Posts in the category Publications

02/04/2013

Autophagy. 2013 Feb 4 ; 9(4)
Improvement of ER stress-induced diabetes by stimulating autophagy.
Bachar-Wikstrom E, Wikstrom JD, Kaiser N, Cerasi E, Leibowitz G.
Source:
Endocrinology and Metabolism Service; Department of Medicine; Hadassah-Hebrew University Medical Center; Jerusalem, Israel.
Abstract:
Pancreatic β-cell dysfunction is central in diabetes. The diabetic milieu may impair proinsulin folding, leading to β-cell endoplasmic reticulum (ER) stress and apoptosis, and thus a worsening of the diabetes. Autophagy is crucial for the well-being of the β-cell; however, the impact of stimulating autophagy on β-cell adaptation to ER stress is unknown. We studied the crosstalk …

12/28/2012

Diabetes. 2012 Dec 28
Stimulation of Autophagy Improves Endoplasmic Reticulum Stress-Induced Diabetes.
Bachar-Wikstrom E, Wikstrom JD, Ariav Y, Tirosh B, Kaiser N, Cerasi E, Leibowitz G.
Source:
Endocrinology and Metabolism Service, Department of Medicine, Hadassah Medical Center, Jerusalem, Israel.
Abstract:
Accumulation of misfolded proinsulin in the β-cell leads to dysfunction induced by endoplasmic reticulum (ER) stress, with diabetes as a consequence. Autophagy helps cellular adaptation to stress via clearance of misfolded proteins and damaged organelles. We studied the effects of proinsulin misfolding on autophagy and the impact of stimulating autophagy on diabetes progression in Akita mice, …

04/27/2011
Comments to Lee et al: Glucagon receptor knockout prevents insulin-deficient type 1 diabetes in mice.

Diabetes 60:391-397, 2011.
Accumulating evidence during the last several decades has suggested that glucagon is of key importance for diabetes hyperglycemia. Thus, patients with type 2 diabetes have hyperglucagonemia and increased hepatic glucose output, and the hyperglycemia seems to be caused by a defective suppression of glucagon during hyperglycemia (1). A recent experimental study by Lee and collaborators examined the role of glucagon in mice with type 1 diabetes induced by streptozotin (2). They approached this aim by using a mouse model with genetic deletion of the glucagon receptors. This model …

04/27/2011
Comments to Bagger et al: Impaired regulation of the incretin effect in patients with type 2 diabetes.

J Clin Endocrinol Metab 96:737-745 (2011)
The incretin effect is defined as the augmented insulin secretion after oral versus intrave-nous glucose administration and is due to the release from the gut of the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) after oral glucose; these incretin hormones augment glucose-stimulated insulin secretion (1). The incretin function is of key importance for normal glucose levels after oral glucose. It has also been shown that the incretin effect is impaired in type 2 diabetes (2). This is mainly due to impaired action …

03/30/2011
Metformin: what cellular target?

Metformin, discovered in the 1920s appeared on the market in 1957. It belongs to one of the major families of products acting on insulin resistance in patients suffering from type 2 diabetes.
The target of its action is the mitochondrion1, more specifically complex 1, the entry point of NADH reduction which allows preservation of the proton gradient required for ATP production at the level of the mitochondrial membrane. However, the molecular target of metformin within complex 1 remains unknown.
Metformin is considered to have as a dominant cell action …