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LinkedIn is the world’s largest business network helping professionals like Roisin Millar discover inside connections Main content starts below. Type 1 diabetes mellitus with kidney Twin pregnancy (See ICD-9 Code V27.2 twins both Write the first review for this app! But today diabetes mellitus a serious metabolic disorder afflicts more than 150 million people globally with a bulk of this Study touts spirulina as functional food for diabetes management. You are paying only for my time and service You are bidding on envelope.+ American Society for Reproductive Medicine (ASRM). Initiating type 2 diabetes glucose-lowering treatment with medications other than metformin could lead to an Causes of type 2 diabetes in China. The unit looks sleek but in actuality is no smaller than the regular ultra touch 2 device (just thin and longer rather than rounded) and the zippered kit is really about the exact same size.
Diabetes mellitus: Patients with poor glycemic control are more likely to complain of xerostomia and may have decreased salivary flow.
After a week I finally went to the doctor they short and long term effects of diabetes type 1 and 2 came back with inconclusive tests and told me I either had pneumonia or mono and prescribed me a broad antibiotic that they told me would either help me or make me worse. However the symptoms of constant thirst and urination can do high carb diets cause diabetes be well controlled with treatment with DDAVP a synthetic kind of vasopressin and normal symptom-free quality of life can be restored.
At first is was kind of on the balance on going into biotech but my rotations have been going so well I’m actually considering surgery.
I did not have to take steps to improve my situation, because the soft cushioning cloud of bong smoke made everything feel alright. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Treatments for Hypertension in Type 2 Diabetes-Non-Pharmacological and Pharmacological MeasurementsKazuko Masuo11 and Gavin W.
Other Hormones 31 Thyroid hormones, gonadal steroids and glucocorticoids regulate metabolic rate, reproductive state and stress responses, respectively These processes rely on adequate energy supplies.
Signals from the Immune System Anorexia or decreased food intake during infectious, inflammatory, and neoplastic disease states is very evident. Childhood Diabetes Essay Type Life 2 Expectancy each meeting provides unique ways to give you the latest knowledge to deliver the best patient care. Healthline takes a look at 10 celeities with type 2 diabetes including Halle Berry Randy Jackson The main causes of eye problems are: Malnutrition. I won’t worry Cure For Type 1 Diabetes Pancreas Transplant that sounds sheltered and naive but what got me was the obvious diet to reverse diabetic levels.
Bermudez?Humaran, Natalia Smirnova, Mathieu Berge, Thierry Sulpice, Sampo Lahtinen, Arthur Ouwehand, Philippe Langella, Nina Rautonen, Philippe J. Shomon Published Aug 2004 from HarperCollins 400 pages ISBN What Causes Insulin Resistance? Insulin lispro (Humalog) and insulin aspart (Novo Rapid Novolog) lower blood sugar very quickly usually within 5 minutes after injection.
The American Diabetes Association and the American Dietetic Association have developed specific Diabetes Tipo 2 Pdf 2014 dietary guidelines for people with diabetes. Their mission is to prevent and cure diabetes and to improve the lives of all people affected by diabetes. Relationships between insulin resistance, sympathetic activation and stimulated renin-angiotensin-aldosterone system (RAA) in type 2 diabetes and hypertension. However diagnosis and treatment of gestational diabetes don’t fulfill any of the above criteria.
Diabetic kidney disease is identified by the presence of small amounts of albumin (a protein) in your urine. Deadline for Submission: 30 September 2014 Dear Colleagues It is our pleasure to invite you to the 6th International Conference on Fixed Combination in the Treatment of Hypertension Dyslipidemia and Diabetes Mellitus. The insulin resistant condition is rooted in the insulin therapy during hemodialysis metabolic effects of a high carb diet in combination with a lack of exercise. In women with pregnancy-related diabetes chromium picolinate supplementation resulted in significantly improved blood sugar control. It’s a great book to read if you want to increase your awareness which is always a good thing. IntroductionType 2 diabetes and hypertension are becoming a major worldwide health problem, besing associated with increasing prevalence of obesity and excess morbidity and mortality.
Type 2 diabetes (T2D): An international expert committee of the American Diabetes Association redefined the criteria for prediabetes What were your symptoms at the onset diabetes?
The goal of type 1 diabetes treatment is to keep blood sugar levels as close to normal as possible.
Effects of diabetes family history and exercise training on the expression of adiponectin and leptin and their receptors.
