How to Epidemic of Diabetes Has Affected Millions Around?
The epidemic of diabetes has affected millions around the world and the work towards finding pharmacologic and non-pharmacologic ways to treat the metabolic disorder is ongoing. The role of exercise in conjunction with a controlled diet in improving the insulin sensitivity, glucose uptake, and improving overall health of type 2 diabetes is being understood. More physiological parameters have been studied and the impact of exercise on reducing obesity, inflammation, hypertension, cardiovascular disease, atherosclerosis and improving the lipid profile is being understood. The benefits of aerobic exercise have been known for long and the high expenditure of energy during aerobic exercise has made this mode popular. But research has found that resistance training offers significant advantage and a combination of aerobic exercise and resistance training is now recommended to improve the glycemic control among type 2 diabetes patients (Colberg, et al., 2010). The improvement in insulin sensitivity, and transport of glucose to the surface of the cell membrane improve import of glucose into the cell. The primary metabolic problem in type 2 diabetes is insulin resistance and the ability of insulin to bind to its receptor and elicit glucose transport into the cell is hindered, thereby increasing fasting and postprandial blood glucose levels and glycated haemoglobin exceeds normal range of 5.0 to 6.0. If left uncontrolled, hyperglycemia causes vascular damage and leads to several complications. Therefore exercise provides better glycemic control by altering the physiological parameters for the better. Several markers of inflammation have been found to reduce as a consequence of exercise in animal and human studies (Jorge, et al., 2011). Oxidative stress is reduced and the generation of free radicals is not allowed to cause damage in tissues due to the antioxidant effect of exercise. Several studies on the physiology of exercise have found that it improves endothelial function, reduces arterial stiffening and improves endothelial function. The maintenance of glycemic control, a normal lipid profile and reducing abnormalities related to blood pressure are the primary goals of a diabetes management program. Studies on the effects of physical exercise have shown that exercise provides these benefits through several physiological pathways and so exercise is highly recommended to achieve better glycemic control. The oxidative damage caused by reactive oxygen species can be reduced through the generation of anti-inflammatory cytokines that are generated in response to exercise. The isometric contraction of skeletal muscles during resistance training improves the uptake of glucose and reduces oxidative stress.
The mechanism of cellular glucose transport in type 2 diabetes patients is impaired. Exercise improves the uptake of glucose in skeletal muscles. Although levels of insulin may be normal or high in type 2 diabetes patients. But the insulin is not able to transport glucose to the cells due to the phenomenon of insulin resistance in tissues of the liver and skeletal muscle and the adipose tissue. Insulin resistance is a typical feature of impaired sugar metabolism in individuals with type 2 diabetes. The pancreas responds to the high blood sugar levels by increasing the secretion of insulin.
There is a lot of evidence of the effect of exercise on the management of blood glucose levels and thereby the overall quality of life. Exercise results in weight loss as and is an additional benefit, lower glycated haemoglobin, better mobility and kidney function, lower triglyceride levels and reduced need for medication are important outcomes for a person with type 2 diabetes (Espeland, et al., 2014; Group., 2014). The complications of diabetes due to long term hyperglycemia include retinopathy, neuropathy, nephropathy and cardiovacular disease among others. The goal of improving glycemic control not only reduces fasting blood glucose and postprandial blood glucose levels, the risk of complications is also reduced. Following a low calorie diet and regular exercise with adherence to medication can help in improving blood glucose levels and the associated morbidities of hypertension and dyslipidemia in type 2 diabetes patients. A low grade chronic inflammation occurs due to release of inflammatory cytokines from the adipose tissues. Exercise causes release of myokines from skeletal muscles which has been recently recognised to hve endocrine function and reduces the inflammation systemically. Various benefits of physical activity can reduce the damage caused by a sedentary lifestyle, which causes diabetes in many individuals.
Exercise is known to improve insulin sensitivity. The contraction of muscles during exercise causes activation of the 5'-AMP-activated protein kinase which in turn caused the glucose translocator protein, GLUT-4 to the sarcolemma of the skeletal muscle cell. The acivation of the protein kinase occurs due to high calcium concentration in the cytoplasm or due to a high ratio of AMP to ATP in the cell which points at the fact that the energy status of the cell is challenged due to less influx of glucose into the cell. Exercise reduces inflammation by reducing the high sensitivity C-reactive protein and tumor necrosis factor-α (Jorge, et al., 2011).
