<unk>  and diabetes<unk>  <unk>  is a 30- or 31-amino-acid-long<unk>  hormone deriving from the tissue-specific posttranslational processing of the proglucagon<unk> . It is produced and secreted by intestinal enteroendocrine L-cells and certain neurons within the nucleus of the solitary tract in the brainstem upon food consumption. The initial product<unk>  (1–37) is susceptible to amidation and proteolytic cleavage, which gives rise to the two truncated and equipotent biologically active forms,<unk>  (7–36) amide and<unk>  (7–37). Active<unk>  protein secondary structure includes two α-helices from amino acid position 13–20 and 24–35 separated by a linker region. Alongside glucose-dependent insulinotropic<unk>  (GIP),<unk>  is an incretin; thus, it has the ability to decrease blood sugar levels in a glucose-dependent manner by enhancing the secretion of insulin. Beside the insulinotropic effects,<unk>  has been associated with numerous regulatory and protective effects. Unlike GIP, the action of<unk>  is preserved in patients with type 2 diabetes and substantial pharmaceutical research has therefore been directed towards the development of<unk> -based treatment. Endogenous<unk>  is rapidly degraded primarily by dipeptidyl<unk> se-4 (DPP-4), as well as neutral endopeptidase 24.11 (NEP 24.11) and renal clearance, resulting in a half-life of approximately 2 minutes. Consequently, only 10–15 % of<unk>  reaches circulation intact, leading to fasting plasma levels of only 0–15 pmol/L. To overcome this,<unk>  receptor agonists and DPP-4 inhibitors have been developed to increase<unk>  activity. As opposed to common treatment agents such as insulin and sulphonylurea,<unk> -based treatment has been associated with weight loss and a lower risk of hypoglycemia, two important considerations for patients with type 2 diabetes.
Glucagon-like peptide-1
Incretin
Proglucagon
Delta-sleep-inducing peptide
Nesfatin-1
Glucagon 
Ghrelin
Histrelin