Uncoupling protein‐3 gene expression in skeletal muscle during development is regulated by nutritional factors that alter circulating non‐esterified fatty acids

Brun, Sònia; Carmona, Mamen; Mampel, Teresa; Viñas, Octavi; Giralt, Marta; Iglesias, Roser; Villarroya, Francesc

doi:10.1016/s0014-5793(99)00722-x

Cited by 57 publications

(50 citation statements)

References 21 publications

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“…In itro and in i o experiments demonstrated that fatty acids or certain retinoids promote UCP2 and\or UCP3 expression in white and brown adipocytes, myocytes and pancreatic islets [171,172,177,206,[229][230][231][232][233][234][235][236][237][238]. Expression of UCP2 and\or UCP3 in skeletal muscles, heart or adipose tissue can be induced by various situations characterized by elevated levels of circulating non-esterified fatty acids, such as starvation in humans or rodents [84,169,239,240], high-fat feeding in rodents [30,177] and genetic or experimental diabetes in rodents [31,241,242].…”

Section: Contribution Of Ucps To Dit Energy Partitioning and Lipid Mmentioning

confidence: 99%

The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP

Ricquier¹,

Bouillaud

2000

Biochemical Journal

610

115

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Animal and plant uncoupling protein (UCP) homologues form a subfamily of mitochondrial carriers that are evolutionarily related and possibly derived from a proton\anion transporter ancestor. The brown adipose tissue (BAT) UCP1 has a marked and strongly regulated uncoupling activity, essential to the maintenance of body temperature in small mammals. UCP homologues identified in plants are induced in a cold environment and may be involved in resistance to chilling. The biochemical activities and biological functions of the recently identified mammalian UCP2 and UCP3 are not well known. However, recent data support a role for these UCPs in State 4 respiration, respiration uncoupling and proton leaks in mitochondria. Moreover, genetic studies suggest that UCP2 and UCP3 play a part in

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Section: Contribution Of Ucps To Dit Energy Partitioning and Lipid Mmentioning

confidence: 99%

The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP

Ricquier¹,

Bouillaud

2000

Biochemical Journal

610

115

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“…For example, UCP-3 mRNA abundance is unaltered in situations of enhanced regulatory thermogenesis in muscle, such as long-term cold exposure (6), whereas UCP-3 mRNA is upregulated in situations of depressed muscle thermogenesis, such as starvation (7,8). In fact, most of the physiological or pathological situations reported to date in which UCP-3 gene expression in skeletal muscle is altered (i.e., during instances of high-fat diets, postnatal development, or streptozotozininduced diabetes) are associated with parallel changes in circulating free fatty acids (9)(10)(11). Fatty acids themselves have been reported to upregulate UCP-3 gene expression in muscle (7,12), most likely by activating peroxisome proliferatoractivated receptor (PPAR)-␣ (12), and it has been proposed that UCP-3 could be specifically involved in the regulation of the use of lipids as fuel substrates in skeletal muscle.…”

Section: Impaired Expression Of the Uncoupling Protein-3 Gene In Skelmentioning

confidence: 99%

Impaired expression of the uncoupling protein-3 gene in skeletal muscle during lactation: fibrates and troglitazone reverse lactation-induced downregulation of the uncoupling protein-3 gene.

