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Cytidine triphosphate:phosphocholine cytidylyltransferase-α (CTα) is the rate limiting enzyme in the major pathway for de novo phosphatidylcholine (PC) synthesis. When CTα is deleted specifically in intestinal epithelial cells of adult mice (CTα

Type 2 diabetes mellitus is a disorder characterized by insulin resistance and a relative deficit in insulin secretion, both of which result in elevated blood glucose. Understanding the molecular mechanisms underlying the pathophysiology of diabetes could lead to the development of new therapeutic approaches. An ever-growing body of evidence suggests that members of the NR4A family of nuclear receptors could play a pivotal role in glucose homeostasis. This review aims to present and discuss advances so far in the evaluation of the potential role of NR4A in the regulation of glucose homeostasis and the development of type 2 diabetes.

Insulin resistance and relative insulin deficiency contribute to the pathogenesis of type 2 diabetes. Defective insulin secretion from pancreatic β-cells results from the progressive deterioration of pancreatic β-cell mass and function. Glucagon-like peptide 1 (GLP-1), an incretin hormone secreted by intestinal L cells in response to a meal, improves glycemic control in patients with type 2 diabetes by addressing both the insulin secretion defect as well as the decline in β-cell mass. These observations fostered the development of new therapeutic agents targeting GLP-1 signaling. This review gives an overview our current knowledge of the molecular mechanisms by which GLP-1 enhances β-cell mass and function.