SREBP transcription factors: master regulators of lipid homeostasis

Eberlé, Delphine; Hegarty, Bronwyn; Bossard, Pascale; Ferré, Pascal; Foufelle, Fabienne

doi:10.1016/j.biochi.2004.09.018

Cited by 1,261 publications

(1,051 citation statements)

References 102 publications

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“…In early and mid lactation, the main promoter up-regulated in adipose tissue was PI and the main promoter down-regulated in mammary tissue was PIII. Interestingly, SREBP1, that it is considered a global regulator of lipid synthesis (Eberlé et al, 2004), had a similar response to the ACC-α PIII transcripts in the mammary gland, whereas in adipose tissue had a similar response to ACC-α PI transcripts and FASN. SREBP1 regulates enzymes which synthesize FA and cholesterol from precursor molecules (Horton et al, 2003;Goldstein et al, 2006) and SREBP1 is a major regulator of mammary de novo FA synthesis and the response to dietary factors that modify milk fat in mouse (Anderson et al, 2007) and cow (Harvatine and Bauman, 2006).…”

Section: Discussionmentioning

confidence: 98%

Transcriptional regulation of acetyl-CoA carboxylase α isoforms in dairy ewes during conjugated linoleic acid induced milk fat depression

Ticiani

Urio

Ferreira

et al. 2016

Animal

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Feeding trans-10, cis-12 CLA to lactating ewes reduces milk fat by down-regulating expression of enzymes involved in lipid synthesis in the mammary gland and increases adipose tissue lipogenesis. Acetyl-CoA carboxylase α (ACC-α) is a key regulated enzyme in de novo fatty acid synthesis and is decreased by CLA. In the ovine, the ACC-α gene is expressed from three tissuespecific promoters (PI, PII and PIII). This study evaluated promoter-specific ACC-α expression in mammary and adipose tissue of lactating cross-bred Lacaune/Texel ewes during milk fat depression induced by rumen-unprotected trans-10, cis-12 CLA supplement. In all, 12 ewes arranged in a completely randomized design were fed during early, mid and late lactation one of the following treatments for 14 days: Control (forage + 0.9 kg of concentrate on a dry matter basis) and CLA (forage + 0.9 kg of concentrate + 27 g/day of CLA (29.9% trans-10, cis-12)). Mammary gland and adipose tissue biopsies were taken on day 14 for gene expression analysis by real-time PCR. Milk fat yield and concentration were reduced with CLA supplementation by 27%, 21% and 35% and 28%, 26% and 42% during early, mid and late lactation, respectively. Overall, our results suggest that trans-10, cis-12 CLA down-regulates mammary ACC-α gene expression by decreasing expression from PII and PIII in mammary gland and up-regulates adipose ACC-α gene expression by increasing expression from PI.

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Section: Discussionmentioning

confidence: 98%

Transcriptional regulation of acetyl-CoA carboxylase α isoforms in dairy ewes during conjugated linoleic acid induced milk fat depression

Ticiani

Urio

Ferreira

et al. 2016

Animal

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“…In addition, SREBP1 also acts as an allostatic mediator that induces adaptive responses to maintain optimal membrane lipid composition in adipocytes (Hagen et al 2010), and regulates desaturase gene expression (Eberle et al 2004). Indeed, fatty acids appear to regulate SREBP1 activation in a feedback loop, controlling the ratio of unsaturated and saturated fatty acids.…”

Section: Discussionmentioning

confidence: 99%

Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients

et al. 2014

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Adipose tissue (AT) is a key organ in the regulation of total body lipid homeostasis, which is responsible for the storage and release of fatty acids according to metabolic needs. We aimed to investigate the effect of the quantity and quality of dietary fat on the lipogenesis and lipolysis processes in the AT of metabolic syndrome (MetS) patients. A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to one of four diets: (a) high-saturated fatty acid (HSFA) (b) highmonounsaturated fatty acid, and (c, d) two low-fat, highcomplex carbohydrate diets supplemented with long chain (LC) n-3 (LFHCC n-3) polyunsaturated fatty acids (PUFA) or placebo (LFHCC), for 12 weeks each. A fat challenge reflecting the same fatty acid composition as the original diets was conducted post-intervention. Long-term consumption of the LFHCC diet induced an increase in the fasting expression levels of the sterol regulatory element binding protein-1 and stearoyl-CoA desaturase D9-desaturase genes, whereas the supplementation of this diet with n-3 PUFA reversed this effect (p = 0.007). In contrast, long-term consumption of the HSFA diet increased the expression of the adipose triglyceride lipase (ATGL) gene, at both fasting and postprandial states (both, p \ 0.001). Our results showed the anti-lipogenic effect exerted by LC n-3 PUFA when administered together with a LFHCC diet. Conversely, a diet high in saturated fat increased the expression of the lipolytic gene ATGL relative to the other diets.

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“…4) in an attempt to facilitate understanding of their role(s) in HCD-induced liver steatosis. In addition, one gene, sterol regulatory element-binding protein (SREBP)-1c, which controls the transcription of genes involved in fatty acid synthesis [23], and whose transcription is regulated by insulin [24], was upregulated. Another gene, peroxisome proliferator-activated receptor (PPAR)-a, also a transcription factor, but encoding enzymes involved in fatty acid oxidation [25], was likewise upregulated.…”

Section: Discussionmentioning

confidence: 99%

“…Other abbreviations: SD, standard diet; HCD, high carbohydrate diet. The following values apply for the HCD-to-SD ratio: GCK, 2.00 ± 0.18; Cyp450 reductase, 0.16 ± 0.08; EGFR, 1.23 ± 0.28 such an upregulation could not be accomplished otherwise than through an adequate response of the liver cells to insulin, (iii) nonenzymatic factors involved in lipid synthesis, such as SREBP-1, are also under the control of insulin [24,39]; the expression of this factor that, in turn, controls several major enzymes involved in fatty acid synthesis [40], was upregulated 1.6-fold (Table 3). Taken together, the gene expression data of this and of cited studies are not compatible with an insulin-resistant liver during the phase of NAFLD in which our animals were killed.…”

Section: Discussionmentioning

confidence: 99%

Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

et al. 2007

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SREBP transcription factors: master regulators of lipid homeostasis

Cited by 1,261 publications

References 102 publications

Transcriptional regulation of acetyl-CoA carboxylase α isoforms in dairy ewes during conjugated linoleic acid induced milk fat depression

Transcriptional regulation of acetyl-CoA carboxylase α isoforms in dairy ewes during conjugated linoleic acid induced milk fat depression

Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients

Genome-wide transcriptome expression in the liver of a mouse model of high carbohydrate diet-induced liver steatosis and its significance for the disease

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