The insulin resistance treatment covered here is a summarised collection of the strategies outlined throughout this site.
An insulin resistance diet is the most important strategy to employ if you’re interested in reversing insulin resistance fast! Each of these factors are discussed in more detail in the article titled: Insulin Resistance Diet.
Exercise is effective in increasing insulin sensitivity via two mechanisms: increased translocation of glucose transporters (GLUT4) to the cell membrane and increased post-receptor insulin signalling.
There are a range of supplements that are beneficial for reversing insulin resistance, making them an essential part of an insulin resistance treatment program. The different supplements work through a variety of mechanisms to assist the body in becoming more sensitive to the action of insulin.
There are several other lifestyle factors that can have a positive impact on insulin sensitivity. Improved sleeping habits can also improve other hormone profiles in the body, resulting in greater insulin sensitivity.
Overall, the strategies mentioned are all you need to use for an effective insulin resistance treatment program.
If you, or someone you know has insulin resistance and would like to know how to overcome the condition, then I highly recommend reading, Your Complete Type 2 Diabetes Treatment Plan.
This entry was posted in Insulin Resistance and tagged diabetic sauce recipes, exercise, glucose disposal agents, insulin resistance diet, insulin resistance treatment, supplements for insulin resistance. Cellular insulin resistance may presage frank diabetes by a decade or more and requires compensatory increases in plasma insulin levels to maintain glucose homeostasis in the face of impaired cellular insulin action, principally in skeletal muscle and liver . Myocardial changes seen in insulin-resistant individuals could be caused by the impaired ATP synthesis noted in these patients, despite reduced oxygen delivery or increased workload. Importantly, cardiac dysfunction precedes the development of systemic hyperglycemia, implying that the altered cellular metabolism rather than systemic hyperglycemia is responsible for the cardiac dysfunction . The mechanism whereby hyperglycemia mediates tissue injury through the generation of reactive oxygen species has been elucidated largely through the work of the Brownlee and colleagues. There are changes in the level of the cardiomyocyte, which are not solely attributable to impaired coronary blood flow or interstitial fibrosis, including altered functional activity of ion channels and pumps and changes in gene expression of regulatory and modulatory proteins of Excitation-Contraction (E-C) coupling. Oxidative stress caused by toxic molecules may play a critical role in subcellular remodeling and abnormalities of calcium handling that lead to subsequent diabetic cardiomyopathy.
Cardiomyopathy in streptozotocin-induced type 1 diabetes is characterized by a decrease in the expression of SERCA2 [4,66], a change that is seen in most animal models of heart failure. Besides, advanced glycosylation end products form irreversible cross-links within or between many proteins, such as SERCA2a, causing their inactivation and subsequently leading to abnormal cardiac relaxation and contractility [72,73].
There can be correlation between diabetic cardiomyopathy and microangiopathy, due to the similarities between diabetes and idiopatic miocardiopathy in what concerns the coronary disease . The capacity of the vascular bed to meet metabolic demands may be impaired by abnormal epicardial vessel tone and microvascular dysfunction [76,79]. Even in patients with no known coronary artery disease, microvascular dysfunction and decreased coronary flow reserve can be present. There are 2 important components in the clinical diagnosis of diabetic cardiomyopathy: the detection of myocardial abnormalities and the exclusion of other contributory causes of cardiomyopathy.
The definitive diagnosis of diabetic cardiomyopathy is difficult to be established, principally because the signs, symptoms and finds of diagnostic examinations are unspecific.
Diastolic function parameters in diabetic patients are analogous to those in animal studies.
Studies that have examined both systolic and diastolic dysfunction in both type I and type II diabetes suggest that the latter is more susceptible to preclinical changes. A number of studies in both animals and humans have shown structural changes in parallel with the functional changes of diabetic heart disease, in the absence of hypertension, coronary artery disease, or intraventricular conduction defects [89,90,91].
