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Tina Seidu, Patrick McWhorter, Jessie Myer, Rabita Alamgir, Nicole Eregha, Dilip Bogle, Taylor Lofton, Carolyn Ecelbarger, and Stanley Andrisse

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

Free access

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

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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

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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

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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

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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

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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

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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

Open access

Bettina Geidl-Flueck and Philipp A Gerber

Despite the existence of numerous studies supporting a pathological link between fructose consumption and the development of the metabolic syndrome and its sequelae, such as non-alcoholic fatty liver disease (NAFLD), this link remains a contentious issue. With this article, we shed a light on the impact of sugar/fructose intake on hepatic de novo lipogenesis (DNL), an outcome parameter known to be dysregulated in subjects with type 2 diabetes and/or NAFLD. In this review, we present findings from human intervention studies using physiological doses of sugar as well as mechanistic animal studies. There is evidence from both human and animal studies that fructose is a more potent inducer of hepatic lipogenesis than glucose. This is most likely due to the liver's prominent physiological role in fructose metabolism, which may be disrupted under pathological conditions by increased hepatic expression of fructolytic and lipogenic enzymes. Increased DNL may not only contribute to ectopic fat deposition (i.e., in the liver), but it may also impair several metabolic processes through DNL-related fatty acids (e.g., beta-cell function, insulin secretion, or insulin sensitivity).

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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