Pharmacological treatment of diabetes type 1 quiz,can a type 2 diabetic have ketoacidosis,gl ich logo - Good Point

Join tens of thousands of doctors, health professionals and patients who receive our newsletters. Diabetes, often referred to by doctors as diabetes mellitus, describes a group of metabolic diseases in which the person has high blood glucose (blood sugar), either because insulin production is inadequate, or because the body's cells do not respond properly to insulin, or both.
Patients with high blood sugar will typically experience polyuria (frequent urination), they will become increasingly thirsty (polydipsia) and hungry (polyphagia). In 2013 it was estimated that over 382 million people throughout the world had diabetes (Williams textbook of endocrinology). The most common diabetes symptoms include frequent urination, intense thirst and hunger, weight gain, unusual weight loss, fatigue, cuts and bruises that do not heal, male sexual dysfunction, numbness and tingling in hands and feet. If you have Type 1 and follow a healthy eating plan, do adequate exercise, and take insulin, you can lead a normal life. As the risk of cardiovascular disease is much higher for a diabetic, it is crucial that blood pressure and cholesterol levels are monitored regularly. As smoking might have a serious effect on cardiovascular health, diabetics should stop smoking.
Patients with type 1 diabetes will need to take insulin injections for the rest of their life.
Between 2001 and 2009, the prevalence of type 1 diabetes among the under 20s in the USA rose 23%, according to SEARCH for Diabetes in Youth data issued by the CDC (Centers for Disease Control and Prevention). The body does not produce enough insulin for proper function, or the cells in the body do not react to insulin (insulin resistance). Some people may be able to control their type 2 diabetes symptoms by losing weight, following a healthy diet, doing plenty of exercise, and monitoring their blood glucose levels. Overweight and obese people have a much higher risk of developing type 2 diabetes compared to those with a healthy body weight. Being overweight, physically inactive and eating the wrong foods all contribute to our risk of developing type 2 diabetes. Men whose testosterone levels are low have been found to have a higher risk of developing type 2 diabetes.
For more information on how type 1 and type 2 diabetes compare, see our article: the difference between type 1 and type 2 diabetes.
The majority of gestational diabetes patients can control their diabetes with exercise and diet.
Scientists from the National Institutes of Health and Harvard University found that women whose diets before becoming pregnant were high in animal fat and cholesterol had a higher risk for gestational diabetes, compared to their counterparts whose diets were low in cholesterol and animal fats. Studies have indicated that even at the prediabetes stage, some damage to the circulatory system and the heart may already have occurred. A person with diabetes has a condition in which the quantity of glucose in the blood is too elevated (hyperglycemia). In 1675, Thomas Willis added mellitus to the term, although it is commonly referred to simply as diabetes.
In ancient China people observed that ants would be attracted to some people's urine, because it was sweet.
Researchers from the Mayo Clinic Arizona in Scottsdale showed that gastric bypass surgery can reverse type 2 diabetes in a high proportion of patients. Patients with type 1 are treated with regular insulin injections, as well as a special diet and exercise.
Patients with Type 2 diabetes are usually treated with tablets, exercise and a special diet, but sometimes insulin injections are also required. If diabetes is not adequately controlled the patient has a significantly higher risk of developing complications. Ketoacidosis - a combination of ketosis and acidosis; accumulation of ketone bodies and acidity in the blood. Neuropathy - diabetic neuropathy is a type of nerve damage which can lead to several different problems. HHNS (Hyperosmolar Hyperglycemic Nonketotic Syndrome) - blood glucose levels shoot up too high, and there are no ketones present in the blood or urine.
Disclaimer: This informational section on Medical News Today is regularly reviewed and updated, and provided for general information purposes only. Please note that although you may feel free to cite and quote this article, it may not be re-produced in full without the permission of Medical News Today. Learn all about diabetes, a lifelong metabolism disorder that causes high blood sugar levels. Learn all about type 1 and type 2 diabetes and the differences between the two conditions in our article about the diabetes mellitus metabolism disorder. 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. Published May 16, 2013 at 595 × 254 in Oral and Injectable (Non-insulin) Pharmacological Agents for Type 2 Diabetes.
The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Hyperglycemia - when blood glucose is too high - can also have a bad effect on the patient.
Some people may refer to this type as insulin-dependent diabetes, juvenile diabetes, or early-onset diabetes. However, type 2 diabetes is typically a progressive disease - it gradually gets worse - and the patient will probably end up have to take insulin, usually in tablet form. People with a lot of visceral fat, also known as central obesity, belly fat, or abdominal obesity, are especially at risk. Drinking just one can of (non-diet) soda per day can raise our risk of developing type 2 diabetes by 22%, researchers from Imperial College London reported in the journal Diabetologia. Experts are not completely sure why, but say that as we age we tend to put on weight and become less physically active. Researchers from the University of Edinburgh, Scotland, say that low testosterone levels are linked to insulin resistance.
