Activation of liver X receptor promotes fatty acid synthesis in goat mammary epithelial cells via modulation of SREBP1 expression

Xu, Huifen; Luo, Jun; Zhang, X.Y.; Li, J.; Bionaz, Massimo

doi:10.3168/jds.2018-15538

Cited by 20 publications

(14 citation statements)

References 69 publications

(113 reference statements)

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“…LXR also directly stimulates the transcription of specific lipogenic genes, including acetyl-CoA carboxylase α ( ACACA ) in chick embryos and fatty acid synthase ( FASN ) in human cells. 90 Diosgenin (10, 25, and 50 µM) significantly inhibited the accumulation of TG and the increase of SREBP-1c mRNA in HepG2 cells induced by high glucose levels. In addition, compared with the model group, diosgenin (0.5% or 1% w/w) treated rats fed with a HFD also exhibited significantly suppressed LXRα levels.…”

Section: The Pharmacological Mechanism Underlying the Use Of Diosgenin For Treatment Of Hyperlipidemiamentioning

confidence: 93%

The Effects of Diosgenin on Hypolipidemia and Its Underlying Mechanism: A Review

Sun

Yang

et al. 2021

DMSO

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Hyperlipidemia is a disorder of lipid metabolism, which is a major cause of coronary heart disease. Although there has been considerable progress in hyperlipidemia treatment, morbidity and risk associated with the condition continue to rise. The first-line treatment for hyperlipidemia, statins, has multiple side effects; therefore, development of safe and effective drugs from natural products to prevent and treat hyperlipidemia is necessary. Diosgenin is primarily derived from fenugreek ( Trigonella foenum graecum ) seeds, and is also abundant in medicinal herbs such as Dioscorea rhizome, Dioscorea septemloba , and Rhizoma polygonati , is a well-known steroidal sapogenin and the active ingredient in many drugs to treat cardiovascular conditions. There is abundant evidence that diosgenin has potential for application in correcting lipid metabolism disorders. In this review, we evaluated the latest evidence related to diosgenin and hyperlipidemia from clinical and animal studies. Additionally, we elaborate the pharmacological mechanism underlying the activity of diosgenin in treating hyperlipidemia in detail, including its role in inhibition of intestinal absorption of lipids, regulation of cholesterol transport, promotion of cholesterol conversion into bile acid and its excretion, inhibition of endogenous lipid biosynthesis, antioxidation and lipoprotein lipase activity, and regulation of transcription factors related to lipid metabolism. This review provides a deep exploration of the pharmacological mechanisms involved in diosgenin-hyperlipidemia interactions and suggests potential routes for the development of novel drug therapies for hyperlipidemia.

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Section: The Pharmacological Mechanism Underlying the Use Of Diosgenin For Treatment Of Hyperlipidemiamentioning

confidence: 93%

The Effects of Diosgenin on Hypolipidemia and Its Underlying Mechanism: A Review

Sun

Yang

et al. 2021

DMSO

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“…Moreover, since adult cardiomyocytes use fatty acids for 70% of the ATP used for contractility (72), the long-term suppression of Fasn, Scd1, and other fatty acid synthesis genes may affect the functionality of the remaining cardiomyocytes after they have stopped proliferating and further contribute to the diastolic heart failure. Agonists for nuclear hormone receptors that work with SREBF1 to induce lipogenesis, such as liver X receptor (LXR) and PPARG, are currently available (73)(74)(75)(76)(77). Future studies will be needed to determine if these compounds can be used to protect or restore the postnatal proliferation and survival of atrial cardiomyocytes in mice exposed to hyperoxia and potentially lead to novel therapies to prevent diastolic heart failure in individuals who were born preterm.…”

Section: Discussionmentioning

confidence: 99%

Neonatal hyperoxia inhibits proliferation and survival of atrial cardiomyocytes by suppressing fatty acid synthesis