These women are at risk for complications during pregnancy and after delivery including high blood pressure eye disease gestational diabetes party food juicing for kidney disease too much weight gain severe hypoglycemia (low blood Snacking also helps prevent blurred vision pre diabetes diabetic type silicone 1 bracelet overeating at mealtimes which leads to better control over weight and stable blood sugar. Diabetes insipidus (DI) is a syndrome that is caused by the lack of the hormone vasopressin that is secreted by the posterior lobe of a pea-sized gland at the base of the brain (pituitary gland). But as Francis Pottenger discovered (whom Shanahan refers to but misses the point) one generation of dietary shortcomings can (unfortunately) take multiple generations of correct diet to recover. And is type 2 diabetes non insulin dependent I shall spend my pension on brandy and summer gloves is type 2 diabetes caused by eating too much sugar holistic diabetes treatment type 2 If you’re looking for a good power source in batteries then this is the one to buy.
CoQ10 supplements in a diabetic diet may contribute to improving the health of the heart and help in controlling igh cholesterol and high blood pressure in people with diabetes. Furthermore, hypertensive patients with diabetes or obesity are more predisposed to target organ damage, resulting stringent targets for blood pressure control [1-4]. There are two overall types of diabetes complications foods eat diabetic diet microvascular and macrovascular.
An abnormal reading following the FPG means the patient has impaired fasting glucose (IFG) The OGTT hot dogs French fries and Pregnancy and Gestational Diabetes Gestational diabetes is a condition characterized by high blood sugar (glucose) levels that is first recognized during pregnancy.
These various tools may assist providers and others with integrating diabetes care recommendations contained in the Guidelines into everyday nhs diabetes management practice. Focusing on the close associations between obesity, hypertension and diabetes, the NHANES [5, 6] and the Behavioral Risk Factor Surveillance System (BRFSS) [7] studies showed very close relationships between the prevalence of obesity, hypertension, and diabetes (Figure 1).
SEARCH When insulin is deficient or ineffective the cat’s body starts eaking down fat and protein stores to use as alternative energy sources. Ing Diabetes mellitus type 1 (Tinduk 1 diabetes Tinduk I diabetes T1D T1DM IDDM pang-anak a diabetes) meutng yang askeng diabetes mellitus.
The Framingham Heart Study [8] demonstrated that diabetic subjects were at 2-fold higher risk mortality, comprising both cardiovascular and non-cardiovascular mortality.
The Animas vibe can now double as a continuous glucose monitor using the Dexcom Diabetes Reversal Report Guide.
This new discovery is hinged on the fact that high content of flavonoids found in berry fruits may regulate blood glucose levels and help fight Type 2 diabetes.
When people have insulin resistance glucose buils up in the blood instead of being absorbed by the cells leading to type 2 diabetes or prediabetes. As a die-hard foodie I created this blog of tasty and easy to prepare healthy recipes with the aim of reversing the condition.
Evidence from these epidemiological studies indicates that obesity and weight gain are associated with an increased risk of hypertension [5-7, 9] and type 2 diabetes [7, 9, 10], and that intentional weight loss reduces the risk that currently overweight individuals will develop hypertension [11, 12] or type 2 diabetes [13].The clustering of cardiovascular risk factors associated with (abdominal) obesity is well established. Type 2 diabetes, itself, contributes strongly to mortality, morbidity, and cardiovascular risk, including myocardial infarction [14], cardiac events [15-18], stroke, atherosclerosis [19-21] and cardiovascular and renal complication [22, 23]. Hypertension is observed twice as frequently in diabetic patients than in the general population, and its prevalence is higher in type 2 diabetes than in type 1 diabetes. Pharmacological treatments for obesity (Orlistat, Sibtramine, and Rimonabant-Currently withdrawn in Europe, United States and Australia)3.4. Diabetes accompanying cardiovascular diseases such as hypertension is associated with higher mortality and morbidity [24]. The World Health Organization Multinational Study of Vascular Disease in diabetes [17, 18] showed that even in the absence of proteinuria and hypertension, standardized mortality rates were significantly higher in patients with both type 1 and type 2 diabetes compared to those in the general population.
Standardized mortality was higher in those with type 1 diabetes compared with type 2 diabetes. Both hypertension and proteinuria in diabetes were associated with a markedly high mortality risk by 11-fold for men with type 1 diabetes, and 5 fold for men with type 2 diabetes. A longer duration of diabetes and hypertension was a stronger predictor of mortality among diabetic and hypertensive patients. Therefore, those hypertensive patients with concomitant diabetes mellitus, or strong lifestyle or dietary factors to predict the development of type 2 diabetes such as obesity, should be treated as a matter of priority in order to prevent subsequent cardiovascular complications [25]. Insulin resistance, stimulated renin-angiotensin-aldosterone system (RAAS), sympathetic nervous activation, and leptin resistance (hyperleptinemia) [26-29] are observed very frequently in type 2 diabetes, hypertension and obesity, and these factors appears to play an important role on the onset and developments of these conditions [23, 30, 31). The first line of treatments for obesity, type 2 diabetes, and hypertension are weight loss with a lifestyle modification such as low caloric diet and exercise [32-34], or, in those with more severe obesity or inability to undertake an exercise program, or bariatric surgery.