Similar structural alterations have been described in diabetic hearts without significant epicardial coronary disease in humans. Insulin Resistance is known to be a condition that is associated with the unresponsiveness of the cells of the body towards insulin. In many places, all around the world, this herb is used to boost the levels of insulin as well as maintain the levels of blood sugar. This herb is known to have an impact on the pancreas, causing it regulate the levels of blood sugar.
Fenugreek is a herb that is helpful in treating insulin resistance.It has been stated that fenugreek is a herb that has been used for hundreds of years in order to treat a host of health conditions. Fenugreek is known to be bitter in taste and the seed is mostly used in order to treat health conditions. According to several health professionals, bitter melon is a herb that is beneficial in the treatment of this condition. This herb is used widely in places like India for hundreds of years to treat conditions such as diabetes. Cinnamon is known to possess anti-oxidant polyphenol compounds which may prove to be beneficial in boosting insulin sensitivity.
According to several research studies, it has been found that this herb is effective in decreasing insulin resistance when conducted on laboratory animals. According to a study conducted on the effectiveness of vanadium, it was pointed out that this herb is helpful in increasing the uptake of glucose by around five times from the fat cells than without the herb.
Not only does it include an insulin resistance diet, but it also includes foods, spices, and herbs to improve insulin resistance, exercise, supplements, and positive lifestyle factors.
Best of all, the more strategies you use simultaneously, the faster your results will come! If you would like more information about a particular strategy, a link will direct you to the article that explains it in more detail. Plus, since nutritional habits are the primary cause of insulin resistance in the first place, it is important that you realise that you need to create a completely new approach to nutrition if you’re serious about getting an effective insulin resistance treatment. A strong body of research demonstrates the benefits that exercise offers when it comes to reversing insulin resistance. It should last at least 20-30 minutes and should include both aerobic exercise and resistance exercise (weight training).
The best supplements for insulin resistance are discussed in the article titled: Top 5 Supplements For Insulin Resistance.
Systemic hyperinsulinemia may accentuate cellular insulin action in insulin responsive tissues, such as the myocardium, that do not manifest cellular insulin resistance. Insulin resistance results in decreased myocardial glucose uptake and oxidation, increased fatty acid oxidation, and altered myocyte gene expression .The slow rate of glucose transport across the sarcolemma into the myocardium restricts the glucose usage in the hearts of patients with insulin resistance [38,47].
Treatment of insulin resistance in these models (with troglitazone, metformin, or exercise) prevents myocardial dysfunction, but therapy aimed at hyperglycemia itself without treating insulin resistance (sulfonylureas) showed no effect [60,61]. Hyperglycemia leads to increased glucose oxidation and mitochondrial generation of superoxide . The cellular defects associated with E-C coupling manifest as prolonged action potentials, slowed cytosolic Ca2+ fluxes and slowed myocyte shortening and lengthening [2,64,65]. Alterations in regulatory proteins and contractile proteins, sarcoplasmic (endoplasmic) reticulum Ca2+-ATPase (SERCA2) and Na-Ca2 exchanger function may be important contributors to abnormal myocardial carbohydrate and lipid metabolism in diabetes.
In animal models of type 2 diabetes or insulin resistance, SERCA2 activity is also compromised, but a decrease in the expression of the protein is not always apparent .
These changes include abnormal capillary permeability, microaneurysm formation, subendothelial matrix deposition, and fibrosis surrounding arterioles. About 72% of normotense diabetic patients present in around 72 % of the diabetic patients without arterial high blood pressure were watched obvious disease of small pots, whereas in non-diabetics this finding was only 12 % . Diabetics have impaired endothelium-dependent relaxation , a defect that may be related to inactivation of nitric oxide by advanced glycosylation end products and increased generation of free radicals .
An important challenge in the clinical diagnosis of diabetic cardiomyopathy has been the lack of any pathognomonic histological changes or imaging characteristics associated with the diagnosis .
The diagnosis of diabetic cardiomyopathy currently rests on noninvasive imaging techniques that can demonstrate myocardial dysfunction across the spectra of clinical presentation .
Left ventricular ejection time is often reduced, and the length of the pre-ejection period and the ratio of pre-ejection period to left ventricular ejection time are often increased.
