The Impact of ACE Inhibitors or Angiotensin II Type 1 Receptor Blockers on the Development of New-Onset Type 2 Diabetes

Gillespie, Effie L.; White, C. Michael; Kardas, Michael J.; Lindberg, Michael; Coleman, Craig I.

doi:10.2337/diacare.28.9.2261

Cited by 200 publications

(139 citation statements)

References 22 publications

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“…In a recent meta-analysis of the randomized, controlled, clinical trials using ACEI or ARB to prevent new-onset type 2 diabetes as a primary or secondary end point, it was concluded that ACEI and ARB have a significant ability to reduce the occurrence of new-onset type 2 diabetes among patients with hypertension, coronary artery disease, and heart failure (39).…”

Section: Discussionmentioning

confidence: 99%

Insulin Resistance, Inflammatory Biomarkers, and Adipokines in Patients with Chronic Kidney Disease

Vinuesa

Goicoechea

Kanter

et al. 2006

Journal of the American Society of Nephrology

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Patients with chronic kidney disease (CKD) present a high prevalence of insulin resistance (IR). Some studies suggest that angiotensin II may influence some cellular pathways that contribute to the pathogenesis of IR and stimulate the release of proinflammatory cytokines. Fifty-two patients who had stages 3 and 4 CKD and no diabetes were administered an angiotensin receptor blocker (ARB), olmesartan (40 mg), for 16 wk. Before and after ARB treatment, metabolic and inflammatory parameters and adipokines were measured. IR was calculated by Homeostasis Model Assessment (HOMA) index. Baseline data were compared with data that were obtained from 25 healthy control individuals of similar age and normal renal function. Compared with control subjects, patients with CKD presented significantly higher BP and waist circumference, higher triglycerides and lower HDL levels, higher insulin levels, and higher mean HOMA index (6.0 ؎ 2.7 versus 2.9 ؎ 2.2 U/ml ؋ mmol/L; P < 0.001). In addition, patients with CKD had increased levels of high-sensitivity C-reactive protein, TNF-␣, and IL-6. In patients with CKD, leptin was positively correlated to abdominal obesity, insulin levels, and IL-6, and adiponectin was inversely correlated to abdominal obesity and insulin levels. Olmesartan treatment resulted in a significant decrease of BP, urinary protein excretion, plasma glucose (99 ؎ 16 versus 92 ؎ 14 mg/dl; P < 0.05), insulin (23.1 ؎ 8.8 versus 19.9 ؎ 9; P < 0.05), HOMA index (6.0 ؎ 2.7 versus 4.7 ؎ 2.8; P < 0.05), and glycated hemoglobin (5.33 ؎ 0.58 versus 4.85 ؎ 0.81%; P < 0.01). At the same time, there was a significant reduction of high-sensitivity C-reactive protein levels, from 4.45 mg/L (2.45 to 9.00) to 3.55 mg/L (1.80 to 5.40; P < 0.05) and fibrinogen (412 ؎ 100 versus 370 ؎ 105 mg/dl; P < 0.05). There were no significant differences in adipokine levels after olmesartan treatment. These data demonstrate that patients with CKD have a high prevalence of IR, metabolic syndrome, and chronic inflammation and that the administration of the ARB olmesartan improves IR and inflammation markers in these patients. Plasma adipokine levels that are related to several metabolic risk factors in patients with CKD were not modified by ARB therapy.

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Section: Discussionmentioning

confidence: 99%

Insulin Resistance, Inflammatory Biomarkers, and Adipokines in Patients with Chronic Kidney Disease

Vinuesa

Goicoechea

Kanter

et al. 2006

Journal of the American Society of Nephrology

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Section: Raas Inhibition In the Clinical Settingmentioning

confidence: 99%

“…[31][32][33] In addition, some studies suggest a beneficial influence of RAAS blockade on insulin resistance and glucose homeostasis. 31,34 Possible mechanisms responsible for the reduced incidence of diabetes in these trials include improvement in insulin mediated glucose uptake, enhanced endothelial function, increased nitric oxide activation, reduced inflammatory response, and increased bradykinin levels. 35 On the other hand, it has been established that MR antagonism favourably affects cardiovascular outcomes in the clinical setting, as has been established in the RALES (Randomized Aldactone Evaluation Study) and EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study) trials.…”