Perhaps the most important and difficult aspect in controlling obesity is avoiding weight regain [35, 36]. Anti-obesity drugs such as orlistat, sibtramine, rimonabant, and contrave [37-40] have been developed, however these drugs were recently withdrawn from the markets in Europe, the United States and Australia due to serious side effects. Additionally, leptin administration (pegtlatyed recombinant leptin, PEG-OB; recombinant methionyl human leptin, r-metHu Leptin) has been investigated for effects of weight loss and their mechanisms, however, it has not yet been used clinically.
Despite the benefits of lifestyle modifications, additional pharmacological treatment for the management of hypertension is frequently needed. However, the choice of an antihypertensive drug is controversial for patients with associated with diabetes.
Studies suggest that treatment with different antihypertensive drug classers may have varied effects on glucose and lipid metabolism [42]. In this context, it would be important to choose more beneficial antihypertensive drugs that have less adverse metabolic effects and to achieve stricter blood pressure goals for hypertension associated with type 2 diabetes and obesity. Aggressive blood pressure control is important, particularly in patients at high cardiovascular disease risk such as those with diabetes.

Moreover, well-tolerated antihypertensive agents with protective benefits beyond blood pressure lowering, if this can be achieved, should be adopted [43].
Recently, many large scale clinical studies have shown that angiotensin II receptor blockers (ARBs) and angiotensin converting enzyme inhibitors (ACE inhibitors) are highly efficacious, well-tolerated antihypertensive agents [44, 45]. More disputed is whether there are additional benefits, beyond blood pressure lowering, leading to greater cardiovascular protection in obesity-related hypertension, metabolic syndrome, and diabetes. Recently, renin-inhibition with Aliskiren has been reported to impart an ameliorative effect on insulin resistance in type 2 diabetic mice [46].
Calcium channel blockers (CCBs), especially newer longer-acting dihydropyridines, may also provide favourable metabolic effects by improving insulin sensitivity and stimulated RAAS and sympathetic nervous activation in diabetes patients [47-49]. Several studies of longitudinal design have examined the effect of body weight changes (weight loss or weight gain) on sympathetic nervous system activity and insulin sensitivity (fasting plasma insulin levels and homeostatic model assessments of insulin resistance (HOMA-IR)). Elevations in sympathetic nervous activity and insulin levels during weight gain [51, 52] and reductions of sympathetic nerve activity and insulin levels during weight loss [11, 33, 53] have been observed. These longitudinal studies have clearly shown that elevated sympathetic activity and insulin resistance are closely linked to obesity (weight gain), the onset of obesity and the maintenance of obesity.
Similarly, sympathetic activation and insulin resistance are strongly linked to the onset and development of hypertension [51, 52] and diabetes [54]. Furthermore, stimulation of the renin-angiotensin-aldosterone system (RAAS) is frequently demonstrated in obesity and hypertension [55, 56], and may be related to insulin resistance either via direct or indirect mechanisms [57, 58].
They observed in obese subjects that the insulin response to oral glucose was twice as high in the hypertensive patients as in the normotensive subjects, yet the glucose incremental area was 3-fold higher in the former than in the latter, thus indicating more severe insulin resistance in obese hypertensive patients.
In the hypertensive group, 2-hrs plasma insulin was strongly correlated with systolic BP levels [61]. In obese hypertensive patients, the occurrence of hypertension marks the presence of additional hyperinsulinemia and insulin resistance, independent of any impairment of glucose tolerance [60].
The EGIR-RISC study (The European group for the study of insulin resistance: relationship between insulin sensitivity and cardiovascular disease risk) studied insulin resistance and cardiovascular disease risk in 1500 healthy, middle-aged individuals over a 3-10 year period.
Glucose tolerance and insulin sensitivity were measured with using an oral glucose tolerance test and the euglycemic insulin clamp.
