Hormonal Regulation of Stearoyl Coenzyme-A Desaturase 1 Activity and Gene Expression in Primary Cultures of Chicken Hepatocytes

Lefèvre, Pascal; Diot, Christian; Legrand, Philippe; Douaire, Madeleine

doi:10.1006/abbi.1999.1315

Cited by 33 publications

(18 citation statements)

References 46 publications

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“…We confirmed the marked induction of SCD-1 mRNA in ob͞ob liver compared with WT mice and observed that hepatic SCD-1 expression was decreased by 50% in the double-null mice compared with ob͞ob animals. Insulin increases SCD-1 activity (26,27); however, despite their reduced adiposity, MCH Ϫ/Ϫ ob͞ob mice were as hyperinsulinemic as ob͞ob mice. Thus, the decrease in SCD-1 expression in MCH Ϫ/Ϫ ob͞ob mice was not due to decreased insulin, which suggests that MCH may be involved in pathways regulating SCD-1 expression.…”

Section: Discussionmentioning

confidence: 99%

Melanin-concentrating hormone is a critical mediator of the leptin-deficient phenotype

Segal-Lieberman

Bradley

Kokkotou

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

215

143

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Energy homeostasis is regulated by a complex network involving peripheral and central signals that determine food intake and energy expenditure. Melanin-concentrating hormone (MCH) plays an essential role in this process. Animals treated with MCH develop hyperphagia and obesity. Ablation of the prepro-MCH gene leads to a lean phenotype, as does ablation of the rodent MCH receptor, MCHR-1. MCH is overexpressed in the leptin-deficient ob͞ob mouse, and we hypothesized that ablation of MCH in this animal would lead to attenuation of its obese phenotype. Compared with ob͞ob animals, mice lacking both leptin and MCH (double null) had a dramatic reduction in body fat. Surprisingly, the hyperphagia of the ob͞ob mouse was unaffected. Instead, leanness was secondary to a marked increase in energy expenditure resulting from both increased resting energy expenditure and locomotor activity. Furthermore, double-null mice showed improvements in other parameters impaired in ob͞ob mice. Compared with ob͞ob mice, double-null animals had increased basal body temperature, improved response to cold exposure, lower plasma glucocorticoid levels, improved glucose tolerance, and reduced expression of stearoyl-CoA desaturase 1 (SCD-1). These results highlight the importance of MCH in integration of energy homeostasis downstream of leptin and, in particular, the role of MCH in regulation of energy expenditure.M elanin-concentrating hormone (MCH), a 19-aa neuropeptide, is the product of the prepro-MCH gene and is expressed exclusively within the lateral hypothalamus. MCH neurons make monosynaptic projections throughout the neuraxis including the cortex and hindbrain, suggesting that MCH regulates complex motivated behaviors (1). A role for MCH in energy homeostasis emerged from studies demonstrating differential MCH gene expression in leptin-deficient ob͞ob mice, where MCH mRNA was overexpressed 2-to 3-fold compared with normal-weight littermates, in both fed and fasted states (2). Furthermore, MCH administration into the lateral ventricle of rats caused an acute and rapid increase in feeding (2, 4). Genetic evidence for a role of MCH in energy balance was derived from a model of MCH gene ablation, which produced a lean phenotype associated with a decrease in feeding and an increase in resting energy expenditure (3), and also from a model of transgene-derived eutopic overexpression, which produced mild obesity (5). Recently, chronic infusions of MCH were shown to produce hyperphagia and obesity in mice (6) and rats (7).Based on the foregoing evidence, we hypothesized that MCH contributed to the hyperphagia seen in ob͞ob mice (8) and predicted that mice lacking both MCH and leptin would show an attenuated obesity phenotype secondary to decreased feeding. Therefore, we performed a series of crosses of MCH Ϫ/Ϫ mice and ob͞ϩ mice to generate mice lacking both leptin and MCH, i.e., MCH Ϫ/Ϫ ob͞ob mice, designated double null. Double-null mice had marked attenuation of obesity and associated metabolic and endocrine abnormalities of leptin deficie...

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Section: Discussionmentioning

confidence: 99%

Melanin-concentrating hormone is a critical mediator of the leptin-deficient phenotype

Segal-Lieberman

Bradley

Kokkotou

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

215

143

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“…The Scd family, also known as ␦-9-desaturase in humans and asebia in mice, is composed of iron-containing enzymes that catalyze a rate-limiting step in the synthesis of monounsaturated fatty acids by introducing the first double bond, mainly in oleate and palmitoleate. Scd expression is modulated by dietary factors (e.g., polyunsaturated fatty acids, cholesterol, vitamin A [21][22][23]), hormonal signals (e.g., insulin, glucagon [24]), environmental factors (e.g., temperature changes, thiazolinediones, metals, alcohol, phenolic compounds [25][26][27][28]), peroxisomal proliferators (29), and developmental processes (30). Altered Scd activity has been observed in a wide range of disorders, including diabetes, atherosclerosis, cancer, obesity, and viral infections (25,31,32).…”

