ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes.
<h4>Background</h4>Free fatty acids released from adipose tissue affect the synthesis of apolipoprotein B-containing lipoproteins and glucose metabolism in the liver. Whether there also exists a reciprocal metabolic arm affecting energy metabolism in white adipose tissue is unknown.<h...
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2008
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oai:doaj.org-article:18acd09f2f934361b3faaae2d2d5215a2021-11-25T06:18:27ZApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes.1932-620310.1371/journal.pone.0003771https://doaj.org/article/18acd09f2f934361b3faaae2d2d5215a2008-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19020660/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Free fatty acids released from adipose tissue affect the synthesis of apolipoprotein B-containing lipoproteins and glucose metabolism in the liver. Whether there also exists a reciprocal metabolic arm affecting energy metabolism in white adipose tissue is unknown.<h4>Methods and findings</h4>We investigated the effects of apoB-containing lipoproteins on catecholamine-induced lipolysis in adipocytes from subcutaneous fat cells of obese but otherwise healthy men, fat pads from mice with plasma lipoproteins containing high or intermediate levels of apoB100 or no apoB100, primary cultured adipocytes, and 3T3-L1 cells. In subcutaneous fat cells, the rate of lipolysis was inversely related to plasma apoB levels. In human primary adipocytes, LDL inhibited lipolysis in a concentration-dependent fashion. In contrast, VLDL had no effect. Lipolysis was increased in fat pads from mice lacking plasma apoB100, reduced in apoB100-only mice, and intermediate in wild-type mice. Mice lacking apoB100 also had higher oxygen consumption and lipid oxidation. In 3T3-L1 cells, apoB100-containing lipoproteins inhibited lipolysis in a dose-dependent fashion, but lipoproteins containing apoB48 had no effect. ApoB100-LDL mediated inhibition of lipolysis was abolished in fat pads of mice deficient in the LDL receptor (Ldlr(-/-)Apob(100/100)).<h4>Conclusions</h4>Our results show that the binding of apoB100-LDL to adipocytes via the LDL receptor inhibits intracellular noradrenaline-induced lipolysis in adipocytes. Thus, apoB100-LDL is a novel signaling molecule from the liver to peripheral fat deposits that may be an important link between atherogenic dyslipidemias and facets of the metabolic syndrome.Josefin SkogsbergAndrea DickerMikael RydénGaby AströmRoland NilssonHasanuzzaman BhuiyanSigurd VitolsAline MairalDominique LanginPeteris AlbertsErik WalumJesper TegnérAnders HamstenPeter ArnerJohan BjörkegrenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 11, p e3771 (2008) |
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Medicine R Science Q |
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Medicine R Science Q Josefin Skogsberg Andrea Dicker Mikael Rydén Gaby Aström Roland Nilsson Hasanuzzaman Bhuiyan Sigurd Vitols Aline Mairal Dominique Langin Peteris Alberts Erik Walum Jesper Tegnér Anders Hamsten Peter Arner Johan Björkegren ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| description |
<h4>Background</h4>Free fatty acids released from adipose tissue affect the synthesis of apolipoprotein B-containing lipoproteins and glucose metabolism in the liver. Whether there also exists a reciprocal metabolic arm affecting energy metabolism in white adipose tissue is unknown.<h4>Methods and findings</h4>We investigated the effects of apoB-containing lipoproteins on catecholamine-induced lipolysis in adipocytes from subcutaneous fat cells of obese but otherwise healthy men, fat pads from mice with plasma lipoproteins containing high or intermediate levels of apoB100 or no apoB100, primary cultured adipocytes, and 3T3-L1 cells. In subcutaneous fat cells, the rate of lipolysis was inversely related to plasma apoB levels. In human primary adipocytes, LDL inhibited lipolysis in a concentration-dependent fashion. In contrast, VLDL had no effect. Lipolysis was increased in fat pads from mice lacking plasma apoB100, reduced in apoB100-only mice, and intermediate in wild-type mice. Mice lacking apoB100 also had higher oxygen consumption and lipid oxidation. In 3T3-L1 cells, apoB100-containing lipoproteins inhibited lipolysis in a dose-dependent fashion, but lipoproteins containing apoB48 had no effect. ApoB100-LDL mediated inhibition of lipolysis was abolished in fat pads of mice deficient in the LDL receptor (Ldlr(-/-)Apob(100/100)).<h4>Conclusions</h4>Our results show that the binding of apoB100-LDL to adipocytes via the LDL receptor inhibits intracellular noradrenaline-induced lipolysis in adipocytes. Thus, apoB100-LDL is a novel signaling molecule from the liver to peripheral fat deposits that may be an important link between atherogenic dyslipidemias and facets of the metabolic syndrome. |
| format |
article |
| author |
Josefin Skogsberg Andrea Dicker Mikael Rydén Gaby Aström Roland Nilsson Hasanuzzaman Bhuiyan Sigurd Vitols Aline Mairal Dominique Langin Peteris Alberts Erik Walum Jesper Tegnér Anders Hamsten Peter Arner Johan Björkegren |
| author_facet |
Josefin Skogsberg Andrea Dicker Mikael Rydén Gaby Aström Roland Nilsson Hasanuzzaman Bhuiyan Sigurd Vitols Aline Mairal Dominique Langin Peteris Alberts Erik Walum Jesper Tegnér Anders Hamsten Peter Arner Johan Björkegren |
| author_sort |
Josefin Skogsberg |
| title |
ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| title_short |
ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| title_full |
ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| title_fullStr |
ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| title_full_unstemmed |
ApoB100-LDL acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| title_sort |
apob100-ldl acts as a metabolic signal from liver to peripheral fat causing inhibition of lipolysis in adipocytes. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2008 |
| url |
https://doaj.org/article/18acd09f2f934361b3faaae2d2d5215a |
| work_keys_str_mv |
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| _version_ |
1718413908176273408 |