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Haoyong Yu, Mingliang Zhang, Yunqin Ma, Junxi Lu, Jiemin Pan, Pan Pan, Haibing Chen, and Weiping Jia

triglyceride measured in two groups. (D) Triglycerides in liver measured by hematoxylin-eosin staining. All data are presented as mean ±  s.e.m. ( n  = 3). * P  < 0.05 vs vehicle-treated group. 5-ALA promoted lipolysis and fatty acid beta

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Fei Xiao, Ying Du, Ziquan Lv, Shanghai Chen, Jianmin Zhu, Hongguang Sheng, and Feifan Guo

five EAAs significantly reduced abdominal fat mass, which was also likely caused by increased energy expenditure. In contrast, lipolysis-related genes and proteins were differentially regulated by different EAAs. These results suggest a crucial role of

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Marina R Pulido, Yoana Rabanal-Ruiz, Farid Almabouada, Alberto Díaz-Ruiz, María A Burrell, María J Vázquez, Justo P Castaño, Rhonda D Kineman, Raúl M Luque, Carlos Diéguez, Rafael Vázquez-Martínez, and María M Malagón

of adipose tissue as an inert energy depot and unveiled the complex regulation of adipose tissue lipolysis and lipogenesis. Indeed, regulation of lipid metabolism in adipocytes depends on a fine balance between multiple factors, both extracellular and

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C Bolduc, M Larose, M Yoshioka, P Ye, P Belleau, C Labrie, J Morissette, V Raymond, F Labrie, and J St-Amand

upregulated (Table 2 ). Genes involved in lipolysis, such as hormone-sensitive lipase, were also upregulated by DHT. Apolipoprotein E and low-density lipoprotein receptor-related protein 1 gene expression was increased by DHT, whereas a switch of transcript

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Verónica Sancho, María V Trigo, Nieves González, Isabel Valverde, Willy J Malaisse, and María L Villanueva-Peñacarrillo

-glucose content was corrected for the unspecific d -glucose uptake value, obtained in cell samples from each experiment treated in parallel with 0.175 mM cytochalasin B ( Perea et al. 1997 ). Lipolysis Lipolysis was

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Luke A Noon, Artem Bakmanidis, Adrian J L Clark, Peter J O’Shaughnessy, and Peter J King

The ACTH receptor melanocortin 2 receptor (MC2-R) is a G-protein-coupled receptor principally expressed in the adrenal cortex and the adipocyte, where it stimulates steroidogenesis and lipolysis respectively. The coding region of the murine gene is encoded by a single exon, although three upstream non-coding exons have been documented, one of which is incorporated by alternative splicing in adrenal cells. We have detected a novel transcript in adipocytes, which includes a previously unidentified 86 bp exon upstream of the coding region. This transcript appears with slower kinetics during a time course of differentiation of 3T3-L1 cells and is much more highly expressed in these cells and murine adipose tissues than in the Y1 murine adrenocortical cell line, also it is undetectable in murine foetal testes. Inclusion of this exon extends the 5′ UTR to 468 bp and introduces three upstream open reading frames. These are typical features of mRNAs under translational control and imply that the MC2-R gene is regulated both transcriptionally and post-transcriptionally during adipogenesis.

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L Lundholm, S Moverare, KR Steffensen, M Nilsson, M Otsuki, C Ohlsson, JA Gustafsson, and K Dahlman-Wright

Estrogens reduce adipose tissue mass in both humans and animals. The molecular mechanisms for this effect are, however, not well characterized. We took a gene expression profiling approach to study the direct effects of estrogen on mouse white adipose tissue (WAT). Female ovariectomized mice were treated for 10, 24 and 48 h with 17beta-estradiol or vehicle. RNA was extracted from gonadal fat and hybridized to Affymetrix MG-U74Av2 arrays. 17beta-Estradiol was shown to decrease mRNA expression of liver X receptor (LXR) alpha after 10 h of treatment compared with the vehicle control. The expression of several LXRalpha target genes, such as sterol regulatory element-binding protein 1c, apolipoprotein E, phospholipid transfer protein, ATP-binding cassette A1 and ATP-binding cassette G1, was similarly decreased. We furthermore identified a 1.5 kb LXRalpha promoter fragment that is negatively regulated by estrogen. Several genes involved in lipogenesis and lipolysis were identified as novel targets that could mediate estrogenic effects on adipose tissue. Finally, we show that ERalpha is the main estrogen receptor expressed in mouse white adipose tissue (WAT) with mRNA levels several hundred times higher than those of ERbeta mRNA.

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Z López-Ibarra, J Modrego, M Valero-Muñoz, P Rodríguez-Sierra, J J Zamorano-León, A González-Cantalapiedra, N de las Heras, S Ballesteros, V Lahera, and A J López-Farré

body ( Dawkins & Hull 1964 ). The two main metabolic processes of WAT are lipogenesis and lipolysis. In this regard, WAT accommodates caloric excess by expanding to store triglycerides and compensates for caloric deficit through the mobilization of free

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Haihua Yang and Linghai Yang

signaling. Metformin also increases cellular AMP to inhibit adenylyl cyclase (AC) and thus suppresses cAMP synthesis. (C) Regulation of lipolysis in adipocyte. Glucagon and epinephrine increase lipolysis in adipocytes by stimulating PKA

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Hui Juan Zhu, Hui Pan, Xu Zhe Zhang, Nai Shi Li, Lin Jie Wang, Hong Bo Yang, and Feng Ying Gong

BCA Protein Assay Reagent kit (Pierce, Rockford, IL, USA). Intracellular lipid contents, which were determined by the two methods just described, were normalized against the protein. Lipolysis assay 3T3-L1 cells were differentiated and treated with