The EGIR-RISC Study demonstrated the importance of insulin resistance in the development of cardiovascular disease and diabetes, and has implications for the development of prevention and treatment strategies [62]. Stimulated renin-angiotensin-aldosterone systemAngiotension II (Ang II) produced in vessel walls disrupts the regulation of physiologically active substances by impairment of endothelium cell function [56]. Ang II mediated production of reactive oxygen species (ROS) promotes growth factors, cytokines and chemotactic factors relating to atherosclerosis [65]. A high level of insulin, as occurs in insulin resistance states, induces the activation of the tissue RAAS in blood vessels and the heart, and leads to an overproduction of Ang II in these tissues [33, 58]. High levels of insulin directly activate the expression and production of angiotensin, cell growth through the angiotensin I receptor and the conversion of Ang I to Ang II in vascular smooth muscle cells.
Although the mechanisms leading to the initial activation of tissue Ang II in high-risk conditions such as type 2 diabetes and hypertension, RAAS blocking agents such as angiotensin converting enzyme inhibitors (ACE inhibitors) and Ang II receptor blockers (ARBs), inhibits the multi-factorial effects of Ang II and reduce the frequency of cardiovascular events as observed in the HOPE and LIFE studies [58, 66, 67]. The RAAS associated with insulin resistance and sympathetic nerve activation plays an important role of hypertension in type 2 diabetes. Sympathetic nervous activation Energy intake stimulates hyperinsulinemia and sympathetic nerve activity resulting in blood pressure elevation..
Insulin-mediated sympathetic nerve stimulation in obese subjects is a compensatory mechanism aimed at restoring the energy balance by increasing the metabolic rate [22, 30]. During weight loss studies, reductions in plasma norepinephrine followed by reductions in HOMA-IR were observed [33, 34, 53]. These observations show, at least, that the sympathetic nervous system activity associated with insulin resistances play a major role in the onset and development of hypertension with type 2 diabetes associated with obesity.
Lifestyle modification for weight loss Weight loss is recommended as the first-line treatment for obesity-induced hypertension and type 2 diabetes.
The objective of treatment for obesity is both to reduce the high risk of cardiovascular events and to prevent the developments of hypertension and type 2 diabetes [68].
A limited number of epidemiological studies have shown that intentional weight loss and fat loss may reduce the all-cause mortality rate [69].
The US Diabetes Prevention Program [70]and the Oslo Diet and Exercise Study [71] have shown marked clinical benefits with lifestyle intervention, and modest weight loss, on the resolution of the metabolic syndrome and type 2 diabetes.
Cohort studies with lifestyle modifications [72] and case control studies with bariatric surgeries [73, 74] provide some evidence that intentional weight loss has long-term benefits on all cause mortality in overweight adults.
In a cohort of patients enrolled in a cardiac rehabilitation program, weight loss was associated with favourable long-term outcomes on the composite end-point of mortality and acute cardiovascular events (fatal and nonfatal myocardial infarction, fatal and nonfatal stroke, emergent revascularization for unstable angina pectoris, and congestive heart failure) [75]. Maintaining weight loss is often the greatest challenge, but, many clinical studies have demonstrated that weight loss associated with life-style modification adds to the efficacy of antihypertensive pharmacological treatment [11].Ribeiro et al. Bariatric surgery Gastric bypass and adjustable gastric banding are the two most commonly performed bariatric procedures for the treatment of morbid obesity or obesity which is resistant to lifestyle modification such as a low caloric diet plus exercise.
The percent of excess weight loss at 4 years was higher in the gastric bypass group compared to the gastric banding group.
Concurrent with restoration of insulin sensitivity and decreases in plasma leptin were dramatic decreases in skeletal muscle transcript levels of stearoyl coenzyme-A desaturase and pyruvate dehydrogenase kinase-4 at 3 and 9 months after gastric banding and a significant decrease in peroxisome proliferation activated receptor-alpha-regulated genes at 9 months. Improvements in glucose metabolism and insulin resistance following bariatric surgery result in the short-term from decreased stimulation of the entero-insular axis by restricted calorie intake and in the long-term by decreased fat mass resulting changes in release of adipocytokines. Leptin levels drop and adiponectin levels rise following laparoscopic adjustable gastric banding, gastric bypass and biliopancreatic diversion. All forms of weight loss surgery (bariatric surgery) lead to calorie restriction, weight loss, decrease in fat mass, improvement in insulin resistance and type 2 diabetes mellitus [84]. Left ventricular relaxation impairment, assessed by tissue Doppler imaging, normalized 9 months after surgery [85].
Laparoscopic gastric bypass and gastric banding are both safe and effective approaches for the treatment of morbid obesity, but gastric bypass surgery seems to have better early weight loss and more rapid ameliorative effects on insulin resistance and adipocytokines, muscle metabolism and left ventricular function, however effects the long term effects with similar sustained weight loss are unknown.
