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In the teleost, Fundulus grandis, injections of prolactin early in the light phase cause an immediate 50% depression in the rate of hepatic lipogenesis ([14C]acetate incorporation); 10 h later, that rate has returned to levels not different from controls. Injections of prolactin late in the light phase cause an even more dramatic immediate depression of lipogenesis (79%) followed by a gradual increase in lipogenic rate which is 2·6 times higher than the control rate after 24 h. The stimulation of lipogenesis by prolactin is blocked by simultaneous treatment with indomethacin, an inhibitor of prostaglandin synthesis. These circadian phase-dependent effects of prolactin on hepatic lipogenesis are discussed with reference to possible mechanisms of action exerted by endogenous prolactin rhythms.

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A. M. Alves, A. J. Thody, C. Fisher, and S. Shuster


Lipogenesis was measured in isolated preputial gland cells of female rats after ovariectomy and after the administration of oestradiol benzoate. Ovariectomy decreased preputial gland cell lipogenesis and also altered the pattern of lipid synthesis, producing a relative decrease in the proportion of polar lipids and an increase in the proportion of 'triglycerides'. Although daily administration of 2 or 10 μg oestradiol benzoate for 7 days produced slight increases in preputial gland cell lipogenesis in ovariectomized rats, the effects were not significant. A single injection of 10 μg oestradiol benzoate, however, produced significant increases in preputial gland cell lipogenesis of ovariectomized rats at both 2 and 24 h and, moreover, at 24 h the pattern of polar lipid and triglyceride labelling was restored to normal. Prior administration of actinomycin D reduced the lipogenic effect of oestradiol benzoate. Oestradiol benzoate had little or no effect on preputial gland cell lipogenesis in male rats. These results confirm that oestrogen is able to stimulate preputial lipogenesis in female rats. Whether this action of oestrogen is related to its pheromone-producing effect on the preputial glands is not yet known.

J. Endocr. (1986) 109, 1–7

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Ken Takao, Katsumi Iizuka, Yanyan Liu, Teruaki Sakurai, Sodai Kubota, Saki Kubota-Okamoto, Toshinori Imaizumi, Yoshihiro Takahashi, Yermek Rakhat, Satoko Komori, Tokuyuki Hirose, Kenta Nonomura, Takehiro Kato, Masami Mizuno, Tetsuya Suwa, Yukio Horikawa, Masakatsu Sone, and Daisuke Yabe

hepatic lipogenesis is impaired in Chrebp −/− mice, which have reduced hepatic triglyceride content and reduced plasma triglyceride levels ( Iizuka et al. 2004 ). Interestingly, Chrebp −/− mice show reduced plasma cholesterol levels due to decreased

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A.-M. Mendes, R. J. Madon, and D. J. Flint


Cortisol implants in normal and diabetic rats reduced body weight, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in isolated adipocytes, whilst insulin sensitivity was unchanged. In normal but not diabetic rats these changes were accompanied by increased serum glucose and insulin concentrations.

In contrast, progesterone implants in normal and diabetic rats increased body weight gain, adiposity, insulin receptor concentration and both basal and insulin-stimulated rates of lipogenesis in adipose tissue, again without affecting insulin sensitivity. Progesterone did not affect serum insulin concentrations in normal or diabetic rats but accelerated the decline in serum glucose concentrations which occurred during an overnight fast in diabetic rats.

The results suggest that (1) cortisol inhibits lipogenesis in adipose tissue without affecting insulin sensitivity, (2) cortisol reduces insulin binding in adipose tissue without a requirement for hyperinsulinaemia, which might itself indirectly lead to down-regulation of the insulin receptor, and (3) in diabetic rats progesterone stimulates lipogenesis in adipose tissue without any increase in food intake or serum insulin concentrations suggesting that progesterone may have a direct anabolic role in adipose tissue.

J. Endocr. (1985) 106, 225–231

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R G Vernon


The intracellular signalling systems involved in the chronic insulin-antagonistic, anti-lipogenic effects and also the lipolytic effect of GH have been investigated in sheep adipose tissue in an in vitro tissue culture system. During culture, chronic exposure to GH decreased the rate of lipogenesis and prevented the increase in lipogenesis induced by insulin. GH also increased glycerol release into the culture medium. GH had no acute, insulin-like effect on lipogenesis in sheep adipose tissue.

Pretreatment with phorbol ester to down-regulate isoforms of protein kinase C or addition of the protein serine kinase inhibitor staurosporine decreased the anti-lipogenic effect of GH while the protein serine kinase inhibitor H7 eliminated it completely. Pretreatment with phorbol ester or addition of H7 also decreased the insulin-antagonistic effect of GH on lipogenesis. Addition of the protein serine phosphatase inhibitor okadaic acid or the phosphatidyl choline phospholipase C inhibitor D609 both diminished the anti-lipogenic and insulin-antagonistic effects of GH.