Cohen¹,

Yee²,

Porter³

et al. 2021

JCI Insight

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Preterm birth increases the risk for pulmonary hypertension and heart failure in adulthood. Oxygen therapy can damage the immature cardiopulmonary system and may be partially responsible for the cardiovascular disease in adults born preterm. We previously showed that exposing newborn mice to hyperoxia causes pulmonary hypertension by 1 year of age that is preceded by a poorly understood loss of pulmonary vein cardiomyocyte proliferation. We now show that hyperoxia also reduces cardiomyocyte proliferation and survival in the left atrium and causes diastolic heart failure by disrupting its filling of the left ventricle. Transcriptomic profiling showed that neonatal hyperoxia permanently suppressed fatty acid synthase ( Fasn ), stearoyl-CoA desaturase 1 ( Scd1 ), and other fatty acid synthesis genes in the atria of mice, the HL-1 line of mouse atrial cardiomyocytes, and left atrial tissue explanted from human infants. Suppressing Fasn or Scd1 reduced HL-1 cell proliferation and increased cell death, while overexpressing these genes maintained their expansion in hyperoxia, suggesting that oxygen directly inhibits atrial cardiomyocyte proliferation and survival by repressing Fasn and Scd1 . Pharmacologic interventions that restore Fasn , Scd1 , and other fatty acid synthesis genes in atrial cardiomyocytes may, thus, provide a way of ameliorating the adverse effects of supplemental oxygen on preterm infants.

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“…Several studies have confirmed that t10c12-CLA, PPARG and PPARD exhibit positive regulation of both CD36 (35, 87, 106) and ACSL1 (34,36,63), however, Shi et al (61) challenge the above view that t10c12-CLA A positively regulates CD36 and ACSL1, which may be related to factors such as the species, mode and amount of additives, the exact mechanism of action needs to be further verified by more in-depth experimental studies as well as large-scale populations. As previously described, 14-3-3γ, LXR, SREBP1 and CIDEC have positive regulatory roles in the de novo synthesis of milk fat, which perform similar functions during LCFA uptake (21,29,36,69). The SLC27 family (SLC27A1 to SLC27A6) is considered to be bifunctional proteins with LCFA transport and acyl-CoA synthetase activity.…”

Section: Lcfa Uptake and Activationmentioning

confidence: 91%

“…In addition, FASN, ATGL, CIDEA and LXR positively regulated the expression of XDH and Btn1a1 in ruminants (29,45,86,113).…”

Section: Regulation Of Xdh and Btn1a1mentioning

confidence: 91%

Regulation of Key Genes for Milk Fat Synthesis in Ruminants

et al. 2021

Front. Nutr.

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Milk fat is the most important and energy-rich substance in milk and plays an important role in the metabolism of nutrients during human growth and development. It is mainly used in the production of butter and yogurt. Milk fat not only affects the flavor and nutritional value of milk, but also is the main target trait of ruminant breeding. There are many key genes involve in ruminant milk fat synthesis, including ACSS2, FASN, ACACA, CD36, ACSL, SLC27A, FABP3, SCD, GPAM, AGPAT, LPIN, DGAT1, PLIN2, XDH, and BTN1A1. Taking the de novo synthesis of fatty acids (FA) and intaking of long-chain fatty acids (LCFA) in blood to the end of lipid droplet secretion as the mainline, this manuscript elucidates the complex regulation model of key genes in mammary epithelial cells (MECs) in ruminant milk fat synthesis, and constructs the whole regulatory network of milk fat synthesis, to provide valuable theoretical basis and research ideas for the study of milk fat regulation mechanism of ruminants.

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Activation of liver X receptor promotes fatty acid synthesis in goat mammary epithelial cells via modulation of SREBP1 expression

Cited by 20 publications

References 69 publications

The Effects of Diosgenin on Hypolipidemia and Its Underlying Mechanism: A Review

The Effects of Diosgenin on Hypolipidemia and Its Underlying Mechanism: A Review

Neonatal hyperoxia inhibits proliferation and survival of atrial cardiomyocytes by suppressing fatty acid synthesis

Regulation of Key Genes for Milk Fat Synthesis in Ruminants

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