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Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle.
Am J Physiol Endocrinol Metab. 2014 May 01; 306(9):E1085-92.AJ

Abstract

Exercise can effectively ameliorate type 2 diabetes and insulin resistance. Here we show that the mRNA levels of one of peroxisome proliferator-activated receptor (PPAR) family members, PPARγ1, and genes related to energy metabolism, including PPARγ coactivator-1 protein-1α (PGC-1α) and lipoprotein lipase (LPL), increased in the gastrocnemius muscle of habitual exercise-trained mice. When mice were intraperitoneally administered an AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), the mRNA levels of the aforementioned three genes increased in gastrocnemius muscle. AICAR treatment to C2C12 differentiated myotubes also increased PPARγ1 mRNA levels, but not PPARα and -δ mRNA levels, concomitant with increased PGC-1α mRNA levels. An AMPK inhibitor, compound C, blocked these AICAR effects. AICAR treatment increased the half-life of PPARγ1 mRNA nearly threefold (4-12 h) by activating AMPK. When C2C12 myoblast cells infected with a PPARγ1 expression lentivirus were differentiated into myotubes, PPARγ1 overexpression dramatically increased LPL mRNA levels more than 40-fold. In contrast, when PPARγ1 expression was suppressed in C2C12 myotubes, LPL mRNA levels were significantly reduced, and the effect of AICAR on increased LPL gene expression was almost completely blocked. These results indicated that PPARγ1 was intimately involved in LPL gene expression in skeletal muscle and the AMPK-PPARγ1 pathway may play a role in exercise-induced LPL expression. Thus, we identified a novel critical role for PPARγ1 in response to AMPK activation for controlling the expression of a subset of genes associated with metabolic regulation in skeletal muscle.

Authors+Show Affiliations

Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan; and.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24644240

Citation

Sasaki, Takashi, et al. "Role of AMPK and PPARγ1 in Exercise-induced Lipoprotein Lipase in Skeletal Muscle." American Journal of Physiology. Endocrinology and Metabolism, vol. 306, no. 9, 2014, pp. E1085-92.
Sasaki T, Nakata R, Inoue H, et al. Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle. Am J Physiol Endocrinol Metab. 2014;306(9):E1085-92.
Sasaki, T., Nakata, R., Inoue, H., Shimizu, M., Inoue, J., & Sato, R. (2014). Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle. American Journal of Physiology. Endocrinology and Metabolism, 306(9), E1085-92. https://doi.org/10.1152/ajpendo.00691.2013
Sasaki T, et al. Role of AMPK and PPARγ1 in Exercise-induced Lipoprotein Lipase in Skeletal Muscle. Am J Physiol Endocrinol Metab. 2014 May 1;306(9):E1085-92. PubMed PMID: 24644240.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle. AU - Sasaki,Takashi, AU - Nakata,Rieko, AU - Inoue,Hiroyasu, AU - Shimizu,Makoto, AU - Inoue,Jun, AU - Sato,Ryuichiro, Y1 - 2014/03/18/ PY - 2014/3/20/entrez PY - 2014/3/20/pubmed PY - 2014/7/2/medline KW - AMP-activated protein kinase KW - C2C12 cells KW - exercise KW - lipoprotein lipase KW - peroxisome proliferator-activated receptor-γ1 SP - E1085 EP - 92 JF - American journal of physiology. Endocrinology and metabolism JO - Am J Physiol Endocrinol Metab VL - 306 IS - 9 N2 - Exercise can effectively ameliorate type 2 diabetes and insulin resistance. Here we show that the mRNA levels of one of peroxisome proliferator-activated receptor (PPAR) family members, PPARγ1, and genes related to energy metabolism, including PPARγ coactivator-1 protein-1α (PGC-1α) and lipoprotein lipase (LPL), increased in the gastrocnemius muscle of habitual exercise-trained mice. When mice were intraperitoneally administered an AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), the mRNA levels of the aforementioned three genes increased in gastrocnemius muscle. AICAR treatment to C2C12 differentiated myotubes also increased PPARγ1 mRNA levels, but not PPARα and -δ mRNA levels, concomitant with increased PGC-1α mRNA levels. An AMPK inhibitor, compound C, blocked these AICAR effects. AICAR treatment increased the half-life of PPARγ1 mRNA nearly threefold (4-12 h) by activating AMPK. When C2C12 myoblast cells infected with a PPARγ1 expression lentivirus were differentiated into myotubes, PPARγ1 overexpression dramatically increased LPL mRNA levels more than 40-fold. In contrast, when PPARγ1 expression was suppressed in C2C12 myotubes, LPL mRNA levels were significantly reduced, and the effect of AICAR on increased LPL gene expression was almost completely blocked. These results indicated that PPARγ1 was intimately involved in LPL gene expression in skeletal muscle and the AMPK-PPARγ1 pathway may play a role in exercise-induced LPL expression. Thus, we identified a novel critical role for PPARγ1 in response to AMPK activation for controlling the expression of a subset of genes associated with metabolic regulation in skeletal muscle. SN - 1522-1555 UR - https://www.unboundmedicine.com/medline/citation/24644240/Role_of_AMPK_and_PPARγ1_in_exercise_induced_lipoprotein_lipase_in_skeletal_muscle_ L2 - https://journals.physiology.org/doi/10.1152/ajpendo.00691.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -