resistance, but are only approved therapies for type 2 diabetes, not insulin resistance, ''per se''. By contrast, growth hormone replacement therapy may be associated with increased insulin resistance.Metformin has become one of the more commonly prescribed medications for insulin resistance, and currently a newer drug, exenatide (marketed as Byetta), is being used. Exenatide has not been approved except for use in diabetics, but often improves insulin resistance by the same mechanism as it does diabetes. It also has been used to aid in weight loss for diabetics and those with insulin resistance, and is being studied for this use as well as for weight loss in people who have gained weight while on antidepressants.
The ''Diabetes Prevention Program'' showed that exercise and diet were nearly twice as effective as metformin at reducing the risk of progressing to type 2 diabetes.Many people with insulin resistance currently follow the lead of some diabetics, and add cinnamon in therapeutic doses to their diet to help control blood sugar.



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