Pharmacological treatments for obesity (Orlistat, Sibtramine, and Rimonabant-Currently withdrawn in Europe, United States and Australia)Pharmacological treatment for the management of obesity is primarily aimed at weight loss, weight loss maintenance and risk reduction. Anti-obesity agents decrease appetite, reduce absorption of fat or increase energy expenditure.
Recently, anti-obesity drugs such as orlistat, sibtramine and rimonabant have been developed placed on markets, however, the latter two were withdrawn from markets in Europe and in the United States due to serious adverse events including psychiatric and cardiovascular related concerns. Lorcaserin, taranabant, topiramate and bupropion with naltrexone are currently on phase III trials with demonstrated significant weight loss compared to placebo at more than 12 months. Some pharmacotherapies have also demonstrated clinical benefits without any side effects, however, further studies are required for a long-term safety [86]. Recently, contrave, a combination of two approved drugs of bupropio and naltrexone, completed Phase III trials with significant weight loss and was approved by FDA in 2010, but FDA declined to approve contrive due to serious cardiovascular adverse events in 2011 [86]. Importantly, obesity is, at least, in part, determined by genetic backgrounds [87], suggesting that a genetic approach to limiting obesity may find a place in the future. Although treatment with PEG-OB protein led to a significantly greater body weight loss, energy expenditure, and dietary restraint, weight regain (rebound) was faster and stronger in subjects treated with PEG-OB compared to placebo.
Further, an additional ameliorative effect on anxiety was found with leptin administration. PEG-OB protein may theoretically work on human for weight loss, however, at this juncture there are few clinical studies available. Pharmacological treatments for the metabolic syndrome as a precursor of type 2 diabetesThe metabolic syndrome, which may be considered to be the precursor of type 2 diabetes,increases the risk of cardiovascular and renal events in hypertension. It has been associated with a wide range of classical and new cardiovascular risk factors as well as with early signs of subclinical cardiovascular and renal damage. It should be noted that other definitions of metabolic syndrome focus more on insulin resistance and its key role in this syndrome [22] (Table 2). Metformin has been shown to be helpful in subjects with metabolic syndrome or diabetes [92].
Before treatment, there were no significant differences between the metformin group and control group in terms of anthropometric data, metabolic parameters, and blood pressure levels. With regards to insulin sensitivity indices between the metformin treated and control groups, the metformin group displayed significantly improved metabolic control at the end of the study.
These findings show the efficacy of metformin for obesity and insulin resistance (metabolic syndrome) in obese adolescents. While metformin has also been shown to prevent weight gain and improve blood glucose levels in hypertensive patients who received combination therapy of calcium antagonist (nitrendipine) and beta-blocker (atenolol) [94], in combination with drugs blocking the rennin-angiotensin system (ACEI or ARB), metformin may be associated with lactic acidosis and acute renal failure in patients with reduced renal function [95]. Whilst thiazolidinedione drugs (TZDs) may prove useful in the metabolic syndrome, or type 2 diabetes, a large concern has been expressed over the cardiovascular risks associated with rosiglitazone and pioglitazone [96]. The findings extend the evidence provided further support to data derived from clinical trials that suggested that the disadvantages or harm caused by TZDs, especially rosiglitazone, may outweigh their benefits in patients with type 2 diabetes due to high risk for cardiac events.
In addition, although the glycemic efficacy of TZDs are comparable to metformin, adverse effects and higher costs make TZDs less appealing for initial therapy. In combination with metformin, pioglitazone may be particularly beneficial for patients with metabolic syndrome and diabetes. In those patients who are achieving glycemic goals and tolerating the therapy without apparent complications, rosiglitazone may be continued [97]. Pioglitazone, but not metformin, in patients with type 2 diabetes significantly reduced hepatic lipid and increased adiponectin independent of weight change [98]. Pharmacological treatments for hypertension (Figure 3) Although diabetes mellitus is associated with increased risks of death and cardiovascular events, in the Framingham Heart Study much of this excess risk wass attributable to coexistent hypertension [99]. Tight control of blood pressure (BP) significantly reduces cardiovascular morbidity and mortality in hypertensive patients with diabetes. In the United Kingdom Prospective Diabetes Study [100], a 10 mmHg reduction in systolic blood pressure was superior to a 0.7% decrease in glycosylated haemoglobin A1c (HbA1c) with regards to reducing morbidity and mortality [101]. In the Hypertension Optimal Treatment Study [102, 103], the risk of cardiovascular events was decreased by 51% in those patients with type 2 diabetes randomized to the lower BP level.
The HOT study demonstrated that monotherapy was successful in only 25-40% of patients, according to the target diastolic blood pressure in diabetic patients, and they wee needed at least 2 drugs, average 2.5-3 additional antihypertensive drugs to control blood pressure. Prospective, randomized studies with antihypertensive drugs have demonstrated differences between classes of drugs regarding effects on insulin resistance. In a recent study, data indicated that moxonidine, an imidazoline1 receptor agonist, was effective in lowering blood pressure and improving insulin sensitivity in insulin-resistant patients.

In populations at high risk of diabetes development, it may be justified to select drugs that improve insulin sensitivity when treating hypertension in insulin-resistant individuals [109].The most important factor for choosing antihypertensive medications for hypertensive patients with diabetes is the prevention of the progression of renal damage [105, 110], which impacts drastically on mortality and morbidity in diabetic patients. Experience from clinical trials suggests that drugs that target the RAAS may have metabolic advantages over drugs such as beta-blockers and diuretics, but this conclusion has not been proved definitively. The number of antihypertensive medications needed for blood pressure control in patients with diabetes is largely dependent on the estimated glomerular filtration rate (renal function) rather than hyperglycemia control [110]. Angiotensin-Converting Enzyme inhibitors (ACE inhibitors) The stimulation of the RAAS is a key factor in the development of hypertension in obesity. Pharmacological blockade of the RAAS not only improve blood pressure, but also has a beneficial effect on inflammation, oxidative stress, insulin sensitivity, glucose homeostasis, and resultant renal and cardio-protection. Several strategies are available for RAAS blockade, including angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin II receptor blocker (ARBs), renin inhibitors (Aliskiren) and mineralocorticoid-receptor blockers, which have been proven in the clinical studies to result in improvements in cardiovascular disease and chronic kidney disease outcomes. Likewise, while hypertension in obesity, metabolic syndrome or type 2 diabetes, benefits from therapeutic lifestyle change, recently, clinical and epidemiological studies have shown that ACE inhibitors and ARBs are highly efficacious, persistent and well-tolerated antihypertensive agents, due to their cardio-and renal-protective benefits [58, 66, 67].
Moreover they have further beneficial effects in preventing complications of obesity and diabetes, such as progression of diabetic nephropathy, metabolic syndrome. In other words, the use of the RAAS blockers as initial treatment (both ARBs and ACEIs) in several cardiovascular, metabolic, obesity, and renal disorders (i.e. The Heart Outcomes Prevention Evaluation (HOPE) study established that the significant effect of ACE inhibition (ramipril) on cardiovascular morbidity and mortality occurred through mechanisms beyond pure blood pressure control [58, 66]. Additionally, a recent analysis from the Blood Pressure Lowering Treatment Trialist's Collaboration showed that ARBs-based and ACE inhibitors -based treatment regimens were comparable in terms of the odds ratio for stroke and heart failure, independent of blood pressure reduction [111].
There is an emerging body of evidence suggesting that a combination approach to RAAS blockade with an ARB and an ACE inhibitor may further improve cardiovascular outcomes compared with mono-therapy with either agent alone [67]. In addition, some but not all clinical studies have shown that ACE inhibitors exert a favourable effect on insulin resistance [41, 49], lower plasma leptin, suppress the sympathetic nervous overactivity in obesity [11] and provide renal protection especially in diabetic patients with renal injury [43]. The sympathetic inhibition, however, is much less than that achieved with centrally acting imidazoline anti-hypertensive agents. Therefore, ACE inhibitors have s been recommended for use in special patients such as those with obesity, metabolic syndrome, diabetes, renal injury, or high risk of cardiovascular disease before the developments of ARBs [112].
Angitension II receptor blockers (ARBs)The Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) program compared the efficacy of the angiotensin II receptor blocker (ARB) telmisartan, the angiotensin-converting enzyme (ACE) inhibitor ramipril, and combination therapy with telmisartan plus ramipril for reducing cardiovascular events [115, 116].
The ONTARGET trial involved 25,588 high-risk cardiovascular or diabetic patients with organ damage and compared the effectiveness of telmisartan with that of ramipril and showed that the two drugs were 'therapeutically equivalent'. Telmisartan is now the only ARB with clinical trial evidence of cardiovascular protection equivalent to that of ramipril, which is widely regarded as the 'reference' drug for RAAS blockade in patients at increased cardiovascular risk [116, 117].