et al. 2000

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The expression of uncoupling protein (UCP)-3 mRNA in skeletal muscle is dramatically reduced during lactation in mice. The reduction in UCP-3 mRNA levels lowers the amount of the UCP-3 protein in skeletal muscle mitochondria during lactation. Spontaneous or abrupt weaning reverses the downregulation of the UCP-3 mRNA but not the reduction in UCP-3 protein levels. In lactating and virgin mice, however, fasting increases UCP-3 mRNA levels. Changes in UCP-3 mRNA occur in parallel with modifications in the levels of free fatty acids, which are reduced in lactation and are upregulated due to weaning or fasting. Modifications in the energy nutritional stress of lactating dams achieved by manipulating litter sizes do not influence UCP-3 mRNA levels in skeletal muscle. Conversely, when mice are fed a high-fat diet after parturition, the downregulation of UCP-3 mRNA and UCP-3 protein levels due to lactation is partially reversed, as is the reduction in serum free fatty acid levels. Treatment of lactating mice with a single injection of bezafibrate, an activator of the peroxisome proliferator-activated receptor (PPAR), raises UCP-3 mRNA in skeletal muscle to levels similar to those in virgin mice. 4-chloro-6-[(2,3-xylidine)-pirimidinylthio] acetic acid (WY-14,643), a specific ligand of the PPAR-␣ subtype, causes the most dramatic increase in UCP-3 mRNA, whereas troglitazone, a specific activator of PPAR-␥, also significantly increases UCP-3 mRNA abundance in skeletal muscle of lactating mice. However, in virgin mice, bezafibrate and WY-14,643 do not significantly affect UCP-3 mRNA expression, whereas troglitazone is at least as effective as it is in lactating dams. It is proposed that the UCP-3 gene is regulated in skeletal muscle during lactation in response to changes in circulating free fatty acids by mechanisms involving activation of PPARs. The impaired expression of the UCP-3 gene is consistent with the involvement of UCP-3 gene regulation in the reduction of the use of fatty acids as fuel by the skeletal muscle and in impaired adaptative thermogenesis, both of which are major metabolic adaptations that occur during lactation.

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“…It is not known, however, whether there are breed-related differences in UCP2 or 3 expression and abundance in adipose tissue or skeletal muscle of these pigs. UCP1 and, more recently, UCP2 and 3 have been shown to be regulated by free fatty acids (Brun et al 1999, Samec et al 1999. With the observed differences in milk composition, it is possible that fatty acids may play a role in the regulation of uncoupling activity in pigs.…”

Section: Introductionmentioning

confidence: 99%

“…UCP3 has a number of proposed roles in the regulation of fatty acid metabolism (Brun et al 1999, Himms-Hagen & Harper 2001, Schrauwen et al 2001, Wang et al 2003, protecting against obesity (Walder et al 1998) and ROS accumulation (Vidal-Puig et al 2000). These functions, however, have been disputed (Nedergaard & Cannon 2003), and to date their function has been described only in rodents.…”

Section: Introductionmentioning

confidence: 99%

Influence of genotype on the differential ontogeny of uncoupling protein 2 and 3 in subcutaneous adipose tissue and muscle in neonatal pigs

Mostyn¹,

Litten²,

Perkins³

et al. 2004

Journal of Endocrinology

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The present study aimed to determine whether porcine genotype and/or postnatal age influenced mRNA abundance or protein expression of uncoupling protein (UCP)2 or 3 in subcutaneous adipose tissue (AT) and skeletal muscle (SM) and the extent to which these differences are associated with breed-specific discordance in endocrine and metabolic profiles. Piglets from commercial and Meishan litters were ranked according to birth weight. Tissue samples were obtained from the three median piglets from each litter on either day 0, 4, 7, 14 or 21 of neonatal life. UCP2 protein abundance in AT was similar between genotypes on the first day of life, but it was elevated at all subsequent postnatal ages (P<0·05) in AT of Meishan piglets. In contrast, UCP2 mRNA abundance was lower in Meishans up to 14 days of age. UCP2 mRNA expression was not correlated with protein abundance in either breed at any age. UCP3 mRNA in AT was similar between breeds up to day 7; thereafter, expression was higher (general linear model, P<0·05) in Meishan piglets. Conversely, UCP3 mRNA expression in SM was higher in commercial piglets after day 7. Colonic temperature remained lower in Meishan than commercial piglets throughout the study; this was most obvious in the immediate post-partum period when Meishan piglets had lower (P<0·05) plasma triiodothyronine. In conclusion, we have demonstrated that porcine genotype influences the expression and abundance of UCP2 and 3, an influence which may, in part, be due to the distinctive endocrine profiles associated with each genotype.

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Uncoupling protein‐3 gene expression in skeletal muscle during development is regulated by nutritional factors that alter circulating non‐esterified fatty acids

Cited by 57 publications

References 21 publications

The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP

The uncoupling protein homologues: UCP1, UCP2, UCP3, StUCP and AtUCP

Impaired expression of the uncoupling protein-3 gene in skeletal muscle during lactation: fibrates and troglitazone reverse lactation-induced downregulation of the uncoupling protein-3 gene.

Influence of genotype on the differential ontogeny of uncoupling protein 2 and 3 in subcutaneous adipose tissue and muscle in neonatal pigs

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