The effects of resistance training on increasing insulin sensitivity became evident only after 1990, before this, aerobic exercise was largely recommended. The effects of resistance training on reducing obesity, lowering HbA1c and reduction in systolic blood pressure have been proven to be beneficial in individuals with type 2 diabetes (Strasser, et al., 2010). Recommendations for resistance training to be done twice a week have benefits for patients with intraabdominal obesity and reduction in inflammation due to obesity. Although the expenditure of energy is greater in aerobic exercise, the benefits of resistnce training in reducing central adiposity make it necessary in the management of type 2 diabetes (Strasser, et al., 2012).
A low grade systemic inflammation is associated with chronic diseases such as, diabetes. Insulin resistance and atherosclerosis are understood to arise due to prolonged low grade inflammation. Regular physical exercise offers protection against non-communicable diseases and can be used for as part of treatement. Due to physical exercise, there is a release of several anti-inflammatory cytokines that protect the body from chronic non-communicable diseases of diabetes, cancer and cardiovascular disease. It is now known that cytokines are produced by the skeletal muscles in response to exercise, these are referred to as myokines and the skeletal muscle is considered to be an endocrine gland that releases anti-inflammatory cytokines that provide beneficial effects on other tissues and organs. In patients with chronic disease, the low concentrations of C-reactive protein- an inflammatory marker, TNF-α and IL-6 have been shown to be predictors of myocardial infarction. The origin of the TNF- α is mainly the adipose tissue. TNF-α is known to cause insulin resistance through an alteration in the signal transduction caused by insulin. It increases the phosphorylation of p70 S6 kinase, that of kinase-1/2 which is also regulated through an extrcellular signal and the phosphorylation of c-Jun NH(2)-terminal kinase. There is a concomitant increase in serine phosphorylation accompanied by a lesser phosphorylation of the tyrosine of insulin receptor substrate-1. The phosphorylation of Akt substrate 160 was also impaired, this is the most proximal step to the insulin signalling cascade that reguates the translocation of GLUT-4 to the sarcolemma and is key to glucose uptake by cells (Mathur, et al., 2008). It has been shown that exercise helps in reducing inflammation. And since atherosclerosis is a consequence of vascular inflammation it may be reduced due to reduced inflammtion of the endothelial lining after prolonged adherence to exercise.
When the balance between production of free radicals in the body and the endogenous antioxidants in the human body is disturbed, it can led to oxidative stress. Oxidative stress causes oxidative damage and may induce signalling pthways that are an outcome of the stress. Insulin resistance, cardiovascular disease and the metabolic syndrome are outcomes of oxidative stress. Exercise induced oxidative stress has been found to be beneficial effects. Production of reactive oxygen species in the mitochondria of skeletal muscle cells helps in adaptation of muscle when exercise is performed through certain signalling pathways. The generation of certain reactive oxygen species during exercise is tied to some benefits of exercise. The free radicals produced during exercise can improve insulin sensitivity and cause prevention of type 2 diabetes onset. The effect of the reactive oxygen species generated during exercise is so important that it may be lost if antioxidant supplements are taken in the form of vitmin C and vitamin E supplements, then the benefits of exercise in improving insulin sensitivity may be lost (Ristow, et al., 2009). Endurance exercise can reduce systemic oxidative damage and is known to improve the immune response and release of anti-inflammatory cytokines that are a hallmark of obesity, even if weight loss does not occur. Exercise is non-pharmacological intervention that reduces inflammation (Samjoo, et al., 2013).
The peroxisome proliferator-activated receptor-gamma (PPARgamma) coactivator-1α regulates substrate utilization as a consequence of exercise. The expression of contractile protein in muscle fibres of the skeletal muscle is controlled by Calcium ion dependent signalling pathways, NO, reactive oxygen species, AMPK, and p38 MPK and helps in angiogenesis and mitochondrial biogenesis. The metabolic adptations of skeletal muscle triggered by PPAR gamma coactivator-1α also helps to improve insulin sensitivity in individuals who exercise (Lira, et al., 2010).