Section: Raas Inhibition In the Clinical Settingmentioning

confidence: 99%

Role of aldosterone and angiotensin II in insulin resistance: an update

Lastra-Lastra

Sowers

Restrepo-Erazo

et al. 2009

Clinical Endocrinology

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SummaryThe role of the Renin-Angiotensin-Aldosterone system (RAAS) on the development of insulin resistance and cardiovascular disease is an area of growing interest. Most of the deleterious actions of the RAAS on insulin sensitivity appear to be mediated through activation of the Angiotensin II (Ang II) Receptor type 1 (AT 1 R) and increased production of mineralocorticoids. The underlying mechanisms leading to impaired insulin sensitivity remain to be fully elucidated, but involve increased production of reactive oxygen species and oxidative stress. Both experimental and clinical studies also implicate aldosterone in the development of insulin resistance, hypertension, endothelial dysfunction, cardiovascular tissue fibrosis, remodelling, inflammation and oxidative stress. There is abundant evidence linking aldosterone, through non-genomic actions, to defective intracellular insulin signalling, impaired glucose homeostasis and systemic insulin resistance not only in skeletal muscle and liver but also in cardiovascular tissue. Blockade of the different components of the RAAS, in particular Ang II and AT 1 R, results in attenuation of insulin resistance, glucose homeostasis, as well as decreased cardiovascular disease morbidity and mortality. These beneficial effects go beyond to those expected with isolated control of hypertension. This review focuses on the role of Ang II and aldosterone in the pathogenesis of insulin resistance, as well as in clinical relevance of RAAS blockade in the prevention and treatment of the metabolic syndrome and cardiovascular disease.

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“…Routine ACE inhibition in patients with diabetes before albuminuria may prevent nephropathy and be cost-effective/saving (62,63). More widespread use of ACE inhibition in the general hypertensive population over the longer run actually may prevent or at least delay new-onset diabetes (64). Younger black individuals who currently have low-normal GFR (60 to 80 ml/min per 1.73 m 2 ) especially with genetic/family risk and are identified through high-yield screening approaches may be critical to improving outcomes in this population (65).…”

Section: Failure Of Therapy and Future Of Ckdmentioning

confidence: 99%

The Chronic Kidney Disease Epidemic

Kiberd¹

2006

Journal of the American Society of Nephrology

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Estimating the prevalence of chronic kidney disease (CKD) is no simple task. The overall prevalence is relatively low but may be higher in select populations that are not accessible to surveys (e.g., certain ethnic groups, the sick or elderly). Moreover, the tests that define CKD lack precision and transportability to healthy populations. During the past decade, it is not clear that CKD has grown substantially. Some epidemiologic factors that are associated with CKD (obesity and diabetes) are increasing, whereas others (uncontrolled hypertension and smoking) are decreasing. Reasons for the discrepancy between a stable CKD population and ongoing ESRD growth remain speculative. There is evidence that ESRD rates may be stabilizing and that efforts to reduce progression in high-risk groups may be starting to show benefit. Expanding the definition of CKD and increasing detection may be required to reduce overall ESRD prevalence. One concern is that many of the well-defined high-risk patient groups (diabetes and black) are still undertreated. Increasing the investigation and treatment of low-risk patients may not be the answer. Clinical inertia (failure to initiate or change therapy) may be a more significant and modifiable barrier toward reducing ESRD, and this deserves increased attention. Furthermore, reducing CKD prevalence will require controlling the precipitating causes. The incremental benefit of detecting CKD in low-risk patients, use of expensive therapies in CKD, or new strategies such as the treatment of prehypertension require solid evidence, not only of the variety that shows benefit (hard end points) but also to whom, when, and at what cost.

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The Impact of ACE Inhibitors or Angiotensin II Type 1 Receptor Blockers on the Development of New-Onset Type 2 Diabetes

Cited by 200 publications

References 22 publications

Insulin Resistance, Inflammatory Biomarkers, and Adipokines in Patients with Chronic Kidney Disease

Insulin Resistance, Inflammatory Biomarkers, and Adipokines in Patients with Chronic Kidney Disease

Role of aldosterone and angiotensin II in insulin resistance: an update

The Chronic Kidney Disease Epidemic

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