Adipose triglyceride lipase expression in human adipose tissue and muscle. Role in insulin resistance and response to training and pioglitazone

Aiwei Yao-Borengasser, Vijayalakshmi Varma, Robert H. Coker, Gouri Ranganathan, Bounleut Phanavanh, Neda Rasouli, Philip A. Kern

Research output: Contribution to journalArticlepeer-review

50 Scopus citations


Adipose triglyceride lipase (ATGL) catalyzes the first step in adipocyte and muscle triglyceride hydrolysis, and comparative gene identification-58 (CGI-58) is an essential cofactor. We studied the expression of ATGL and CGI-58 in human adipose and muscle and examined correlations with markers of muscle fatty acid oxidation. Nondiabetic volunteers were studied. Subjects with impaired glucose tolerance were treated with pioglitazone or metformin for 10 weeks. Subjects with normal glucose tolerance underwent a 12-week training program. We examined changes in ATGL and CGI-58 with obesity and insulin resistance, and effects of exercise and pioglitazone. Adipose triglyceride lipase messenger RNA (mRNA) expression showed no correlation with either body mass index or insulin sensitivity index in either adipose or muscle. However, adipose ATGL protein levels were inversely correlated with body mass index (r = -0.64, P < .02) and positively correlated with insulin sensitivity index (r = 0.67, P < .02). In muscle, ATGL mRNA demonstrated a strong positive relationship with carnitine palmitoyltransferase I mRNA (r = 0.82, P < .0001) and the adiponectin receptors AdipoR1 mRNA (r = 0.71, P < .0001) and AdipoR2 mRNA (r = 0.74, P < .0001). Muscle CGI-58 mRNA was inversely correlated with intramyocellular triglyceride in both type 1 (r = -0.35, P < .05) and type 2 (r = -0.40, P < .05) fibers. Exercise training resulted in increased muscle ATGL, and pioglitazone increased adipose ATGL by 31% (P < .05). Pioglitazone also increased ATGL in adipocytes. Adipose ATGL protein is decreased with insulin resistance and obesity; and muscle ATGL mRNA is associated with markers of fatty acid oxidation in muscle, as is CGI-58. The regulation of ATGL and CGI-58 has important implications for the control of lipotoxicity.

Original languageEnglish
Pages (from-to)1012-1020
Number of pages9
JournalMetabolism: Clinical and Experimental
Issue number7
StatePublished - Jul 2011

Bibliographical note

Funding Information:
We wish to thank Regina Dennis for assistance with recruitment and the nurses at the General Clinical Research Center for assistance with the procedures. We wish to thank Dr Susan Fried for providing adipose tissue for RNA extraction. Funding: a Merit Review Grant from the Veterans Administration (NR, GR) and grants from the National Institutes of Health ( M01RR14288 , RO1 DK 39176 [PAK], RO1 DK71349 [PAK], and KO1 DK 64716-01 [RHC]). We would also like to acknowledge support from the American Heart Association ( SDA 0335172N [RHC]).

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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