The lack of an association between diabetes and LV diastolic dysfunction in young diabetic subjects (35 yr) may relate to the prevalence of type I diabetes [19,87]. The most prominent histopathological finding in diabetic patients is fibrosis, which may be perivascular, interstitial, or both. There are many natural ways by which you can treat this condition. There are several herbs which are beneficial in treating Insulin Resistance. Gymnema is known to possess a sweetish taste and is found mostly in India as well as in some parts of Africa.
Prior to consuming this herb, it is advisable that you consult your physician regarding the dosage as well as the side-effects of this herb.
Fenugreek is considered to be helpful in the treatment of conditions such as diabetes, digestive conditions as well as poor appetite.
Bitter melon is considered to be helpful in lowering the levels of blood sugar in those suffering from type 1 and 2 Diabetes.
This herb is considered to be beneficial when consumed along with some glucose or about 12-14 hours before consuming glucose.
This is discussed in more detail in the article titled: Reverse Insulin Resistance With Exercise.
This results in an increased appetite, which may then in turn cause greater food to be consumed. In this regard, the mitogenic actions of insulin on myocardium during chronic systemic hyperinsulinemia bear directly the commonly observed finding of cardiac hypertrophy in diabetic cardiomyopathy . Excessive myocardial fatty acid uptake could enhance insulin resistance, promote cell dysfunction and trigger myocyte apoptosis, resulting in myocardial dysfunction . These adaptive responses of the heart are inhibited in the setting of insulin resistance (Fig. The prognostic impact of insulin resistance is independent of other variables, including peak oxygen consumption (VO2max) and left ventricular ejection fraction (LVEF), implying that insulin resistance is pathogenic rather than simply a marker for worsened heart failure [25,62]. Taken together, these data provide mechanistic evidence linking hyperglycemia to altered expression and function of both the ryanodine receptor (RyR) and sarco(endo)plasmic reticulum Ca2-ATPase (SERCA2) that may contribute to decreased systolic and diastolic function. These changes likely result from accumulation of toxic molecules such as long-chain acylcarnitines, free radicals, and abnormal membrane lipid content19.
The alteration in SERCA2 activity is most probably dependent on the severity and duration of diabetes. Coronary blood flow reserve in diabetic patients is reduced even in the absence of obstructive coronary artery disease and left ventricular hypertrophy . Besides, abnormalities of the reserve of coronary flow have been solidly demonstrated in diabetic patients without epicardic coronary arterial disease.
The abnormal vasodilator response in diabetes extends to the coronary microcirculation . In the absence of resting flow abnormalities, this is less likely to be a cause of resting left ventricular dysfunction but could contribute to left ventricular dysfunction with stress or exercise.
Besides, the clinical picture and laboratorial what took the suspicion of diabetic cardiomyopathy can be resulting of pathologies very prevalent between the diabetic patients, like arterial high blood pressure, coronary disease and obesity.
In another study using modern stereological techniques to quantify changes in the morphology accompanying streptozotocin-induced diabetes, the results showed that the time to peak tension and relaxation of papillary muscles was prolonged, the heart weight to body weight ratio was increased, and the volume of extracellular components was increased 3-fold in diabetic rats.
