title: GIP: no longer the neglected incretin twin?
abstract: In the design of therapeutics to treat type 2 diabetes, researchers have exploited the observation that oral ingestion of nutrients leads to the secretion of glucose homeostasis-regulating incretin hormones (for example, glucagon-like-peptide-1) from the gut. Here, we discuss two recent papers that suggest that the "other" incretin hormone, gastric inhibitory polypeptide (GIP), also is important in the regulation of glucose homeostasis. These findings warrant further studies to unravel the mechanism of action of GIP in β-cells of the endocrine pancreas and to evaluate the possibility of designing novel therapeutics that target both incretin hormones.
authors.affiliation: Islet Cell Biology and Regenerative Medicine, Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, MA 02215, USA. Rohit.Kulkarni@joslin.harvard.edu
authors.forename: Rohit N
authors.initials: RN
authors.lastname: Kulkarni
mesh_terms: D000818:Animals; D001786:Blood Glucose; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D005749:Gastric Inhibitory Polypeptide / Q000378:metabolism*; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism; D006801:Humans; D054795:Incretins / Q000378:metabolism*; D050417:Insulin-Secreting Cells / Q000378:metabolism; D008954:Models, Biological
chemical_list: D001786:Blood Glucose; D054795:Incretins; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1