Impairment of insulin-stimulated glucose transport and ERK activation by adipocyte-specific knockout of PKC-λ produces a phenotype characterized by diminished adiposity and enhanced insulin suppression of hepatic gluconeogenesis.

Farese, Robert
Sajan, MP
Jurzak, MJ
Samuels, VT
Shulman, GI
Braun, U
Leitges, M
Farese, RV

Publication date

January 2014

Publisher

eScholarship, University of California

Abstract

Tissue-specific knockout (KO) of atypical protein kinase C-λ (PKC-λ) impairs insulin-stimulated glucose transport in muscle (M) and lipid synthesis in liver (L), thereby producing insulin resistance in MλKO mice and insulin-hypersensitivity in LλKO mice.

Extracted data

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Impairment of insulin-stimulated glucose transport and ERK activation by adipocyte-specific knockout of PKC-λ produces a phenotype characterized by diminished adiposity and enhanced insulin suppression of hepatic gluconeogenesis.

Abstract

Extracted data

Impairment of insulin-stimulated glucose transport and ERK activation by adipocyte-specific knockout of PKC-λ produces a phenotype characterized by diminished adiposity and enhanced insulin suppression of hepatic gluconeogenesis.

Abstract

Extracted data

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