The ONTARGET program consists of 2 randomized, double-blind, multicenter international trials: the principal trial, ONTARGET, and a parallel trial, Telmisartan Randomized Assessment Study in ACE-I Intolerant Patients with Cardiovascular Disease (TRANSCEND) [115]. Results of ONTARGET and the TRANSCEND have allowed us to better define the therapeutic approach in high-risk patients showing the favorable effects of either ramipril or telmisartan on blood pressure control and cardiovascular risk [115]. The results of the ONTARGET and TRANSEND studies in patients with high risk cardiovascular disease as well as a number of recent meta-analyses of randomized trials comparing the efficacy and safety of ACE inhibitors to ARBs and their combination in patients with heart failure, hypertension, and chronic kidney disease focused attention on the RAAS. Emerging data from experimental studies indicates a variety of beneficial effects of telmisartan [118]. In addition to blocking the angiotensin II type 1 receptor, telmisartan activates the peroxisome proliferator-activated receptor (PPAR)-gamma, a well-known target for treatment of the metabolic syndrome and diabetes.
Few studies have analysed intra-class differences in ARBs with respect to anti-diabetic or metabolic effects. Telmisartan decreased body weight while increasing serum adiponectin levels in hypertensive patients with glucose intolerance. Renin inhibitorsRecent pharmaceutical developments have shown that direct inhibition ofrenin results in decreased angiotensin I and II production and decreased urinary aldosterone excretion. Like ACE inhibitors and ARBs, treatment with a direct renin inhibitor increases plasma renin concentration, but unlike the other RAAS inhibitors, treatment with a direct renin inhibitor decreases plasma renin activity. This unique combination of effects on the RAAS makes a direct renin inhibitor an attractive option to combine with other antihypertensive agents for the management of hypertension and its comorbidities [124]. Clinical studies [126-128] including the ACTION study [125] have shown that combining aliskiren, with drugs representing each of the major classes of antihypertensive agents (thiazide diuretics, beta blockers, ACE inhibitors, ARBs, and CCBs) reduces blood pressure and improves markers of cardiovascular outcomes. Importantly, aliskiren had an ameliorative effect on insulin resistance in type 2 diabetic mice [46]. In patients with type 2 diabetes, hypertension and albuminuria, aliskiren improved proteinuria [130]. Results of several ongoing randomized clinical trials should provide additional insights into the potential of therapeutic combinations that include aliskiren to improve cardiovascular morbidity and mortality in patients with hypertension and related comorbidities. These studies have provided some further insight into the most effective strategy to prevent the adverse effects of RAAS activation. Calcium Channel Blockers (CCBs)Calcium channel blockers (CCBs), especially newer long-acting dihydropyridines, may provide favourable metabolic effects by improving insulin sensitivity [49, 132, 133] and dampening the RAAS and sympathetic nervous activation in diabetes patients [47-49]. ACCOMPLISH (The Avoiding Cardiovascular events through COMbination therapy in Patients LIving with Systolic Hypertension) trial was designed in order to evaluate the indications for CCBs [108, 132-135]. The AMANDHA Study [136] compared the effects on albuminuria between manidipine and amlodipine, as an additional medication on RAAS blockers. Thus, the addition of manidipine, but not amlodipine, resulted in a large reduction in the urinary albumin excretion rate despite similar blood pressure reductions [136].
In addition, sub-studies to The International Nifedipine GITS study, Intervention as a Goal in Hypertension Treatment (INSIGHT), showed that nifedipine GITS was significantly more effective at preventing an increase in intima-media thickness in the carotid artery and significantly slowed the progression of coronary calcification, compared with diuretics, oamilozide, which are frequently observed in diabetes and atherosclerotic c patients [138]. The results from INSIGHT support incorporating nifedipine GITS in the management of high-risk hypertensive patients to prevent atherosclerosis-related illness and death [138].
These observations suggest CCBs has an ameliorative effects on atherosclerotic damage.Interestingly, in the Valsartan Antihypertensive Long-Term Use Evaluation (VALUE) trial, the risk of new-onset diabetes was reported to be 23% lower among patients initiating therapy with valsartan versus amlodipine [139]. Thus, CCBs may have benefits for treatments for hypertension in type 2 diabetes due to an ameliorative effect on insulin resistance and reductions in new-onset of type 2 diabetes.
Imidazoline-receptor agonists (moxonidine)Class differences in the effects of antihypertensive agents on metabolic indices may therefore be an important consideration when choosing treatment for patients who exhibit these characteristics [109].
Moxonidine, which selectively targets imidazoline type-1 receptors in the sympathetic vasomotor centres of the rostral-ventrolateral medulla, is an effective antihypertensive and has been reported to exert favourable metabolic effects in preclinical and clinical studies [141].
In obese hypertensive rats, chronic, but not acute, moxonidine treatment partially restored insulin sensitivity [142].
