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PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity
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| Zeitschriftentitel: | Diabetes |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Diabetes, 52, 2003, 2, S. 291-299 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Diabetes Association
|
| Schlagwörter: |
| author_facet |
Laplante, Mathieu Sell, Henrike MacNaul, Karen L. Richard, Denis Berger, Joel P. Deshaies, Yves Laplante, Mathieu Sell, Henrike MacNaul, Karen L. Richard, Denis Berger, Joel P. Deshaies, Yves |
|---|---|
| author |
Laplante, Mathieu Sell, Henrike MacNaul, Karen L. Richard, Denis Berger, Joel P. Deshaies, Yves |
| spellingShingle |
Laplante, Mathieu Sell, Henrike MacNaul, Karen L. Richard, Denis Berger, Joel P. Deshaies, Yves Diabetes PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity Endocrinology, Diabetes and Metabolism Internal Medicine |
| author_sort |
laplante, mathieu |
| spelling |
Laplante, Mathieu Sell, Henrike MacNaul, Karen L. Richard, Denis Berger, Joel P. Deshaies, Yves 0012-1797 1939-327X American Diabetes Association Endocrinology, Diabetes and Metabolism Internal Medicine http://dx.doi.org/10.2337/diabetes.52.2.291 <jats:p>This study sought to determine whether the adipose depot−specific (subcutaneous [SF] vs. visceral [VF]) action of peroxisome proliferator−activated receptor-γ (PPAR-γ) agonists on fat deposition extends to the expression of lipoprotein lipase (LPL) and other key adipose lipid metabolism genes, and whether changes in LPL impact triglyceridemia. Rats were fed a standard diet or an obesity-promoting diet for 3 weeks, with or without treatment with COOH, a nonthiazolidinedione PPAR-γ agonist. Treatment effects were essentially similar in both dietary cohorts. COOH did not affect weight gain, but increased SF (inguinal) fat mass twofold and reduced VF (retroperitoneal) accretion by half. Corresponding depot-specific alterations were observed in mRNA levels of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD-1) and the thermogenic modulator uncoupling protein 1 (UCP-1). COOH increased brown adipose tissue (BAT) weight and LPL availability by five- to eightfold. In rats refed standard diet after a 24-h fast, COOH reduced the insulin excursion by half. The agonist increased SF LPL activity and mRNA levels, but had no effect on VF LPL. The two- to threefold postprandial increase in plasma triglycerides (TGs) was abrogated in COOH-treated rats, likely in part because of increased LPL in SF and BAT. Thus PPAR-γ agonist treatment had a powerful, site-specific effect on adipose metabolism and lipid deposition, and greatly impacted the postprandial handling of TG-rich lipoproteins. These depot-specific effects may be mediated by differential regulation of key metabolic genes, including LPL, 11β-HSD-1, and UCP-1.</jats:p> PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity Diabetes |
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American Diabetes Association, 2003 |
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| title |
PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_unstemmed |
PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_full |
PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_fullStr |
PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_full_unstemmed |
PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_short |
PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_sort |
ppar-γ activation mediates adipose depot−specific effects on gene expression and lipoprotein lipase activity |
| topic |
Endocrinology, Diabetes and Metabolism Internal Medicine |
| url |
http://dx.doi.org/10.2337/diabetes.52.2.291 |
| publishDate |
2003 |
| physical |
291-299 |
| description |
<jats:p>This study sought to determine whether the adipose depot−specific (subcutaneous [SF] vs. visceral [VF]) action of peroxisome proliferator−activated receptor-γ (PPAR-γ) agonists on fat deposition extends to the expression of lipoprotein lipase (LPL) and other key adipose lipid metabolism genes, and whether changes in LPL impact triglyceridemia. Rats were fed a standard diet or an obesity-promoting diet for 3 weeks, with or without treatment with COOH, a nonthiazolidinedione PPAR-γ agonist. Treatment effects were essentially similar in both dietary cohorts. COOH did not affect weight gain, but increased SF (inguinal) fat mass twofold and reduced VF (retroperitoneal) accretion by half. Corresponding depot-specific alterations were observed in mRNA levels of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD-1) and the thermogenic modulator uncoupling protein 1 (UCP-1). COOH increased brown adipose tissue (BAT) weight and LPL availability by five- to eightfold. In rats refed standard diet after a 24-h fast, COOH reduced the insulin excursion by half. The agonist increased SF LPL activity and mRNA levels, but had no effect on VF LPL. The two- to threefold postprandial increase in plasma triglycerides (TGs) was abrogated in COOH-treated rats, likely in part because of increased LPL in SF and BAT. Thus PPAR-γ agonist treatment had a powerful, site-specific effect on adipose metabolism and lipid deposition, and greatly impacted the postprandial handling of TG-rich lipoproteins. These depot-specific effects may be mediated by differential regulation of key metabolic genes, including LPL, 11β-HSD-1, and UCP-1.</jats:p> |
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| author | Laplante, Mathieu, Sell, Henrike, MacNaul, Karen L., Richard, Denis, Berger, Joel P., Deshaies, Yves |
