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Acute activation of the mammalian target of rapamycin complex 1 does not impair in vivo insulin action in mice
Author(s) -
Berk Eli Zachary,
Reynolds Thomas Henry
Publication year - 2008
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.22.1_supplement.1226.24
Subject(s) - insulin resistance , insulin , mtorc1 , medicine , endocrinology , in vivo , saline , leucine , glucose tolerance test , intraperitoneal injection , pi3k/akt/mtor pathway , biology , signal transduction , amino acid , biochemistry , microbiology and biotechnology
Recent cell culture studies have shown that the mammalian target of rapamycin complex 1 (mTORC1) plays a role in the development of insulin resistance. However, the ability of mTORC1 to produce whole‐body insulin resistance is not established. The purpose of the present study was to determine the effect of acutely activating mTORC1 with leucine on in vivo insulin action. C57BL/6 male mice (n = 20) received intraperitoneal injections of leucine (1.35 g/Kg body weight) or an equivalent volume of saline. Mice were subjected to an intraperitoneal insulin‐assisted glucose tolerance test (IAGTT) that involved injections of glucose (1 mg/Kg) and insulin (0.15 U/Kg) at 15 and 20 minutes following leucine or saline administration, respectively. Blood glucose was assessed by sampling tail vein blood (~ 5 ul) at baseline and 15, 30, 45, and 60 minutes following the injection of glucose. The blood glucose values were used to calculate the area under the IAGTT curve. The area under the IAGTT curve was similar in leucine treated mice compared to controls (7805 ± 675 vs. 7513 ± 462, p = 0.753), indicating that insulin sensitivity was not altered. In skeletal muscles of mice injected with leucine, mTORC1 signaling was elevated compared to mice that received saline. These results suggest that acute treatment with leucine appears to activate mTOR signaling but does not produce insulin resistance in mice.