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Chromogranin A (CgA) peptide Catestatin (CST: hCgA\n                      <jats:sub>352\u2010372<\/jats:sub>\n                      ) improves glucose tolerance in insulin\u2010resistant mice. Here, we seek to determine whether CST induces hepatic glycogen synthesis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We determined liver glycogen, glucose\u20106\u2010phosphate (G6P), uridine diphosphate glucose (UDPG) and glycogen synthase (GYS2) activities; plasma insulin, glucagon, noradrenaline and adrenaline levels in wild\u2010type (WT) as well as in CST knockout (CST\u2010KO) mice; glycogen synthesis and glycogenolysis in primary hepatocytes. We also analysed phosphorylation signals of insulin receptor (IR), insulin receptor substrate\u20101 (IRS\u20101), phosphatidylinositol\u2010dependent kinase\u20101 (PDK\u20101), GYS2, glycogen synthase kinase\u20103\u03b2 (GSK\u20103\u03b2), AKT (a kinase in AKR mouse that produces Thymoma)\/PKB (protein kinase B) and mammalian\/mechanistic target of rapamycin (mTOR) by immunoblotting.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>CST stimulated glycogen accumulation in fed and fasted liver and in primary hepatocytes. CST reduced plasma noradrenaline and adrenaline levels. CST also directly stimulated glycogenesis and inhibited noradrenaline and adrenaline\u2010induced glycogenolysis in hepatocytes. In addition, CST elevated the levels of UDPG and increased GYS2 activity. CST\u2010KO mice had decreased liver glycogen that was restored by treatment with CST, reinforcing the crucial role of CST in hepatic glycogenesis. CST improved insulin signals downstream of IR and IRS\u20101 by enhancing phospho\u2010AKT signals through the stimulation of PDK\u20101 and mTORC2 (mTOR Complex 2, rapamycin\u2010insensitive complex) activities.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>CST directly promotes the glycogenic pathway by (a) reducing glucose production, (b) increasing glycogen synthesis from UDPG, (c) reducing glycogenolysis and (d) enhancing downstream insulin signalling.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.13775","type":"journal-article","created":{"date-parts":[[2022,1,5]],"date-time":"2022-01-05T08:06:39Z","timestamp":1641369999000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Catestatin induces glycogenesis by stimulating the phosphoinositide 3\u2010kinase\u2010AKT pathway"],"prefix":"10.1111","volume":"235","author":[{"given":"Gautam","family":"Bandyopadhyay","sequence":"first","affiliation":[{"name":"Department of Medicine University of California San Diego  La Jolla California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kechun","family":"Tang","sequence":"additional","affiliation":[{"name":"VA San Diego Healthcare System  San Diego California USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas J. 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