It has been found that resistance training could be more effective in improving insulin sensitivity and glycemic profile as compared to aerobic exercise. The isometric contrctions that occur during resistance training mimic insulin and improve glucose uptake in skeletal muscles. Other benefits of using weights during exercise in repetitive motion involving the same group of muscles is that several physiological parameters such as, regional body composition, hypertension and increase in high density lipoprotein occur. The American Diabetes Assocition and the American Collegeof Sports Medicine have recommended resistance training with aerobic exercise for improvement in insulin activity. The benefits are not restricted to better glucose uptake by the skeletal muscles but help in managing blood pressure, treating dyslipidemia, reducing cardiovascular risk and a general improvement in quality of life by improvement in all the co-morbidities of type 2 diabetes (Suh, et al., 2011).
Postprandial uptake of glucose by skeletal muscle in patients with type 2 diabetes is much less as compared to the 80% uptake in normal individuals. Even the capacity for oxidation of fat and glucose is much less among diabetics as compared to healthy counterparts. Resistance training increases the strength of muscles and muscle mass because of the muscular hypertrophy and remodelling of muscles at the neuromuscular level are induced. The pathway responsible for these changes in metabolism is the phosphatidylinositol-3-kinase - Akt- mammalian target of rapamycin pathway. A long duration of resistance training over 9 months improves the uptake of glucose and fat substrate from muscle in persons with type 2 diabetes. The participants observed an increase in muscle mass of about 1.4 kg which is likely to have mediated the improvement in the muscle metabolism. The role of insulin signalling may also have played a role in better glycemic control and better substrate metabolism following the sessions of resistance training over a long period. The molecular mechanism of better glycemic control operates through the calmodulin-dependent protein kinase(CaMK) II, it acts as a sensor for remodelling of muscle and calcium signalling in the cell. Histone decetylases are an important kind of transcription factors that leave the nucleus upon phosphorylation by CaMK II and in turn activate transcription factor MEF 2 (myocyte enhancing factor 2) which acts on its target genes- the peroxisome-proliferator-activted receptor-gamma coactivator1 alpha (PGC-1α) and the glucose transporter,GLUT4 both of which play a role in improving glycemic control. Studies have also shown that whether the persons with type 2 diabetes perform resistance training or exercise training a higher number of training sessions provide more benefit than sessions that are more intense or are of a particular kind (Pesta, et al., 2017). The activation of PGC-1α and the FOXO1 (forkhead box protein O) triggers the oxidation of fatty acids, promotes the biogenesis of mitochondria and increases the antioxidant effects. The antioxidant effect is increased through superoxide dismutase through the rective oxygen species mediated signalling.There are other benefits- increased resting energy demand and a higher protein turnover in the muscles, these changes help in keeping the glucose uptake higher. Benefits of resistance training exercise in type 2 diabetes management are thus substantial.
Lipid profile refers to the levels of various lipids in the blood that can vary when checked depending on several factors. The low-density lipoprotein (LDL), the high-density lipoprotein (HDL), cholesterol and triglycerides are the lipids that are measured in blood as part of the lipid profile. Higher levels of LDL and triglycerides in the blood increase the risk of cardiovascular disease. Very low density lipoprotein also raises cardiovascular risk even if the levels of LDL are within the normal range. Diabetes and dyslipidaemia are often observed in patients due to hyperglycemia. Aerobic exercise and resistance training are known to improve the lipid profile of patients with type 2 diabetes. Exercise can increase the ability of skeletal muscle cells to utilize lipids rather than glycogen as a source of energy.Activity of lecithin-cholestrol acyltrans is increased after exercise and the activity of the lipoprotein lipase is increased (Mann, et al., 2014).
Regular aerobic exercise can increase the levels of HDL. Intense aerobic exercise is required to decrease the levels of LDL, cholesterol and triglycerides. Longer duration and more intense aerobic exercise can increase the activity of lipoprotein lipase. A combination of aerobic exercise and resistance training can cause improvements in the lipid profile.However two studies that investigated the impact of exercise on lipid profile for 4 and 6 weeks found that short duration of exercise does not lower the levels of lipids in type 2 diabetes patients (Aggarwala, et al., 2016; Gordon, et al., 2008).