| author_facet | Laplante, Mathieu, Sell, Henrike, MacNaul, Karen L., Richard, Denis, Berger, Joel P., Deshaies, Yves, Laplante, Mathieu, Sell, Henrike, MacNaul, Karen L., Richard, Denis, Berger, Joel P., Deshaies, Yves |
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| description | <jats:p>This study sought to determine whether the adipose depot−specific (subcutaneous [SF] vs. visceral [VF]) action of peroxisome proliferator−activated receptor-γ (PPAR-γ) agonists on fat deposition extends to the expression of lipoprotein lipase (LPL) and other key adipose lipid metabolism genes, and whether changes in LPL impact triglyceridemia. Rats were fed a standard diet or an obesity-promoting diet for 3 weeks, with or without treatment with COOH, a nonthiazolidinedione PPAR-γ agonist. Treatment effects were essentially similar in both dietary cohorts. COOH did not affect weight gain, but increased SF (inguinal) fat mass twofold and reduced VF (retroperitoneal) accretion by half. Corresponding depot-specific alterations were observed in mRNA levels of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD-1) and the thermogenic modulator uncoupling protein 1 (UCP-1). COOH increased brown adipose tissue (BAT) weight and LPL availability by five- to eightfold. In rats refed standard diet after a 24-h fast, COOH reduced the insulin excursion by half. The agonist increased SF LPL activity and mRNA levels, but had no effect on VF LPL. The two- to threefold postprandial increase in plasma triglycerides (TGs) was abrogated in COOH-treated rats, likely in part because of increased LPL in SF and BAT. Thus PPAR-γ agonist treatment had a powerful, site-specific effect on adipose metabolism and lipid deposition, and greatly impacted the postprandial handling of TG-rich lipoproteins. These depot-specific effects may be mediated by differential regulation of key metabolic genes, including LPL, 11β-HSD-1, and UCP-1.</jats:p> |
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| imprint | American Diabetes Association, 2003 |
| imprint_str_mv | American Diabetes Association, 2003 |
| institution | DE-Rs1, DE-Pl11, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15 |
| issn | 0012-1797, 1939-327X |
| issn_str_mv | 0012-1797, 1939-327X |
| language | English |
| last_indexed | 2024-03-01T16:20:12.638Z |
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| physical | 291-299 |
| publishDate | 2003 |
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| publisher | American Diabetes Association |
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| series | Diabetes |
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| spelling | Laplante, Mathieu Sell, Henrike MacNaul, Karen L. Richard, Denis Berger, Joel P. Deshaies, Yves 0012-1797 1939-327X American Diabetes Association Endocrinology, Diabetes and Metabolism Internal Medicine http://dx.doi.org/10.2337/diabetes.52.2.291 <jats:p>This study sought to determine whether the adipose depot−specific (subcutaneous [SF] vs. visceral [VF]) action of peroxisome proliferator−activated receptor-γ (PPAR-γ) agonists on fat deposition extends to the expression of lipoprotein lipase (LPL) and other key adipose lipid metabolism genes, and whether changes in LPL impact triglyceridemia. Rats were fed a standard diet or an obesity-promoting diet for 3 weeks, with or without treatment with COOH, a nonthiazolidinedione PPAR-γ agonist. Treatment effects were essentially similar in both dietary cohorts. COOH did not affect weight gain, but increased SF (inguinal) fat mass twofold and reduced VF (retroperitoneal) accretion by half. Corresponding depot-specific alterations were observed in mRNA levels of the glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD-1) and the thermogenic modulator uncoupling protein 1 (UCP-1). COOH increased brown adipose tissue (BAT) weight and LPL availability by five- to eightfold. In rats refed standard diet after a 24-h fast, COOH reduced the insulin excursion by half. The agonist increased SF LPL activity and mRNA levels, but had no effect on VF LPL. The two- to threefold postprandial increase in plasma triglycerides (TGs) was abrogated in COOH-treated rats, likely in part because of increased LPL in SF and BAT. Thus PPAR-γ agonist treatment had a powerful, site-specific effect on adipose metabolism and lipid deposition, and greatly impacted the postprandial handling of TG-rich lipoproteins. These depot-specific effects may be mediated by differential regulation of key metabolic genes, including LPL, 11β-HSD-1, and UCP-1.</jats:p> PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity Diabetes |
| spellingShingle | Laplante, Mathieu, Sell, Henrike, MacNaul, Karen L., Richard, Denis, Berger, Joel P., Deshaies, Yves, Diabetes, PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity, Endocrinology, Diabetes and Metabolism, Internal Medicine |
| title | PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_full | PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_fullStr | PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_full_unstemmed | PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_short | PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| title_sort | ppar-γ activation mediates adipose depot−specific effects on gene expression and lipoprotein lipase activity |
| title_unstemmed | PPAR-γ Activation Mediates Adipose Depot−Specific Effects on Gene Expression and Lipoprotein Lipase Activity |
| topic | Endocrinology, Diabetes and Metabolism, Internal Medicine |
| url | http://dx.doi.org/10.2337/diabetes.52.2.291 |