Abstract
Lipoprotein lipase (LPL) is found in adipose tissue and muscle, and is important for the uptake of triglyceride-rich lipoproteins from plasma. This study examined the regulation of LPI. in adipose tissue and muscle by exercise training in combination with the fed or fasted state. After training male rats on a treadmill for 6 weeks, LPL activity, mass, and mRNA levels were measured in adipose tissue, heart, soleus, and extensor digitorum Iongus (EDL) muscles and corn pared with levels in sedentary rats. Tissue LPL was measured as the heparin-released (HR) and cellular-extracted (EXT) fractions 16 hours following the last bout of exercise, during which time some animals were fasted and others were allowed free access to food. Training led to an increase in HR LPL activity and LPL protein mass in soleus and EDL, but had no effect on adipose tissue and heart LPL. The increase in soleus LPL with exercise was in the HR fraction only, whereas the increase in EDL LPL with training was in both the HR and EXT fractions. All these changes in LPL activity were accompanied by similar changes in LPL immunoreactive mass. However, there were no changes in LPL mRNA levels with training. Feeding induced a large increase in adipose tissue LPL activity and mass in both the HR and EXT fractions; however, there was no change in mRNA levels. In heart, feeding yielded a decrease in HR but no consistent change in EXT activity or mass, and a consistent decrease in mRNA levels. As compared with control rats, trained rats demonstrated different responses to feeding in all tissues, especially in soleus and EDL. Whereas feeding had no effect on LPL in soleus and EDL of control rats, feeding induced a decrease in HR and EXT LPL in the soleus of trained rats. In addition, feeding yielded a significant decrease in EXT LPL of the EDL of trained rats. Thus, these data demonstrate that adipose tissue and heart LPL are highly regulated by feeding and are not responsive to long-term exercise training. On the other hand, skeletal muscle LPL is increased in trained rats, but this increase is blunted considerably by feeding following the last bout of exercise. These changes in LPL activity and mass are mostly unaccompanied by changes in LPL mRNA levels, demonstrating that much physiologic regulation occurs posttranscriptionally.
| Original language | English |
|---|---|
| Pages (from-to) | 1596-1605 |
| Number of pages | 10 |
| Journal | Metabolism: Clinical and Experimental |
| Volume | 44 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 1995 |
Bibliographical note
Funding Information:From the Department of Medicine, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine, Los Angeles; and the Department of Chemistry, California Polytechnic State University, San Luis Obispo, CA. Submitted December 27, 1994; accepted March 22, 1995. Supported by Grant No. DK 39176 from the National Institutes of Health, and a grant from the American Heart Association Greater Los Angeles Affiliate. This study was performed during the tenure of an Established Investigatorship from the American Heart Association. Address reprint requests to Philip A. Kern, MD, Division of Endocrinology, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. Copyright © 1995 by W..B. Saunders Company 0026-0495/95/4412-0015503.00/0
Funding
From the Department of Medicine, Cedars-Sinai Medical Center, University of California at Los Angeles School of Medicine, Los Angeles; and the Department of Chemistry, California Polytechnic State University, San Luis Obispo, CA. Submitted December 27, 1994; accepted March 22, 1995. Supported by Grant No. DK 39176 from the National Institutes of Health, and a grant from the American Heart Association Greater Los Angeles Affiliate. This study was performed during the tenure of an Established Investigatorship from the American Heart Association. Address reprint requests to Philip A. Kern, MD, Division of Endocrinology, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048. Copyright © 1995 by W..B. Saunders Company 0026-0495/95/4412-0015503.00/0
| Funders | Funder number |
|---|---|
| American Heart Association Greater Los Angeles Affiliate | |
| National Institutes of Health (NIH) | |
| National Institute of Diabetes and Digestive and Kidney Diseases | R29DK039176 |
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology
