scholarly journals Regulatory Roles of SREBF1 and SREBF2 in Lipid Metabolism and Deposition in Two Chinese Representative Fat-Tailed Sheep Breeds

Animals ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1317
Author(s):  
Chen Liang ◽  
Liying Qiao ◽  
Yongli Han ◽  
Jianhua Liu ◽  
Jianhai Zhang ◽  
...  

Sterol regulatory element binding proteins (SREBPs) can regulate the lipid homeostasis by regulating its target genes, which are crucial for the cholesterol and fatty acid metabolism. However, the transcriptional regulation role of SREBPs in fat-tailed sheep is unclear. In this study, two Chinese representative breeds of total 80 fat-tailed sheep were employed, serum triglyceride, total cholesterol (TC), non-esterified fatty acid (NEFA), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and mRNA expressions of SREBF1 and SREBF2 in seven different adipose tissues and liver were examined in sheep at the ages of 4, 6, 8, 10, and 12 months, respectively. The subcellular localization and function of SREBP1/2 were predicted through bioinformatics approaches. The results demonstrated that serum TC and NEFA levels among breeds were significantly different, and most serum indices were dynamically altered in an age-dependent manner. The mRNA expression profiling of SREBF1 and SREBF2 are breed-specific with temporal and spatial expressions differences. Further analysis shows that SREBF1/2 transcriptional levels and tail traits are closely related. All investigations simplify that SREBF1/2 play a crucial role in lipid metabolism and deposition during growth and development of the fat-tailed sheep, which also provides a novel insight for revealing the genetic mechanism of different tail type and meat quality.

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2003
Author(s):  
Risa Araki ◽  
Akira Yada ◽  
Hirotsugu Ueda ◽  
Kenichi Tominaga ◽  
Hiroko Isoda

The effectiveness of anthocyanins may differ according to their chemical structures; however, randomized clinical controlled trials (RCTs) or meta-analyses that examine the consequences of these structural differences have not been reported yet. In this meta-analysis, anthocyanins in test foods of 18 selected RCTs were categorized into three types: cyanidin-, delphinidin-, and malvidin-based. Delphinidin-based anthocyanins demonstrated significant effects on triglycerides (mean difference (MD): −0.24, p < 0.01), low-density lipoprotein cholesterol (LDL-C) (MD: −0.28, p < 0.001), and high-density lipoprotein cholesterol (HDL-C) (MD: 0.11, p < 0.01), whereas no significant effects were observed for cyanidin- and malvidin-based anthocyanins. Although non-significant, favorable effects on total cholesterol (TC) and HDL-C were observed for cyanidin- and malvidin-based anthocyanins, respectively (both p < 0.1). The ascending order of effectiveness on TC and LDL-C was delphinidin-, cyanidin-, and malvidin-based anthocyanins, and the differences among the three groups were significant (both p < 0.05). We could not confirm the significant effects of each main anthocyanin on glucose metabolism; however, insulin resistance index changed positively and negatively with cyanidin- and delphinidin-based anthocyanins, respectively. Therefore, foods containing mainly unmethylated anthocyanins, especially with large numbers of OH groups, may improve glucose and lipid metabolism more effectively than those containing methylated anthocyanins.


2007 ◽  
Vol 293 (1) ◽  
pp. R70-R77 ◽  
Author(s):  
Sebastian Luci ◽  
Beatrice Giemsa ◽  
Holger Kluge ◽  
Klaus Eder

This study investigated the effect of clofibrate treatment on expression of target genes of peroxisome proliferator-activated receptor (PPAR)-α and various genes of the lipid metabolism in liver and adipose tissue of pigs. An experiment with 18 pigs was performed in which pigs were fed either a control diet or the same diet supplemented with 5 g clofibrate/kg for 28 days. Pigs treated with clofibrate had heavier livers, moderately increased mRNA concentrations of various PPAR-α target genes in liver and adipose tissue, a higher concentration of 3-hydroxybutyrate, and markedly lower concentrations of triglycerides and cholesterol in plasma and lipoproteins than control pigs ( P < 0.05). mRNA concentrations of sterol regulatory element-binding proteins (SREBP)-1 and -2, insulin-induced genes ( Insig) -1 and Insig-2, and the SREBP target genes acetyl-CoA carboxylase, 3-methyl-3-hydroxyglutaryl-CoA reductase, and low-density lipoprotein receptor in liver and adipose tissue and mRNA concentrations of apolipoproteins A-I, A-II, and C-III in the liver were not different between both groups of pigs. In conclusion, this study shows that clofibrate treatment activates PPAR-α in liver and adipose tissue and has a strong hypotriglyceridemic and hypocholesterolemic effect in pigs. The finding that mRNA concentrations of some proteins responsible for the hypolipidemic action of fibrates in humans were not altered suggests that there were certain differences in the mode of action compared with humans. It is also shown that PPAR-α activation by clofibrate does not affect hepatic expression of SREBP target genes involved in synthesis of triglycerides and cholesterol homeostasis in liver and adipose tissue of pigs.


Author(s):  
Irina S. Sobolevskaya ◽  
◽  
Oleg D. Myadelets ◽  
Natalʼya N. Yarotskaya

The purpose of this study was to substantiate the possibility of correcting lipid metabolism changes at dark deprivation using linseed oil, melatonin, and their combination. Materials and methods. The experiment involved 130 white outbred male rats with a body weight of 170–220 g. The animals were divided into 5 groups: rats under standard fixed lighting conditions (12 hours light/12 hours dark); rats under modelled dark deprivation with round-the-clock lighting (24 hours light); rats under modelled dark deprivation with round-the-clock lighting (24 hours light) receiving intragastric injections of linseed oil, melatonin or their combination from day 1 of the experiment. Serum concentrations of total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total phospholipids (TPL) and atherogenic index (AI) were determined. Results. Long-term dark deprivation led to dyslipoproteinemia, which consists in an increase in serum concentrations of TC by a factor of 1.33 (p = 0.0009), TG by a factor of 1.62 (p = 0.013), LDL-C by a factor of 1.2 (p = 0.026) and TPL by a factor of 1.15 (p = 0.0082). The severity of changes in TC, TG, LDL-C, HDL-C and TPL concentrations varied depending on the duration of the experiment. During the use of linseed oil, melatonin or their combination under dark deprivation, the severity of disorders caused by desynchronosis decreased and lipid metabolism in rat serum normalized, especially at the initial stages of the research. Conclusion. Changes in lipid metabolism due to desynchronosis in rats injected with the substances under study were significantly smaller compared with animals that did not receive them. The most pronounced effects of administering these substances were observed in the group of rats treated with linseed oil and melatonin at the same time.


2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Cheng Liu ◽  
Yanxian Lai ◽  
Songsong Ying ◽  
Junfang Zhan ◽  
Yan Shen

Abstract Background Exosome-derived microRNAs (exo-miRs) as messengers play important roles, in the cross-talk between genetic [ATP-sensitive potassium channels (KATP) genetic variant rs1799858] and environmental [elevated serum low-density lipoprotein cholesterol (LDL-C) level] factors, but the plasma exo-miRs expression profile and its role in biological processes from genotype to phenotype remain unclear. Methods A total of 14 subjects with increased LDL-C serum levels (≥ 1.8 mmol/L) were enrolled in the study. The KATP rs1799858 was genotyped by the Sequenom MassARRAY system. The plasma exo-miRs expression profile was identified by next-generation sequencing. Results 64 exo-miRs were significantly differentially expressed (DE), among which 44 exo-miRs were up-regulated and 20 exo-miRs were down-regulated in those subjects carrying T-allele (TT + CT) of rs1799858 compared to those carrying CC genotype. The top 20 up-regulated DE-exo-miRs were miR-378 family, miR-320 family, miR-208 family, miR-483-5p, miR-22-3p, miR-490-3p, miR-6515-5p, miR-31-5p, miR-210-3p, miR-17-3p, miR-6807-5p, miR-497-5p, miR-33a-5p, miR-3611 and miR-126-5p. The top 20 down-regulated DE-exo-miRs were let-7 family, miR-221/222 family, miR-619-5p, miR-6780a-5p, miR-641, miR-200a-5p, miR-581, miR-605-3p, miR-548ar-3p, miR-135a-3p, miR-451b, miR-509-3-5p, miR-4664-3p and miR-224-5p. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were subsequently implemented to identify the top 10 DE-exo-miRs related specific target genes and signaling pathways. Only 5 DE-exo-miRs were validated by qRT-PCR as follows: miR-31-5p, miR-378d, miR-619-5p, miR-320a-3p and let-7a-5p (all P < 0.05). Conclusion These results firstly indicated the plasma exo-miRs expression profile bridging the link between genotype (KATP rs1799858) and phenotype (higher LDL-C serum level), these 5 DE-exo-miRs may be potential target intermediates for molecular intervention points.