The blood vessels are lined on the inside with a thin layer of the endothelial cells that play a role in maintaining structure and regulation of vascular tension. Dysfunction of the endothelium increases the risk for atherosclerosis and for heart diseases.Nitric oxide bioavailability is necessary for the maintenance of the health and functions of the endothelial lining. The endothelial dysfunction is measured by the flow-mediated dilation (FMD) and occurs in several cardiovascular diseases that include diabetes, hypertension, chronic heart failure and also atherosclerosis. Exercise, when done on a regular basis is beneficial because it promotes an increase in the number of smooth muscle cells and cells of the endothelium. This helps to expand the aortic vessels and an increase in arterial diameter follows. A larger number of smooth muscle cells and endothelial cells increases the number of capillaries and improved outcomes in terms of vasculature are achieved. Exercise is known to improve the bioavailability of nitric oxide and reduces destruction caused due to oxidative stress (Kwon, et al., 2011). In their study on the comparison of the effect of aerobic exercise and resistance training on the endothelial function among a group of Korean women with type 2 diabetes, Kwon et al. found that aerobic exercise was effective in improving endothelial function. The study was of a short duration lasting for 6 weeks. Cohen et al. studied the effects of progressive resistance exercise for 14 months on endothelial function in type 2 diabetes patients who underwent supervised an unsupervised programs. A string of correlation was found between HbA1c levels and endothelial function. Better glycemic control may therefore help in the long term improvements in endothelial function (Cohen, et al., 2008).
It is possible to reduce the oxidative stress by engaging in physical exercise on a regular basis. The oxidative homeostasis of cells is positively affected as a consequence of exercise, because the basal level of oxidative damage is reduced and the cells become increasingly resistant to oxidative stress. Cellular damage is minimized as a result of the reduced oxidative stress. The intrinsic antioxidant potential of the cells increases as a result of physical exercise and there is much lesser DNA damage. The nuclear factor erythroid-2 related factor Nrf-2 is an important transcription factor that is released in response to exercise in healthy and diabetic individuals and causes release of antioxidant enzymes in the cell. These effects occur upon moderate levels of exercise. Exhaustive exercise can have dmaging effects. Another important effect of exercise is the increase in the levels of maximal oxygen consumption VO2max and metabolic activity. This occurs due to repeated contraction of muscle when performing the exercise (de Lamos, et al., 2012).
Exercise is also the cause for increase in levels of serum adiponectin. Adiponectin is a protein hormone and an adipocytokine that is secreted by the white adipose tissue. The anti-inflammatory action of adiponectin provides cardiometabolic benefits due to its regulatory effects on other factors, such as, TNF-α, IL-6 and C reactive protein. The anti-inflammatory action of adiponectin has been shown to last for as long as 48 hours after a session of exercise. Adiponectin has properties that make it an effective antidiabetic, anti-inflammtory and anti-atherogenic molecule. The serum levels of adiponectin are lower in individuals with abdominal obesity and higher body mass index. Adiponectin promotes insulin sensitivity and inhibits the action of inflammatory molecules. It plays a role with insulin in inhibition of hepatic glucose production. It is also known to cause stimulation of fatty acid oxidation in cells of the skeletal muscle. Adiponectin that acts in response to exercise causes increase in levels of nitric oxide production and the AMP activated kinase. It plays a role in reducing C-reactive protein expression and IL-6. Inhibition of TNF-α is also an effect of adiponectin secretion by white adipose tissue. It downregulates the expression of the adhesion molecules in the endothelium and inhibits the nuclear transcription factor κ signalling and reduces cytokine expression by macrophages and thus exhibits its anti-inflammatory effects (Simpson & Singh, 2008).
Plasma levels of adiponectin increase when there is weight loss as a result of diet. This causes an iprovement in insulin sensitivity and lower levels of the inflammatory markers. But when diet intervention is coupled with exercise, robust increase in adiponectin levels results. Reduction of fat mass that occurs as a result of the two simultaneous interventions is believed to play a role in the increase.
