FFA uptake, de novo lipogenesis (DNL), and/or reduced lipid removal. ( Dowman et al. 2010 , Pettinelli et al. 2011 , Berlanga et al. 2014 ). The development of hepatic steatosis in PCOS is unique due to the influence of HA and is multi
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Tina Seidu, Patrick McWhorter, Jessie Myer, Rabita Alamgir, Nicole Eregha, Dilip Bogle, Taylor Lofton, Carolyn Ecelbarger, and Stanley Andrisse
Min Liu, Shuo Xie, Weiwei Liu, Jingjin Li, Chao Li, Wei Huang, Hexin Li, Jinghai Song, and Hong Zhang
lipogenesis and adipogenesis ( Musso et al . 2013 ). Adipose tissue includes adipocytes and a stromal-vascular fraction comprising preadipocytes, fibroblasts, endothelial cells, macrophages, and other immune cells. There are generally two types of adipose
Chunchun Wei, Xianhua Ma, Kai Su, Shasha Qi, Yuangang Zhu, Junjian Lin, Chenxin Wang, Rui Yang, Xiaowei Chen, Weizhong Wang, and Weiping J Zhang
adaptation. Lipoprotein lipase (LPL) is dramatically upregulated during BAT activation to promote uptake of free fatty acids from circulation. β-oxidation can directly provide acetyl-CoA for thermogenesis. However, de novo lipogenesis (DNL) genes, such as
Cho-Rong Bae, Kazuya Hasegawa, Sayaka Akieda-Asai, Yurie Kawasaki, Kazuyo Senba, Youn-Soo Cha, and Yukari Date
lipogenesis, we evaluated the expression of sterol regulatory element-binding transcription factor 1 (SREBF1), carbohydrate-responsive element-binding protein (ChREBP; MLX1PL), and acetyl-CoA carboxylase (ACC) and the phosphorylation of ACC by using western
Bettina Geidl-Flueck and Philipp A Gerber
hypothesized that an increased de novo lipogenesis after fructose intake in parallel with a decreased fatty acid oxidation leads to hepatic fat deposition. ACC, acetyl-CoA-carboxylase; ATP, adenosine triphosphate; CPT1a, carnitine palmitoyltransferase 1A; FA
Paul W Caton, Nanda K Nayuni, Noorafza Q Khan, Elizabeth G Wood, and Roger Corder
et al . 2005 , Bilz et al . 2006 , Rajasekar & Anuradha 2007 , Nagai et al . 2009 ). In humans, consumption of a fructose-rich diet causes insulin resistance, increases uric acid, and stimulates de novo lipogenesis, resulting in increased
A I Martín, E Castillero, M Granado, M López-Menduiña, M A Villanúa, and A López-Calderón
fat stores is not well known. Fat mass loss can be secondary to an increase in lipolysis and/or a decrease in lipogenesis. Lipolysis in WAT is under hormonal control, where the hormone-sensitive lipase (HSL) is the main regulatory pathway in rodent
Christophe Breton
binds to MC4 receptor (MC4R) acts on the opposite way, thereby decreasing food intake and increasing energy expenditure. The adipocyte is a specialised cell that stores excess energy as triacylglycerol (TG) in lipid droplets during lipogenesis. When
Sébastien Desarzens and Nourdine Faresse
in lipogenesis, inflammation and secreted adipokines in diet-induced obese Gr fl/fl and Gr ad-ko mice. As shown in Fig. 5A , Gr deletion has a slight or no effects on lipogenic genes as well as adipokines expression. However, pro
C A Borland, M C Barber, M T Travers, and R G Vernon
Abstract
The chronic inhibitory effect of growth hormone (GH) on lipogenesis in sheep adipose tissue explants was investigated in an in vitro tissue culture system. In the absence of other hormones, GH caused a decrease in the rate of lipogenesis after 6 h of culture. In contrast, when lipogenesis was stimulated by the presence of insulin plus dexamethasone, GH again decreased lipogenesis but after a lag of at least 12 h.
Actinomycin D, an inhibitor of gene transcription, prevented the effect of GH on lipogenesis in both the absence and presence of insulin plus dexamethasone. Actinomycin D added to tissue previously incubated for 6 h in the presence of GH alone prevented further decline in lipogenesis over the next 5 h, suggesting that transcription of a short-lived mediator protein is required for the GH effect to occur.
An increase in ornithine decarboxylase activity was detected in explants exposed to GH, reaching a peak after 12 h incubation; this was prevented by actinomycin D. Methylglyoxal bis-(guanylhydrazone), an inhibitor of polyamine biosynthesis, partially alleviated the effect of GH on lipogenesis; this was reversed by addition of spermidine. However, spermidine did not reverse the effects of actinomycin D, implicating a short-lived protein in addition to ornithine decarboxylase in the action of GH.
In the absence of other hormones GH had no effect on either the expressed (initial) or total activity of acetyl-CoA carboxylase, but GH prevented the increase in both expressed and total activities of the enzyme induced by insulin plus dexamethasone. Varying lipolysis and fatty acid accumulation in adipose tissue by addition of adenosine deaminase plus indomethacin or bovine serum albumin to the culture medium had no effect on lipogenesis and these agents partly alleviated GH inhibition of lipogenesis. No effect of GH was found on the amount of glycerol released by cultured tissue. GH also had no effect on fatty acid esterification.
Thus the chronic inhibitory effects of GH on lipogenesis involve a protein with a very short half-life. The effect also requires polyamines but does not appear to involve changes in fatty acid concentrations in the cell. In addition GH appears to inhibit lipogenesis and to antagonise insulin-stimulation of lipogenesis by different mechanisms.
Journal of Endocrinology (1994) 142, 235–243
