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Jiung-Pang Huang, Sheng-Chieh Hsu, Yaa-Jyuhn James Meir, Po-Shiuan Hsieh, Chih-Chun Chang, Kuan-Hsing Chen, Jan-Kan Chen, and Li-Man Hung

( Guilherme et al . 2008 ). Therefore, the balance between stored and released lipids is exquisitely controlled by adipose tissue. Dysfunctional adipose tissue loses the function of a metabolic homeostasis regulator and promotes lipolysis. Increased

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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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F. M. Ng, N. A. Adamafio, and J. E. Graystone


The effects of two preparations of highly purified human GH (hGH) on lipid metabolism were studied in the GH-deficient little mouse (50–60 days old). Marked decreases in incorporation of [14C]glucose into fatty acid and in the activity of acetyl-CoA carboxylase in the epididymal fat pads were observed after i.p. injection of hGH at a dose of 1·0μg/g body weight or after continuous infusion of hGH by osmotic minipump. The rate of glucose incorporation into fatty acid decreased from 107·0 ± 27·6 (s.e.m.) to 38·1 ± 19·6 μmol/g tissue per h after a single injection of hGH and from 174·1±28·5 to 56·3±20·3 μmol/g tissue per h after continuous infusion of hGH for 2 days. Activity of the lipogenic enzyme acetyl-CoA carboxylase was also reduced by more than 50% in the epididymal fat pad from hGH-treated mice in comparison with the corresponding control animals. Incubation of isolated fat pads with hGH (0·1 μg/ml) revealed similar inhibitory effects of the hormone on fatty acid synthesis and acetyl-CoA carboxylase activity. No lipolytic effect of hGH was found as determined by the rate of glycerol release from epididymal fat pads of little mice following hormone treatment in vivo or in vitro. The results lend strong support to the conclusion that GH inhibits lipogenesis but has no effect on lipolysis in adipose tissues, and indicate that the physiological role of GH in lipid metabolism is concerned mainly with the regulation of anabolic rather than catabolic processes.

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B. Beck


The gastrointestinal hormone, gastric inhibitory polypeptide (GIP), has been isolated and characterized because of its enterogastrone-type effects. It is also named glucose-dependent insulinotropic polypeptide and is actually considered to be the main incretin factor of the entero-insular axis. Besides these well-described effects on gastric secretion and pancreatic β cells, it also has direct metabolic effects on other tissues and organs, such as adipose tissue, liver, muscle, gastrointestinal tract and brain. In adipose tissue it is involved in the activation and regulation of lipoprotein lipase (LPL); it also inhibits glucagon-induced lipolysis and potentiates the effect of insulin on incorporation of fatty acids into triglycerides. It may play a role in the development of obesity because of the hypersensitivity of adipose tissue of obese animals to some of these actions. In the liver it does not modify insulin extraction, and its incretin effects are due only to the stimulation of insulin secretion and synthesis. It reduces hepatic glucose output and inhibits glucagon-stimulated glycogenolysis. It might increase glucose utilization in peripheral tissues such as muscle. GIP also has an effect on the volume and/or electrolyte composition of intestinal secretion and saliva. The functional importance of its effect on the hormones of the anterior pituitary lobe remains to be established, as it has never been detected in the brain.

Its links with insulin are very close and the presence of insulin is sometimes necessary for the greater efficiency of both hormones. GIP can be considered as a true metabolic hormone, with most of its functions tending to increase anabolism.