Some women have very high levels of glucose in their blood, and their bodies are unable to produce enough insulin to transport all of the glucose into their cells, resulting in progressively rising levels of glucose. Between 10% to 20% of them will need to take some kind of blood-glucose-controlling medications.
After eating, the pancreas automatically releases an adequate quantity of insulin to move the glucose present in our blood into the cells, as soon as glucose enters the cells blood-glucose levels drop. This is because the body either does not produce enough insulin, produces no insulin, or has cells that do not respond properly to the insulin the pancreas produces. Mel in Latin means "honey"; the urine and blood of people with diabetes has excess glucose, and glucose is sweet like honey.
They added that within three to five years the disease recurs in approximately 21% of them.
The materials contained within this guide do not constitute medical or pharmaceutical advice, which should be sought from qualified medical and pharmaceutical advisers.
Relationships between insulin resistance, sympathetic activation and stimulated renin-angiotensin-aldosterone system (RAA) in type 2 diabetes and hypertension. The blood glucose levels were measured each day and they could observe that mice with S961 became hyperglycaemic in a dose dependent manner. Comparison of three multiple injection regimens for Type 1 diabetes: morning plus dinner or bedtime administration of insulin detemir vs. The 12-month efficacy and safety of insulin detemir and NPH insulin in basal-bolus therapy for the treatment of type 1 diabetes. Long-term efficacy and safety of insulin detemir compared to neutral protamine Hagedorn insulin in patients with Type 1 diabetes using a treat-to-target basal-bolus regimen with insulin aspart at meals. Comparison of the subcutaneous absorption of insulin glargine (Lantus) and NPH insulin in patients with Type 2 diabetes. Fluctuation of serum basal insulin levels following single and multiple dosing of insulin glargine.
A randomized clinical trial comparing breakfast, dinner, or bedtime administration of insulin glargine in patients with type 1 diabetes.
Twice-daily compared with once-daily glargine in people with Type 1 diabetes using meal-time insulin aspart. Effect of continuous subcutaneous insulin infusion vs multiple daily insulin injection with glargine as basal insulin: an open parallel long-term study.
A one-year, randomized, multicentre trial comparing insulin glargine with NPH insulin in combination with oral agents in patients with type 2 diabetes. Insulin Glargine 4002 Study InvestigatorsThe treat-to-target trial: randomized addition of glargine or human NPH insulin to oral therapy of type 2 diabetic patients.
Costs analysis of type 2 diabetes mellitus treatment with glargine insulin or detemir insulin in Spain.
People usually develop type 1 diabetes before their 40th year, often in early adulthood or teenage years. The scientists believe that the impact of sugary soft drinks on diabetes risk may be a direct one, rather than simply an influence on body weight. Undiagnosed or uncontrolled gestational diabetes can raise the risk of complications during childbirth.
However, glucose cannot enter our cells without insulin being present - insulin makes it possible for our cells to take in the glucose. Yessica Ramos, MD., said "The recurrence rate was mainly influenced by a longstanding history of Type 2 diabetes before the surgery. IntroductionType 2 diabetes and hypertension are becoming a major worldwide health problem, besing associated with increasing prevalence of obesity and excess morbidity and mortality. Management of hyperglycemia in type 2 diabetes mellitus: a consensus algorithm for the initiation and adjustment of therapy. Time-action profile of the long-acting insulin analog insulin glargine (HOE901) in comparison with those of NPH insulin and placebo. Administration of neutral protamine Hagedorn insulin at bedtime versus dinner in type 1 diabetes mellitus to avoid nocturnal hypoglycemia and improve control. Pharmacokinetics and pharmacodynamics of subcuta­neous injection of long-acting human insulin analog glargine, NPH insulin, and ultralente human insulin and continuous subcutaneous infusion of insulin lispro. Lower within-subject variability of insulin detemir in comparison to NPH insulin and insulin glargine in people with type 1 diabetes. Albumin-bound basal insulin analogs (insulin detemir and NN344): comparable time-action profiles but less variability than insulin glargine in type 2 diabetes.
Pharmacokinetics and pharmacodynamics of the long-acting insulin analog glargine after one week of use as compared to its first administration in subjects with Type 1 diabetes mellitus. Comparison of pharmacokinetics and -dynamics of the long-acting insulin analogs glargine and detemir at steady state in type 1 diabetes mellitus: a double-blind, randomized, cross-over study. Pharmacokinetics of 125I-labeled insulin glargine (HOE 901) in healthy men: comparison with NPH insulin and the influence of different subcutaneous injection sites. Effects of exercise on the absorption of insulin glargine in patients with type 1 diabetes. The mechanism of protraction of insulin detemir, a long-acting, acylated analog of human insulin. Correlations of receptor binding and metabolic and mitogenic potencies of insulin analogs designed for clinical use.
Basal activity profiles of NPH and [Ne-palmitoyl Lys (B29)] human insulins in subjects with IDDM.
Comparison of the effects on glucose and lipid metabolism of equipotent doses of insulin detemir and NPH insulin with a 16-h euglycemic clamp.