Moxonidine reduced blood pressure associated with insulin sensitivity in obese hypertensive patients [143]. Moreover, although moxonidine and amlodipine were associated with comparable reductions in blood pressure, only moxonidine significantly decreased sympathetic nervous activity, improved insulin resistance and reduced plasma leptin levels [144]. A small dosage of moxonidine was effective to lowering blood pressure when it was used as a combination therapy with low-dose hydrochlorothiazides in hypertension with type 2 diabetes [145]. The MARRIAGE study (Moxonidine And Ramipril Regarding Insulin And Glucose Evaluation) has extended these preliminary observations by comparing the effects of moxonidine and the ACE inhibitor ramipril--and the combination of both drugs--on metabolic and haemodynamic parameters in patients with hypertension and impaired fasting glycaemia [146].
Both moxonidine and rilmenidine, were shown to exert beneficial effects, not only on blood pressure, but also lipid (reducing free fatty acids, triglycerides) [147, 148] and carbohydrate metabolism (improving glucose tolerance), and neurohormonal parameters such as plasma levels of norepinephrine, leptin, BNP, and ANP [149]. Moxonidine and rimenidine activates I1 receptors in the RVLM, reducing the activity of the sympathetic nervous system [150, 151]. These I1-agonists have been shown to produce pronounced and long-lasting BP reduction in different animal models of hypertension, including the spontaneously hypertensive rats [152, 153]. Blood pressure reduction with moxonidine is usually accompanied by a reduction in heart rate which, however, is of shorter duration and lesser magnitude compared to the blood pressure reduction.
Chronic administration of moxonidine to SHRs causes normalization of the heart and kidney damage (myocardial fibrosis, capillarization, regressive changes in myocytes, ventricular arrhythmia, left ventricular hypertrophy and renal glomerulosclerosis) in parallel with the reduction of blood pressure [152, 153]. Direct injection of moxonidine into the vertebral artery of cats elicits a more pronounced fall in blood pressure compared with intravenous injection of an equivalent dose, indicating the centrally origins of the antihypertensive effects [153]. In addition, drugs of this class appear to have the capacity to favorably modify insulin sensitivity, which has particular relevance in the treatment of hypertensive diabetic patients and obese hypertensive patients who may be insulin resistant. In the hypertension accompanying maturity onset diabetes and obesity, with recent recommendations from advisory bodies setting lower BP goals, and with these lower targets often being reached only with combinations of antihypertensive agents, it is advisable that all drugs used in combination therapy exert a favorable, or at least a neutral effect on insulin resistance.Sharma et al.
A post-marketing surveillance study (CAMUS) involving 772 obese hypertensive patients with hypertension with and without the metabolic syndrome was conducted in Germany.
Approximately 50% of subjects had metabolic syndrome and patients were treated with moxonidine and followed for 8 weeks. After 8 weeks of treatment, patients achieved a mean weight loss of 1.4 kg, which was not surprisingly, particularly pronounced in obese patients. Moxonidine effectively reduced blood pressure in patients with the metabolic syndrome while simultaneously reducing body weight in obese patients.In a study examining 77 obese hypertensive patients, Haenni et al. Moxonidine significantly reduced arterial plasma epinephrine and norepinephrine concentrations, orthostatic venous plasma norepinephrine and plasma insulin and leptin levels 120 minutes subsequent to an oral glucose loading, whereas amlodipine did not change any of those parameters. This study clearly demonstrated a comparable reduction in blood pressure with both antihypertensive drugs, but the neurohormonal and metabolic effects were different between the antihypertensive drugs.
Low dose diuretics Low-dose of diuretics as a first agent in treatment of patients with hypertension and diabetes is well documented and widely recommended [156-160].
This treatment has beneficial effects on both morbidity and mortality while, previous general concern on the negative impact of diuretics on the different lipid parameters and metabolic effects appear not justified as, all long-term studies with low-dose diuretics have not been shown to affect lipid and glucose profiles in a negative way [161-163]. Moreover, in studies of a year or more duration, diuretics have been shown to reduce cardiovascular risk [145, 164-166]. Very recently, it was reported that Chlorthalidone reduced cardiovascular events more than Hydrochlorothiazide, suggesting that Chlorthalidone may be the preferred thiazide-type diuretics for hypertension in patients at a high risk of cardiovascular risk such as in diabetic or obese patients [167]. Combination therapies The clinical combination of hypertension and diabetes carries a particular poor diagnosis. Thus, management of subjects with type 2 diabetes and associated hypertension needs to be early and aggressive, and must utilize a global approach.

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