2020 ◽  
Vol 11 ◽  
Author(s):  
Katsumi Iizuka ◽  
Ken Takao ◽  
Daisuke Yabe

Carbohydrate response element-binding protein (ChREBP) plays an important role in the development of type 2 diabetes, dyslipidemia, and non-alcoholic fatty liver disease, as well as tumorigenesis. ChREBP is highly expressed in lipogenic organs, such as liver, intestine, and adipose tissue, in which it regulates the production of acetyl CoA from glucose by inducing Pklr and Acyl expression. It has recently been demonstrated that ChREBP plays a role in the conversion of gut microbiota-derived acetate to acetyl CoA by activating its target gene, Acss2, in the liver. ChREBP regulates fatty acid synthesis, elongation, and desaturation by inducing Acc1 and Fasn, elongation of long-chain fatty acids family member 6 (encoded by Elovl6), and Scd1 expression, respectively. ChREBP also regulates the formation of very low-density lipoprotein by inducing the expression of Mtp. Furthermore, it plays a crucial role in peripheral lipid metabolism by inducing Fgf21 expression, as well as that of Angptl3 and Angptl8, which are known to reduce peripheral lipoprotein lipase activity. In addition, ChREBP is involved in the production of palmitic-acid-5-hydroxystearic-acid, which increases insulin sensitivity in adipose tissue. Curiously, ChREBP is indirectly involved in fatty acid β-oxidation and subsequent ketogenesis. Thus, ChREBP regulates whole-body lipid metabolism by controlling the transcription of lipogenic enzymes and liver-derived cytokines.


2012 ◽  
Vol 30 (3) ◽  
pp. 141-144
Author(s):  
Mimi Parvin ◽  
Muhammad Saiedullah ◽  
Aminul Haque Khan ◽  
Muhammad Rezwanur Rahman ◽  
Md Saiful Islam

Objective: A modification of Friedewald’s formula was proposed to calculate LDL cholesterol in Bangladeshi population up to serum triglyceride concentration of 1000 mg/dL. The aim of this study was to validate the modification of Friedewald’s formula in Bangladeshi population.Methods: Serum total cholesterol, triglyceride, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol concentrations were measured in specimens obtained form 314 adult Bangladeshi subjects selected conveniently. LDL cholesterol concentrations were also calculated by modified Friedewald’s formula and original Friedewald’s formula. Results were expressed as mean ± SD and calculated LDL cholesterol was compared with measured LDL cholesterol by two-tailed paired t test and Pearson’s correlation coefficient (r).Results: The mean ± SD of measured LDL cholesterol was 138.3 ± 54.58 mg/dL. LDL cholesterol calculated by modified Friedewald’s formula and original Friedewald’s formula were 135.9 ± 59.26 mg/dL (P>0.05) and 123.5 ± 65.75 mg/dL (P<0.001) respectively. Compared to measured LDL cholesterol, calculated LDL cholesterol were 2.47 mg/ dL and 17.20 mg/dL lower for modified formula and original formula respectively. The correlation coefficient (r) with measured LDL cholesterol was 0.8601 (P<0.0001) for LDL cholesterol calculated by the modified Friedewald’s formula and 0.8565 (P<0.0001) for the LDL cholesterol calculated by the original Friedewald’s formula.Conclusion: The study validates the modified Friedewald’s formula to calculate LDL cholesterol in Bangladeshi    population. DOI: http://dx.doi.org/10.3329/jbcps.v30i3.12463 J Bangladesh Coll Phys Surg 2012; 30: 141-144


2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Zoe Irwin ◽  
Emeir M. McSorley ◽  
Mary M. Slevin ◽  
Lisa Rowan ◽  
Paul McMillen ◽  
...  