Bitter melon is also consumed as food as well as a medicine. This herb is known to be helpful in treating a host of health conditions such as diabetes, cancer, insulin resistance as well as disorders of the immune system. Cortisol is the primary stress hormone and has the effect of decreasing insulin sensitivity. Hyperglycemia-induced oxidative stress also activates poly(ADP-ribose) polymerase-1 (PARP) . Changes in gene expression that affect E-C coupling and cellular metabolism contribute to myocardial dysfunction in diabetic cardiomyopathy. Impaired SERCA function has been consistently found to coincide with myocyte insulin resistance in animal and in vitro models of type 1 and 2 diabetes68,69. Hyperglycemia also can lead to an enhanced synthesis of vasoconstrictor prostanoids by the endothelium and activation of protein kinase C. Perivascular and interstitial fibrosis and miocardic hypertrophy were also frequent finds in diabetics . Besides, microcirculatory dysfunction in diabetics may be due in part to downregulation of the expression of vascular endothelial growth factor (VEGF). In addition, a mismatch between coronary blood flow and myocardial glucose uptake has been demonstrated . The clinical demonstration of the diabetic cardiomyopathy is usually characterized for dyspnea due to the pulmonary congestion resulting from the diastolic dysfunction of the left ventricle. Left ventricular diastolic dysfunction appears to be quite common in well-controlled type II diabetic patients without clinically detectable heart disease . The mechanism of protection of type I diabetic patients may relate to protective effects of insulin therapy and lack of insulin resistance. At the same time, this study also demonstrated that the volume, surface density, and total surface area of capillaries as well as volume fraction of myocyte mitochondria were reduced, and oxygen diffusion distance to myocyte mitochondria was increased in the diabetic animals . Thus, the increased myocardial tissue reflectivity in diabetics may represent an early marker of diabetic cardiomyopathy . Before using any of these herbs, it is advisable that you consult your doctor regarding the dosage as well as the possible side-effects.
Although the initial myocardial metabolic switch in heart failure is down-regulation of FFA metabolism, the opposite occurs (up-regulation of FFA metabolism) in the setting of insulin resistance [53,54]. The activation of the PARP regulates several cellular reactions like repair of DNA, gene expression and cellular overlife.
At the cellular level, defective E-C coupling has been implicated as one of the root causes of the contractile dysfunction associated with diabetic cardiomyopathy. Furthermore, instigating insulin treatment in diabetic rats restored SERCA2a levels to normal, increased intracellular Ca2+ transient currents, and improved myocardial function following ischemia-reperfusion [70,71]. This vasoconstriction can promote myocardial hypertrophy, endothelial dysfunction, and ventricular hypertrophy . Subsequently, with the advancement of the disease, compromising of the systolic performance can occur, aggravating the severity of heart failure. Indeed, animal data suggest correction of abnormal function with insulin therapy, with indices of cardiac performance significantly greater in insulin-treated rats when compared with control rats .
This increased reliance on FFA metabolism leads to increased oxygen consumption, decreased cardiac efficiency, and the potential for lipotoxicity [55,56]. The effects of PARP include increase in the formation of advanced glycosilation end products (AGE’s), through the diversion of the route of degradation of the glucose. One of the most consistent and early changes seen in the hearts of individuals with diabetes is the prolongation of the ventricular action potential . Protein kinase C, an intracellular signaling molecule, is activated in diabetes and can lead to endothelial dysfunction by reducing the bioavailability of nitric oxide while increasing oxygen-derived free radical production.
The signs and symptoms of right heart failure, as well as the clinical form of dilated cardiomyopathy with global heart failure, are not common in the diabetic cardiomyopathy .
Insulin resistance at its most fundamental level inhibits uptake and metabolism of glucose. Meantime, the excessive activation of the PARP can begin several cellular processes and cause cellular damage. It also can enhance leukocyte adhesion, increase albumin permeability, and impair fibrinolysis [74,75]. It is important to emphasize that with our current knowledge, there is still no consensus in the precise imaging definition of diabetic cardiomyopathy, but evidence of hypertrophy or diastolic dysfunction is likely crucial to support a diagnosis of diabetic cardiomyopathy, but is not specific to it . It is likely this effect— preventing the heart from using its adaptive energy response to an insult—which contributes to heart failure and the vicious cycle of neurohormonal activation, serving to potentiate the myocardial dysfunction and further increasing energy requirements [25,51,57,58]. In addition, hyperglycemia contributes to altered cardiac structure through posttranslational modification of the extracellular matrix . Therefore, activation of this enzyme contributes significantly to the development of microvascular complications, as seen in diabetic neuropathy and nephropathy. The response to hypoglycemic therapy further confirms the correlation of myocardial functional and structural changes with glycemic control.
Taken together, hyperglycemia, through multiple pathways, causes cardiac cellular and functional changes, possibly contributing to the development of cardiomyopathy .
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