Copyright
©The Author(s) 2023.
World J Diabetes. May 15, 2023; 14(5): 549-559
Published online May 15, 2023. doi: 10.4239/wjd.v14.i5.549
Published online May 15, 2023. doi: 10.4239/wjd.v14.i5.549
Figure 2 Intracellular mechanism of incretin hormones.
The binding of glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 with their respective receptors increase cyclic adenosine monophosphate and activation of protein kinase A. This result in the increase of Ca2+ levels, mediating the fusion of insulin-containing granules with the plasma membrane and insulin secretion from pancreatic β cells. ATP: Adenosine triphosphate; cAMP: Cyclic adenosine monophosphate; Ca2+: Calcium; [Ca2+]i: Calcium influx; EPAC2: Exchange protein activated by cAMP2; GIPR: Glucose-dependent insulinotropic polypeptide receptor; GLP-1R: Glucagon-like peptide-1 receptor; KATP-channel: ATP-sensitive potassium channel; K+: Kalium; PKA: Protein kinase A; VDCC: Voltage-gated calcium channels.
- Citation: Wibawa IDN, Mariadi IK, Somayana G, Krisnawardani Kumbara CIY, Sindhughosa DA. Diabetes and fatty liver: Involvement of incretin and its benefit for fatty liver management. World J Diabetes 2023; 14(5): 549-559
- URL: https://www.wjgnet.com/1948-9358/full/v14/i5/549.htm
- DOI: https://dx.doi.org/10.4239/wjd.v14.i5.549