Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain.
Obesity is a global epidemic that contributes to the increasing medical burdens related to type 2 diabetes, cardiovascular disease and cancer. A better understanding of the mechanisms regulating adipose tissue expansion could lead to therapeutics that eliminate or reduce obesity-associated morbidity...
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2014
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oai:doaj.org-article:6dbfe82749764926b256929ef4c5b2942021-11-25T05:56:51ZLaminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain.1932-620310.1371/journal.pone.0109854https://doaj.org/article/6dbfe82749764926b256929ef4c5b2942014-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0109854https://doaj.org/toc/1932-6203Obesity is a global epidemic that contributes to the increasing medical burdens related to type 2 diabetes, cardiovascular disease and cancer. A better understanding of the mechanisms regulating adipose tissue expansion could lead to therapeutics that eliminate or reduce obesity-associated morbidity and mortality. The extracellular matrix (ECM) has been shown to regulate the development and function of numerous tissues and organs. However, there is little understanding of its function in adipose tissue. In this manuscript we describe the role of laminin α4, a specialized ECM protein surrounding adipocytes, on weight gain and adipose tissue function. Adipose tissue accumulation, lipogenesis, and structure were examined in mice with a null mutation of the laminin α4 gene (Lama4-/-) and compared to wild-type (Lama4+/+) control animals. Lama4-/- mice exhibited reduced weight gain in response to both age and high fat diet. Interestingly, the mice had decreased adipose tissue mass and altered lipogenesis in a depot-specific manner. In particular, epididymal adipose tissue mass was specifically decreased in knock-out mice, and there was also a defect in lipogenesis in this depot as well. In contrast, no such differences were observed in subcutaneous adipose tissue at 14 weeks. The results suggest that laminin α4 influences adipose tissue structure and function in a depot-specific manner. Alterations in laminin composition offers insight into the roll the ECM potentially plays in modulating cellular behavior in adipose tissue expansion.Marcella K VaicikJill Thyboll KortesmaaSofia Movérare-SkrticJarkko KortesmaaRaija SoininenGöran BergströmClaes OhlssonLi Yen ChongBjörn RozellMargo EmontRonald N CohenEric M BreyKarl TryggvasonPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 10, p e109854 (2014) |
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Medicine R Science Q Marcella K Vaicik Jill Thyboll Kortesmaa Sofia Movérare-Skrtic Jarkko Kortesmaa Raija Soininen Göran Bergström Claes Ohlsson Li Yen Chong Björn Rozell Margo Emont Ronald N Cohen Eric M Brey Karl Tryggvason Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| description |
Obesity is a global epidemic that contributes to the increasing medical burdens related to type 2 diabetes, cardiovascular disease and cancer. A better understanding of the mechanisms regulating adipose tissue expansion could lead to therapeutics that eliminate or reduce obesity-associated morbidity and mortality. The extracellular matrix (ECM) has been shown to regulate the development and function of numerous tissues and organs. However, there is little understanding of its function in adipose tissue. In this manuscript we describe the role of laminin α4, a specialized ECM protein surrounding adipocytes, on weight gain and adipose tissue function. Adipose tissue accumulation, lipogenesis, and structure were examined in mice with a null mutation of the laminin α4 gene (Lama4-/-) and compared to wild-type (Lama4+/+) control animals. Lama4-/- mice exhibited reduced weight gain in response to both age and high fat diet. Interestingly, the mice had decreased adipose tissue mass and altered lipogenesis in a depot-specific manner. In particular, epididymal adipose tissue mass was specifically decreased in knock-out mice, and there was also a defect in lipogenesis in this depot as well. In contrast, no such differences were observed in subcutaneous adipose tissue at 14 weeks. The results suggest that laminin α4 influences adipose tissue structure and function in a depot-specific manner. Alterations in laminin composition offers insight into the roll the ECM potentially plays in modulating cellular behavior in adipose tissue expansion. |
| format |
article |
| author |
Marcella K Vaicik Jill Thyboll Kortesmaa Sofia Movérare-Skrtic Jarkko Kortesmaa Raija Soininen Göran Bergström Claes Ohlsson Li Yen Chong Björn Rozell Margo Emont Ronald N Cohen Eric M Brey Karl Tryggvason |
| author_facet |
Marcella K Vaicik Jill Thyboll Kortesmaa Sofia Movérare-Skrtic Jarkko Kortesmaa Raija Soininen Göran Bergström Claes Ohlsson Li Yen Chong Björn Rozell Margo Emont Ronald N Cohen Eric M Brey Karl Tryggvason |
| author_sort |
Marcella K Vaicik |
| title |
Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| title_short |
Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| title_full |
Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| title_fullStr |
Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| title_full_unstemmed |
Laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| title_sort |
laminin α4 deficient mice exhibit decreased capacity for adipose tissue expansion and weight gain. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2014 |
| url |
https://doaj.org/article/6dbfe82749764926b256929ef4c5b294 |
| work_keys_str_mv |
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