Exercise also benefits patients with arterial stiffness. Arterial stiffening occurs as a consequence of ageing and may be seen in patients with dyslipidemia, chronic kidney disease, diabetes and therosclerosis. The stiffenened arteries cause the systolic wave to reflect faster when it returns from the peripheral arteries of smaller diameter back to the heart and this augments pressure at the central aorta. This can lead to higher ventricular load and a reduction in coronary perfusion ensues that can lead to myocardial hypertrophy and ischaemia and even infarction. Arterial stiffness therefore is a predictor of cardiovascular disease.
Stiffening of arterial walls largely occurs due to inflammation (Park & Lakatta, 2012). The effect of aerobic exercise, resistance training and a combination of the two were studied by Ashor et al. to determine the best exercise intervention that can reverse arterial stiffening. Improvement in pulse wave velocity and augmentation index was observed. Lessened arterial stiffness was more evident in patients who had more stiffness and performed aerobic exercise for a longer duration of time. Though intense aerobic exercise yielded better outcomes than more frequent or long aerobic exercise interventions. Only resistance training or a combination of aerobic and resistance training did not yield better outcomes in terms of pulse wave velocity or augmentation index. Inflammation and oxidative stress (Patel, et al., 2011) are the main reasons that lead to arterial stiffening (Park & Lakatta, 2012). Ageing is also associated with stiffening of vascular walls. But in individuals who continue to exercise, stiffening is not observed due to the anti-inflammatory benefits of exercise (Seals, et al., 2008). The stiffening occurs due to the breakdown of elastin and collagen deposition. Smooth muscle proliferation also results in the stiffening of walls. Constant exposure to cytokines and free radicals, lower levels of NO and a higher concentration of angiotensin, prostaglandins and endothelin cause progressive stiffening of vascular walls. It has been evidenced in animal studies that animals that were exercised has more elastin and less collagen than the animls who had not been exercised (Roque, et al., 2013). Exercise has antioxidant effects due to raised levels of superoxide dismutases and lower level of NADPH oxidase. Interleukin 4 and interleukin 10 are anti-inflammatory cytokines that are raised as a result of exercise and protect the arterial walls from stiffening (Teixeira-Lemos, et al., 2011).
In conclusion, it is evident that the onset of diabetes may be a consequence of sedentary lifestyles among modern populations around the world. The problems of insulin insensitivity and insulin resistance can be reveresed through proper diet and exercise. Physical exercise is a major intervention that can counter many of the physiological outcomes of hyperglycemia. The altered insulin signalling pathway in type 2 diabetes makes it difficult for cells to utilize glucose. Exercise reduces the chronic inflammation by release of anti-inflammatory cytokines. The effect of inflammation due to TNFα, C reactive protein causes severe damage and my even led to myocardial infarction. The production of myokines by the skeletal muscle after exercise counters the effects of imflammation and restores insulin sensitivity. Arterial stiffening, loss of endothelial function and the propensity for dyslipidemia due to hyperglycemia can be reveresed by exercise. Aerobic exercise has been known to alleviate arterial stiffening while resistance training did not provide benefit. Resistance training is now recommended with aerobic exercise to help in the management of type 2 diabetes. The isolateral contraction of muscles through repetitions of resistance training improve the insulin sensitivity. The increase in muscle mass also helps to increase glucose uptake in muscles. Adiponectin, a protein hormone released by white adipose tissue in response to exercise is responsible for bioaugmentation of nitric oxide and causes production of AMP kinase. It reduces the production inflammatory markers TNFα and C-reactive protein. Exercise also benefits because it increases the production anti-inflammatory enzymes, such as superoxide dismutases and causes a decrease in NADPH. Intense bouts of exercise offer some physiological gains while frequent and prolonged exercise sessions provide other benefits. Cells improve in the maintenance of overall oxidative homeostasis and the chances of oxidative damage of DNA and other cellular components is reduced. Mitochondrial biogenesis is another favourable outcome of physical exercise, it is particularly important because loss of mitochondria in skeletal muscle fibres reduced the capacity of cells to generate energy. The several advantages of exercise in improving physiological parameters and even curing dyslipidemia and hypertension besides other co-morbidities of type 2 diabetes makes it an indispensable interventio
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