{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T14:00:11Z","timestamp":1758808811292},"reference-count":51,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,6,13]],"date-time":"2005-06-13T00:00:00Z","timestamp":1118620800000},"content-version":"vor","delay-in-days":12,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2005,6]]},"abstract":"<jats:p>Several recent reports using cell lines have suggested that both Akt and atypical protein kinase C (aPKC) \u03b6\/\u03bb are translocated to the plasma membrane (PM) in response to insulin. However, it has yet to be determined in skeletal muscle whether: (1) insulin increases PM\u2010associated Akt2, aPKC \u03b6 and\/or \u03bb protein concentration, (2) the activity of these kinases is altered by insulin at the PM, and (3) high fat feeding alters the insulin\u2010stimulated PM concentration and\/or activity of Akt2 and aPKC \u03b6\/\u03bb. Sprague\u2010Dawley rats were randomly assigned to either normal (<jats:italic>n<\/jats:italic>= 16) or high fat (<jats:italic>n<\/jats:italic>= 16) dietary groups. Following a 12 week dietary period, animals were subjected to hind limb perfusions in the presence (<jats:italic>n<\/jats:italic>= 8 per group) or absence (<jats:italic>n<\/jats:italic>= 8 per group) of insulin. In normal skeletal muscle, total PI3\u2010kinase, Akt2 and aPKC \u03b6\/\u03bb activities were increased by insulin. PM\u2010associated aPKC \u03b6 and \u03bb, and aPKC \u03b6\/\u03bb activity, but not Akt2 or Akt2 activity, were increased by insulin in normal muscle. High fat feeding did not alter total skeletal muscle Akt2, aPKC \u03b6 or aPKC \u03bb protein concentration. Insulin\u2010stimulated total PI3\u2010kinase, Akt2 and aPKC \u03b6\/\u03bb activities were reduced in the high fat fed animals. Insulin\u2010stimulated PM aPKC \u03b6, aPKC \u03bb, aPKC \u03b6\/\u03bb activity and GLUT4 protein concentration were also reduced in high fat fed animals. These findings suggest that in skeletal muscle, insulin stimulates translocation of aPKC \u03b6 and \u03bb, but not Akt2, to the PM. In addition, high fat feeding impairs insulin\u2010stimulated activation of total aPKC \u03b6\/\u03bb and Akt2, as well as PM association and activation of aPKC \u03b6 and \u03bb.<\/jats:p>","DOI":"10.1113\/jphysiol.2005.086694","type":"journal-article","created":{"date-parts":[[2005,4,1]],"date-time":"2005-04-01T01:13:33Z","timestamp":1112318013000},"page":"627-636","source":"Crossref","is-referenced-by-count":13,"title":["Insulin\u2010stimulated plasma membrane association and activation of Akt2, aPKC \u03b6 and aPKC \u03bb in high fat fed rodent skeletal muscle"],"prefix":"10.1113","volume":"565","author":[{"given":"Henry J.","family":"Herr","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey R.","family":"Bernard","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Donald 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