Chronic exposure of adipose tissue to GH had no effect on the total activity of acetyl CoA carboxylase or its activation status but it did diminish the increase in activation status induced by insulin. H7 and okadaic acid also diminished the increase in activation status of acetyl CoA carboxylase induced by insulin but did not alter the effect of GH on this variable. Okadaic acid decreased total acetyl CoA carboxylase activity.

Pretreatment with phorbol ester or the addition of H7, staurosporine or okadaic acid increased glycerol release into the culture medium to the same extent as GH itself; the effects of GH and these various agents were not additive.

These studies suggest that the anti-lipogenic, insulin-antagonistic effects of GH involve both protein serine kinases and phosphatases, possibly including one or more isoforms of protein kinase C, and a phosphatidyl choline-specific phospholipase C. Comparison with studies by others on the GH enhancement of preadipocyte differentiation and prolactin stimulation of lipogenesis in mammary tissue suggests involvement of protein kinase C at an early stage in all three systems. In contrast, effects of okadaic acid vary with the system, suggesting the involvement of protein serine phosphatase activity in a late stage of the action of GH. The effects of GH on lipogenesis and lipolysis do not occur via identical mechanisms.

Journal of Endocrinology (1996) 150, 129–140

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SK Jacobi, KM Ajuwon, TE Weber, JL Kuske, CJ Dyer, and ME Spurlock

Adiponectin is an adipocyte-derived hormone that has been implicated recently in the regulation of inflammation in immunocytes, and in lipid metabolism and glucose homeostasis in liver, skeletal muscle and adipocytes. However, information in non-rodent models is limited. We have cloned and sequenced the porcine adiponectin open reading frame and evaluated the regulation of adiponectin in vivo following lipopolysaccharide (LPS) or E. coli administration. The porcine sequence shares approximately 88, 86, 85 and 83% homology with the dog, human, cow and mouse adiponectin respectively, and 79-83% similarity with dog, human, cow and mouse proteins at the amino acid level, based on the translated porcine sequence and GenBank submissions for the other species. Relative serum adiponectin concentrations were not altered in pigs infused with E. coli, and mRNA expression in adipose tissue was not responsive to LPS. However, analysis of serum from very lean vs a substantially fatter genotype of pig indicated that relative circulating adiponectin concentrations are higher (P<0.01) in the lean pigs than in the fatter genotype, and that the difference is established relatively early in the growth curve. Also, incubating pig adipocytes for 6 h with recombinant pig adiponectin resulted in an approximately 30% reduction (P<0.05) in lipogenesis compared with adipocytes under basal conditions and with those incubated in the presence of insulin. This is the first report in any species that adiponectin antagonizes the incorporation of glucose carbon into lipid in the adipocyte, and provides additional evidence that adiponectin acts as an autocrine regulatory factor to regulate energy metabolism.

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The effects of progesterone on isolated rat adipocytes were studied in vitro during various steps of glucose metabolism, transport, lipogenesis and lipolysis. Progesterone decreased the phosphorylation of glucose into glucose-6-phosphate as assessed by measuring the uptake of 2-deoxyglucose but it had no effect on transmembrane transport of glucose as determined by measuring the entry of 3-0-methylglucose into the cell. As glucose phosphorylation is a rate-limiting step of the pentose-phosphate pathway, these data could explain the inhibition of lipogenesis and the enhancement of lipolysis observed when progesterone is present in incubation medium. Progesterone might thus modulate a regulatory step of glucose metabolism and antagonize insulin action in the fat cell.

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Giselle Adriana Abruzzese, Maria Florencia Heber, Silvana Rocio Ferreira, Leandro Martin Velez, Roxana Reynoso, Omar Pedro Pignataro, and Alicia Beatriz Motta

between the uptake and exportation of fatty acids (which in turn can be esterified or to be oxidized) ( Browning & Horton 2004 , Kawano & Cohen 2013 ). However, when the balance between lipolysis and lipogenesis is altered, or fatty acid influx to the

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Lei Yu, Haoran Wang, Xiaoxue Han, Honghui Liu, Dalong Zhu, Wenhuan Feng, Jinhui Wu, and Yan Bi

 < 0.05, **P  < 0.01. Data are represented as the mean ±  s.d. A full color version of this figure is available at . OT reduces hepatic lipogenesis and HIF-2α mediates the alleviation of hepatic

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Jin-Bong Lee, Sung-Jin Yoon, Sang-Hyun Lee, Moo-Seung Lee, Haiyoung Jung, Tae-Don Kim, Suk Ran Yoon, Inpyo Choi, Ik-Soo Kim, Su Wol Chung, Hee Gu Lee, Jeong-Ki Min, and Young-Jun Park

. 2013 , Lefterova et al . 2014 ). In adipocytes, PPARγ is required for differentiation, lipogenesis ( Brun et al . 1996 , Tontonoz & Spiegelman 2008 ) and survival ( Imai et al . 2004 ). In addition to its role in adipocyte differentiation and lipid