Section: Transcripts For Scd Enzymes Are Downregulated In Plinmentioning

confidence: 99%

Coordinated Upregulation of Oxidative Pathways and Downregulation of Lipid Biosynthesis Underlie Obesity Resistance in Perilipin Knockout Mice

et al. 2003

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Obesity is a major risk factor for diabetes and heart disease. We previously reported that the inactivation of the gene for perilipin (plin), an adipocyte lipid droplet surface protein, produced lean and obesity-resistant mice. To dissect the underlying mechanisms involved, we used oligonucleotide microarrays to analyze the gene-expression profile of white adipose tissue (WAT), liver, heart, skeletal muscle, and kidney of plin ؊/؊ and plin ϩ/ϩ mice. As compared with wild-type littermates, the WAT of plin ؊/؊ mice had 270 and 543 transcripts that were significantly up-or downregulated. There was a coordinated upregulation of genes involved in ␤-oxidation, the Krebs cycle, and the electron transport chain concomitant with a downregulation of genes involved in lipid biosynthesis. There was also a significant downregulation of the stearoyl CoA desaturase-1 gene, which has been associated with obesity resistance. Thus, in response to the constitutive activation of lipolysis associated with absence of perilipin, WAT activated pathways to rid itself of the products of lipolysis and activated pathways of energy expenditure that contribute to the observed obesity resistance. The biochemical pathways involved in obesity resistance in plin ؊/؊ mice identified in this study may represent potential targets for the treatment of obesity. Diabetes 52:2666 -2674, 2003 P erilipin (plin) is a member of a family of proteins that coat the surfaces of intracellular neutral lipid storage droplets, mainly in adipocytes and in steroidogenic cells (1,2). Perilipin, in the basal state, prevents access of hormone-sensitive lipase to the lipid droplet (3) and is a major substrate of cAMPdependent protein kinase in adipocytes (4). Specific hormonal or cytokine stimuli, such as catecholamines and tumor necrosis factor-␣, activate lipolysis by phosphorylating perilipin, thereby allowing hormone-sensitive lipase to access the lipid droplet and initiate its lipolytic action (5,6).Plin Ϫ/Ϫ mice are characterized by constitutive lipolysis, normal body weight despite an increase in food consumption, a lean body habitus, and smaller fat depots composed of small adipocytes (7,8). These mice display increased oxygen consumption and are resistant to diet-induced and genetic obesity (7).To explain this phenotype, we hypothesized that there had to be significant changes in the expression of genes involved in pathways for substrate and energy metabolism. We further reasoned that although perilipin is expressed in adipocytes, there should be concomitant changes in other tissues that are important in whole-body metabolism, such as the liver, skeletal muscle, heart, and kidney, to explain the profound changes seen in plin Ϫ/Ϫ mice. To test these hypotheses, we performed oligonucleotide microarray analysis of the above tissues of plin Ϫ/Ϫ mice and compared the data with those obtained from their wild-type littermates. We show a concomitant and coordinated upregulation of multiple genes involved in oxidative catabolic pathways along with downregulation of gene...

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“…Human SCD-5 was abundantly expressed in brain and pancreas (Wang et al 2005). In birds, one SCD isoform (SCD) has been, so far, identified and cloned (GenBank accession number X60465) and very little is known about its tissue distributions and regulation (Lefevre et al 1999(Lefevre et al , 2001.…”

Section: Introductionmentioning

confidence: 99%

The regulation of stearoyl-CoA desaturase gene expression is tissue specific in chickens

Dridi¹,

Taouis²,

Gertler³

et al. 2007

Journal of Endocrinology

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Emerging evidence suggests a potential role of stearoyl-CoA desaturase (SCD)-1 in the control of body weight and energy homeostasis. The present study was conducted to investigate the effects of several energy balance-related factors (leptin, cerulenin, food deprivation, genotype, and gender) on SCD gene expression in chickens. In experiment 1, 6-week-old female and male broiler chickens were used. In experiment 2, two groups of 3-week-old broiler chickens were continuously infused with recombinant chicken leptin (8 mg/kg/h) or vehicle for 6 h. In experiment 3, two groups of 2-week-old broiler chickens received i.v. injections of cerulenin (15 mg/kg) or vehicle. In experiment 4, two broiler chicken lines (fat and lean) were submitted to two nutritional states (food deprivation for 16 or 24 h and feeding ad libitum). At the end of each experiment, tissues were collected for analyzing SCD gene expression. Data from experiment 1 showed that SCD is ubiquitously expressed in chicken tissues with highest levels in the proventriculus followed by the ovary, hypothalamus, kidney, liver, and adipose tissue in female, and hypothalamus, leg muscle, pancreas, liver, and adipose tissue in male. Female chickens exhibited significantly higher SCD mRNA levels in kidney, breast muscle, proventriculus, and intestine than male chickens. However, hypothalamic SCD gene expression was higher in male than in female (P!0 . 05). Leptin increased SCD gene expression in chicken liver (P!0 . 05), whereas cerulenin decreased SCD mRNA levels in muscle. Both leptin and cerulenin significantly reduced food intake (P!0 . 05). Food deprivation for either 16 or 24 h decreased the hepatic SCD gene expression in fat line and lean line chickens compared with their fed counterparts (P!0 . 05). The hypothalamic SCD mRNA levels were decreased in both lines only after 24 h of food deprivation (P!0 . 05). In conclusion, SCD is ubiquitously expressed in chickens and it is regulated by leptin, cerulenin, nutritional state, and gender in a tissue-specific manner.

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Hormonal Regulation of Stearoyl Coenzyme-A Desaturase 1 Activity and Gene Expression in Primary Cultures of Chicken Hepatocytes

Cited by 33 publications

References 46 publications

Melanin-concentrating hormone is a critical mediator of the leptin-deficient phenotype

Melanin-concentrating hormone is a critical mediator of the leptin-deficient phenotype

Coordinated Upregulation of Oxidative Pathways and Downregulation of Lipid Biosynthesis Underlie Obesity Resistance in Perilipin Knockout Mice

The regulation of stearoyl-CoA desaturase gene expression is tissue specific in chickens

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