Sakeneh Zraika

Islet amyloid formation is an important determinant for inducing islet inflammation in high-fat-fed human IAPP transgenic mice.

Effects of sex and hormone replacement therapy use on the prevalence of isolated impaired fasting glucose and isolated impaired glucose tolerance in subjects with a family history of type 2 diabetes.

Superiority of the Modification of Diet in Renal Disease equation over the Cockcroft-Gault equation in screening for impaired kidney function in Japanese Americans.

Glucose- and time-dependence of islet amyloid formation in vitro.

Identification of the amyloid-degrading enzyme neprilysin in mouse islets and potential role in islet amyloidogenesis.

Relationship of liver enzymes to insulin sensitivity and intra-abdominal fat.

Inhibition of glycosaminoglycan synthesis and protein glycosylation with WAS-406 and azaserine result in reduced islet amyloid formation in vitro.

Body mass index is associated with increased creatinine clearance by a mechanism independent of body fat distribution.

β-cell loss and β-cell apoptosis in human type 2 diabetes are related to islet amyloid deposition.

Matrix metalloproteinase-9 reduces islet amyloid formation by degrading islet amyloid polypeptide.

Rosiglitazone treatment does not decrease amyloid deposition in transplanted islets from transgenic mice expressing human islet amyloid polypeptide.

Neprilysin deficiency protects against fat-induced insulin secretory dysfunction by maintaining calcium influx.

One year of sitagliptin treatment protects against islet amyloid-associated β-cell loss and does not induce pancreatitis or pancreatic neoplasia in mice.

Determination of Optimal Sample Size for Quantification of β-Cell Area, Amyloid Area and β-Cell Apoptosis in Isolated Islets.

Matrix Metalloproteinase-9 Protects Islets from Amyloid-induced Toxicity.

The S20G substitution in hIAPP is more amyloidogenic and cytotoxic than wild-type hIAPP in mouse islets.

Improved glycaemia in high-fat-fed neprilysin-deficient mice is associated with reduced DPP-4 activity and increased active GLP-1 levels.

High fat feeding unmasks variable insulin responses in male C57BL/6 mouse substrains.

Neprilysin Is Required for Angiotensin-(1-7)'s Ability to Enhance Insulin Secretion via Its Proteolytic Activity to Generate Angiotensin-(1-2).

Apoptosis Repressor With Caspase Recruitment Domain Ameliorates Amyloid-Induced β-Cell Apoptosis and JNK Pathway Activation.

Neprilysin Deficiency Is Associated With Expansion of Islet β-Cell Mass in High Fat-Fed Mice.

Neprilysin inhibition: a new therapeutic option for type 2 diabetes?