Different brain responses to hypoglycemia induced by equipotent doses of the long-acting insulin analog detemir and human regular insulin in humans. Time-action profile of the soluble, fatty acid acy-lated, long-acting insulin analog NN304. Pharmacokinetic and pharmacodynamic properties of long-acting insulin analog NN304 in comparison to NPH insulin in humans.
A double-blind, randomized, dose-response study investigating the pharmacodynamic and pharmacokinetic properties of the long-acting insulin analog detemir. Time-action profile of insulin detemir and NPH insulin in patients with type 2 diabetes from different ethnic groups. Proportional dose-response relationship and lower within-patient variability of insulin detemir and NPH insulin in subjects with type 1 diabetes mellitus. Effects of the long-acting insulin analog insulin glargine on cultured human skeletal muscle cells: comparisons to insulin and IGF-I. Sustained signalling from the insulin receptor after stimulation with insulin analogs exhibiting increased mitogenic potency.
Insulin and its analogue glargine do not affect variability and proliferation of human coronary artery endothelial and smooth muscle cells. Comparison of the mitogenic potency of regular human insulin and its analogue glargine in normal and transformed human breast epithelial cells.

Proliferation of Colo-357 pancreatic carcinoma cells and survival of patients with pancreatic carcinoma is not altered by insulin glargine. Insulin activation of phosphatidylinositol 3-kinase in the hypothalamic arcuate nucleus: a key mediator of insulin-induced anorexia.
A 26-week, randomized, parallel, treat-to-target trial comparing insulin detemir with NPH insulin as add-on therapy to oral glucose-lowering drugs in insulin-naive people with type 2 diabetes. Insulin analogs (insulin detemir and insulin aspart) versus traditional human insulins (NPH insulin and regular human insulin) in basal-bolus therapy for patients with type 1 diabetes. Insulin detemir used in basal-bolus therapy in people with type 1 diabetes is associated with a lower risk of nocturnal hypoglycemia and less weight gain over 12 months in comparison to NPH insulin.
Similar progression of di­abetic retinopathy with glargine or NPH insulin in Type 2 diabetes [abstract 301-OR].
Early retinopathy progression in four randomized trials comparing insulin glargine and NPH insulin. In Type 1 diabetic patients with good metabolic control blood glucose variability is lower during continuous subcutaneous insulin infusion than during multiple daily injections with glargine.
Glycemic parameters with multiple daily injections using insulin glargine versus insulin pump.
Comparison of a multiple daily injection regimen with once-daily insulin glargine basal insulin and mealtime lispro, to continuous subcutaneous insulin infusion: a randomised, open, parallel study [abstract]. Insulin detemir under steady-state conditions: no accumulation and constant metabolic effect over time with twice daily administration in subjects with Type 1 diabetes.
Insulin detemir improves glycemic control with less hypoglycemia and no weight gain in patients with type 2 diabetes who were insulin naive or treated with NPH or insulin glargine: clinical practice experience from a German subgroup of the PREDICTIVE study. Insulin detemir is associated with more predictable glycemic control and reduced risk of hypoglycemia than NPH insulin in patients with type 1 diabetes on a basal-bolus regimen with premeal insulin aspart. Effects of QD insulin detemir or neutral protamine Hagedorn on blood glucose control in patients with type I diabetes mellitus using a basal-bolus regimen.
Comparison of the soluble basal insulin analog insulin detemir with NPH insulin: a randomized open crossover trial in type 1 diabetic subjects on basal-bolus therapy. A randomised, 52-week, treat-to-target trial comparing insulin detemir with insulin glargine when administered as add-on to glucose-lowering drugs in insulin-naive people with type 2 diabetes. Glucose is a form of sugar in the blood - it is the principal source of fuel for our bodies.
Furthermore, hypertensive patients with diabetes or obesity are more predisposed to target organ damage, resulting stringent targets for blood pressure control [1-4]. Basal insulin therapy in type 2 diabetes: 28-week comparison of insulin glargine (HOE 901) and NPH insulin. Less nocturnal hypoglycemia and better post-dinner glucose control with bedtime insulin glargine compared with bedtime NPH insulin during insulin combination therapy in type 2 diabetes. So, even though the blood has plenty of glucose, the cells are not getting it for their essential energy and growth requirements.
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). The Framingham Heart Study [8] demonstrated that diabetic subjects were at 2-fold higher risk mortality, comprising both cardiovascular and non-cardiovascular mortality.
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]. While proteins and enzymes such as cyclins, CDks and E2Fs, which promote cell proliferation, were observed to be over expressed, the inhibitory factors were seen to be repressed. 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.
This means that the treated b cells in mice are more prone to be proliferating than those of untreated. 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]. However, as the S961 is an antagonist for the insulin receptor, further study was necessary to see if it work directly on b cells or if there is other intermediates in this metabolic action. 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. Now, especially for hypertensive patients with diabetes and obesity, multiple-medications are common [168].

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