Effects of Treatment With Sulfonylurea Drugs or Insulin on Ischemia-Induced Myocardial Dysfunction in Type 2 Diabetes

Scognamiglio, R; Avogaro, Angelo; Kreutzenberg, Saula Vigili de; Negut, Christian; Palisi, Monica; Bagolin, E.; Tiengo, Antonio

doi:10.2337/diabetes.51.3.808

Cited by 89 publications

(48 citation statements)

References 39 publications

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“…These abnormalities were improved when myocytes were incubated with metformin, but glyburide had no beneficial effect (227). Finally, one experiment recently evaluated the relative functional cardiac effects of glyburide versus insulin (228). In this study of patients with type 2 diabetes, left ventricular function was measured by echocardiography after 12-week treatment periods with each agent, attaining similar metabolic control.…”

Section: Sulfonylureasmentioning

confidence: 99%

Management of Diabetes and Hyperglycemia in Hospitals

et al. 2004

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Section: Sulfonylureasmentioning

confidence: 99%

Management of Diabetes and Hyperglycemia in Hospitals

et al. 2004

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“…Thus, in certain populations with an increased incidence and prevalence of cardiovascular disease, treatments that may unexpectedly interfere with natural PC mechanisms (which would be triggered during transient premonitory episodes of ischemia, such as angina) could increase morbidity and mortality. Sulfonylureas are among the most widely used pharmaceuticals in the treatment of type 2 diabetes mellitus but have been associated with an unexpected and unexplained small increase in cardiovascular mortality in large epidemiology studies (57,58). Certain sulfonylureas are known to inhibit the mitoK ATP , and we have found that glibenclamide (the prototype first-generation sulfonylurea) can abolish the MPT protection of Dz as effectively as 5HD can (S.-H. Kim and S.J.…”

Section: Figure 10mentioning

confidence: 99%

Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore

Juhaszova¹,

Zorov²,

Kim³

et al. 2004

J. Clin. Invest.

246

311

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Environmental stresses converge on the mitochondria that can trigger or inhibit cell death. Excitable, postmitotic cells, in response to sublethal noxious stress, engage mechanisms that afford protection from subsequent insults. We show that reoxygenation after prolonged hypoxia reduces the reactive oxygen species (ROS) threshold for the mitochondrial permeability transition (MPT) in cardiomyocytes and that cell survival is steeply negatively correlated with the fraction of depolarized mitochondria. Cell protection that exhibits a memory (preconditioning) results from triggered mitochondrial swelling that causes enhanced substrate oxidation and ROS production, leading to redox activation of PKC, which inhibits glycogen synthase kinase-3β (GSK-3β). Alternatively, receptor tyrosine kinase or certain G protein-coupled receptor activation elicits cell protection (without mitochondrial swelling or durable memory) by inhibiting GSK-3β, via protein kinase B/Akt and mTOR/p70 s6k pathways, PKC pathways, or protein kinase A pathways. The convergence of these pathways via inhibition of GSK-3β on the end effector, the permeability transition pore complex, to limit MPT induction is the general mechanism of cardiomyocyte protection.

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“…Glibenclamide treatment affects ischemic preconditioning, exposing a possible higher risk of cardiovascular mortality in sulfonylurea-treated type 2 diabetic patients with myocardial infarction (44). In addition, myocardial function during ischemic challenge was found to be altered to a higher degree in glibenclamide-treated compared with insulintreated type 2 diabetic subjects (45).…”

Section: Adverse Effects Of Oral Hypoglycemicmentioning

confidence: 99%

Treatment of Type 2 Diabetes With Combined Therapy

Massi‐Benedetti

Orsini-Federici²

2008

Diabetes Care

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Type 2 diabetes is a progressive syndrome that evolves toward complete insulin deficiency during the patient's life. A stepwise approach for its treatment should be tailored according to the natural course of the disease, including adding insulin when hypoglycemic oral agent failure occurs. Treatment with insulin alone should eventually be considered in a relevant number of cases. Experience has shown the protective effects of insulin on ␤-cell survival and function, resulting in more stable metabolic control. On the contrary, treatment with most insulin secretagogues has been associated with increased ␤-cell apoptosis, reduced responsiveness to high glucose, and impairment of myocardial function during ischemic conditions. In addition, macrovascular complications are associated with postprandial hyperglycemia, indicating the need for tight glycemic control. Insulin treatment, especially with rapid-acting analogs, has been demonstrated to successfully control postprandial glucose excursions. Finally, a reason for concern with regard to combined therapy is represented by the evidence that polipharmacy reduces compliance to the treatment regimen. This can be particularly relevant in patients with type 2 diabetes usually taking drugs for complications and for concomitant diseases with consequent deterioration not only of metabolic control but also of other conditions. In conclusion, therapy with insulin alone immediately after hypoglycemic oral agent failure may be a useful and safe therapeutic approach in type 2 diabetes.Diabetes Care 31 (Suppl. 2):S131-S135, 2008

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Effects of Treatment With Sulfonylurea Drugs or Insulin on Ischemia-Induced Myocardial Dysfunction in Type 2 Diabetes

Cited by 89 publications

References 39 publications

Management of Diabetes and Hyperglycemia in Hospitals

Management of Diabetes and Hyperglycemia in Hospitals

Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore

Treatment of Type 2 Diabetes With Combined Therapy

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