AbstractEvidence from observational studies indicates that seaweed consumption may reduce the risk of non-communicable diseases such as cardiovascular disease, type two diabetes, and obesity. Accumulating evidence from in vitro and animal studies suggest seaweed have antihyperlipidemic, anti-inflammatory and antioxidant properties which may in part be attributed to the high content of soluble dietary fibre in seaweeds. The viscosity of seaweed fibres is suggested to mediate antihyperlipdiemic effects via the alteration of lipid/bile acid absorption kinetics to decrease low-density lipoprotein cholesterol (LDL). Thus, there is a need to evaluate the efficacy of seaweed derived dietary fibre in the management of dyslipidemia. Therefore, the aim of this study was to determine the effect of a fibre rich extract from Palmaria palmata on the lipid profile as well as markers of inflammation and oxidative stress in healthy adults. A total of 60 healthy participants (30 male and 30 female) aged 20 to 58 years, were assigned to consume the Palmaria palmata fibre extract (5g/day), Synergy-1 and the placebo (maltodextrin) for a duration of 4 weeks with a minimum 4 week washout between each treatment in a double blind, randomised crossover study conducted over 5 months. Fasting concentrations of cholesterol, triglycerides and high-density lipoprotein cholesterol (HDL) were analysed and low-density lipoprotein cholesterol (LDL) and LDL: HDL ratio was calculated. C-reactive protein (CRP) and Ferric Reducing Ability of Plasma (FRAP) were analysed as markers of inflammation and oxidative stress, respectively. Supplementation for 4 weeks with Palmaria palmata resulted in favourable changes to lipid profiles with a reduced LDL:HDL ratio; however intention-to-treat univariate ANCOVA identified no significant difference between the treatment groups over time on any of the lipid profile markers. A non-significant increase in CRP and triglyceride concentration along with lower FRAP was also observed with Palmaria palmata supplementation. Evidence from this study suggests that Palmaria palmata may have effects on lipid metabolism and appears to mobilise triglycerides. More research is needed in individuals with dyslipidaemia to fully elucidate these effects.


Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2169-2174 ◽  
Author(s):  
Wan Huang ◽  
Anantha Metlakunta ◽  
Nikolas Dedousis ◽  
Heidi K. Ortmeyer ◽  
Maja Stefanovic-Racic ◽  
...  

It is well established that leptin increases the sensitivity of carbohydrate metabolism to the effects of insulin. Leptin and insulin also have potent effects on lipid metabolism. However, the effects of leptin on the regulation of liver lipid metabolism by insulin have not been investigated. The current study addressed the effects of leptin on insulin-regulated hepatic very low-density lipoprotein (VLDL) metabolism in vivo in rats. A 90-min hyperinsulinemic/euglycemic clamp (4 mU/kg · min−1) reduced plasma VLDL triglyceride (TG) by about 50% (P &lt; 0.001 vs. saline control). Importantly, a leptin infusion (0.2 μg/kg · min−1) in combination with insulin reduced plasma VLDL-TG by about 80% (P &lt; 0.001 vs. insulin alone). These effects did not require altered skeletal muscle lipoprotein lipase activity but did include differential effects of insulin and leptin on liver apolipoprotein (apo) B and TG metabolism. Thus, insulin decreased liver and plasma apoB100/B48 levels (∼50%, P &lt; 0.01), increased liver TGs (∼20%, P &lt; 0.05), and had no effect on fatty acid oxidation. Conversely, leptin decreased liver TGs (∼50%, P &lt; 0.01) and increased fatty acid oxidation (∼50%, P &lt; 0.01) but had no effects on liver or plasma apoB levels. Importantly, the TG-depleting and prooxidative effects of leptin were maintained in the presence of insulin. We conclude that leptin additively increases the suppressive effects of insulin on hepatic and systemic VLDL metabolism by stimulating depletion of liver TGs and increasing oxidative metabolism. The net effect of the combined actions of insulin and leptin is to decrease the production and TG content of VLDL particles.


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