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The regulation of hepatic metabolism by insulin
Author(s) -
Birnbaum Morris J,
Leavens Karla
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.303.1
Subject(s) - akt2 , anabolism , lipid metabolism , protein kinase b , endocrinology , biology , insulin receptor , medicine , insulin resistance , insulin , carbohydrate metabolism , adipose tissue , akt1 , signal transduction , biochemistry
Central to the signaling cascade by which insulin regulates metabolism in liver, muscle and adipose tissue is the serine/threonine protein kinase Akt, also known as Protein Kinase B. Each of the three Akt family members has distinct roles in normal physiology. The isoform specificity in hepatic metabolism is evident in liver, in that Akt2 deletion abrogates control of lipogenic gene expression, but insulin is still capable of regulating the genes encoding gluconeogenic proteins. Most impressively, deletion of Akt2 selectively in the liver leads to marked abnormalities in anabolic lipid metabolism, whereas glucose metabolism is relatively normal. Deletion of both Akt2 genes results in significant glucose intolerance. The phenotype of livers deficient in Akt2, which are protected from accumulation of fat in the liver, support the hypothesis insulin resistance under pathological conditions is “selective”, retaining the ability of insulin to regulate anabolic lipid pathways while losing suppression of hepatic glucose output.