Lecithin:Cholesterol Acyltransferase (LCAT) Deficiency Promotes Differentiation of Satellite Cells to Brown Adipocytes in a Cholesterol-dependent Manner

Nesan, Dinushan; Tavallaee, Ghazaleh; Koh, Deborah; Bashiri, Amir; Abdin, Rawand; Ng, Dominic S.

doi:10.1074/jbc.m115.676056

Cited by 7 publications

(4 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Meanwhile, LCAT promoted the PPARγ signalling pathway at the protein and RNA levels, and the effects of LCAT overexpression and interference on preadipocyte differentiation were determined by qPCR and Oil red O staining. However, the research by Nesan et al showed that LCAT deficiency could promote the differentiation of cholesterol-dependent satellite cells into brown adipocytes [ 24 ]. This is contrary to our results, and the reasons for this difference are unclear.…”

Section: Discussionmentioning

confidence: 99%

“…This study is the first to clarify the role of LCAT m 6 A methylation during adipogenesis. Lecithin cholesterol acyltransferase (LCAT) is a key protein in the peripheral high-density lipoprotein metabolism pathway, which has been reported to be mainly involved in cholesterol reverse transport and energy metabolism [22][23][24]. To date, LCAT plays an important role in atherosclerosis and is associated with abdominal subcutaneous fat and abdominal visceral fat [25][26][27][28].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

ALKBH5 regulates chicken adipogenesis by mediating LCAT mRNA stability depending on m6A modification

Chao,

Guo,

et al. 2024

BMC Genomics

View full text Add to dashboard Cite

Background Previous studies have demonstrated the role of N6-methyladenosine (m6A) RNA methylation in various biological processes, our research is the first to elucidate its specific impact on LCAT mRNA stability and adipogenesis in poultry. Results The 6 100-day-old female chickens were categorized into high (n = 3) and low-fat chickens (n = 3) based on their abdominal fat ratios, and their abdominal fat tissues were processed for MeRIP-seq and RNA-seq. An integrated analysis of MeRIP-seq and RNA-seq omics data revealed 16 differentially expressed genes associated with to differential m6A modifications. Among them, ELOVL fatty acid elongase 2 (ELOVL2), pyruvate dehydrogenase kinase 4 (PDK4), fatty acid binding protein 9 (PMP2), fatty acid binding protein 1 (FABP1), lysosomal associated membrane protein 3 (LAMP3), lecithin-cholesterol acyltransferase (LCAT) and solute carrier family 2 member 1 (SLC2A1) have ever been reported to be associated with adipogenesis. Interestingly, LCAT was down-regulated and expressed along with decreased levels of mRNA methylation methylation in the low-fat group. Mechanistically, the highly expressed ALKBH5 gene regulates LCAT RNA demethylation and affects LCAT mRNA stability. In addition, LCAT inhibits preadipocyte proliferation and promotes preadipocyte differentiation, and plays a key role in adipogenesis. Conclusions In conclusion, ALKBH5 mediates RNA stability of LCAT through demethylation and affects chicken adipogenesis. This study provides a theoretical basis for further understanding of RNA methylation regulation in chicken adipogenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ALKBH5 regulates chicken adipogenesis by mediating LCAT mRNA stability depending on m6A modification

Chao,

Guo,

et al. 2024

BMC Genomics

View full text Add to dashboard Cite

show abstract

“…On the other hand, cholesterol from endogenous synthesis and dietary sources both contribute to hepatic inflammasome activation (27), in part through cholesterol crystal formation. The findings also uncovered a critical role for cellular cholesterol in modulating the spontaneous development of classical brown adipose tissue in skeletal muscle from myoblasts in utero and satellite cells in adults (28).…”

Section: Non-classical Metabolic Phenotypes Of Fld: Lessons From Murimentioning

confidence: 90%

Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings

Norum

Remaley

Miettinen

et al. 2020

Journal of Lipid Research

Self Cite

View full text Add to dashboard Cite

Lecithin:cholesterol acyltransferase (LCAT) converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer lab shared structural findings on LCAT and the close homolog lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT null mice were protected from diet-induced obesity, insulin resistance and non-alcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with rhLCAT. Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead towards better treatments for patients with heart disease and FLD.

show abstract

“…In addition to the above‐mentioned proteins and transcriptional factors, lecithin cholesterol acyltransferase (LCAT) deletion can convert SCs to brown adipocytes (Nesan et al, 2015). Ectopic expression of nuclear factor I‐A (NFIA) in myoblasts induces them to brown adipocyte differentiation (Hiraike et al, 2017).…”

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

Factors inducing transdifferentiation of myoblasts into adipocytes

Wang

Shan

2020

Journal Cellular Physiology

View full text Add to dashboard Cite

Fat infiltration in skeletal muscle is observed in several myopathies, is associated with muscular dysfunction, and is strongly correlated with insulin resistance, diabetes, obesity, and aging. In animal production, skeletal muscle fat (also known as intermuscular and intramuscular fat) is positively related to meat quality including tenderness, flavor, and juiciness. Thus, understanding the cell origin and regulation mechanism of skeletal muscle fat infiltration is important for developing therapies against human myopathies as well as for improving meat quality. Notably, age, sarcopenia, oxidative stress, injury, and regeneration can activate adipogenic differentiation potential in myoblasts and affect fat accumulation in skeletal muscle. In addition, several transcriptional and nutritional factors can directly induce transdifferentiation of myoblasts into adipocytes. In this review, we focused on the recent progress in understanding the muscle‐to‐adipocyte differentiation and summarized and discussed the genetic, nutritional, and physiological factors that can induce transdifferentiation of myoblasts into adipocytes. Moreover, the regulatory roles and mechanisms of these factors during the transdifferentiation process were also discussed.

show abstract

Lecithin:Cholesterol Acyltransferase (LCAT) Deficiency Promotes Differentiation of Satellite Cells to Brown Adipocytes in a Cholesterol-dependent Manner

Abstract: Significance: We present a novel lipid-based mechanism to recruit functional BAT.

Cited by 7 publications

References 37 publications

ALKBH5 regulates chicken adipogenesis by mediating LCAT mRNA stability depending on m6A modification

ALKBH5 regulates chicken adipogenesis by mediating LCAT mRNA stability depending on m6A modification

Lecithin:cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings

Factors inducing transdifferentiation of myoblasts into adipocytes

Contact Info

Product

Resources

About