scholarly journals Interesterified Fats Induce Deleterious Effects on Adipose Tissue and Liver in LDLr-KO Mice

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 466 ◽  
Author(s):  
Maria Lavrador ◽  
Milessa Afonso ◽  
Dennys Cintra ◽  
Marcia Koike ◽  
Valeria Nunes ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Tissue Expansion ◽  
Inflammatory Cells ◽  
Neutrophil Infiltration ◽  
Collagen Content ◽  
Protein Levels ◽  
Expression Of Genes ◽  
Interesterified Fats ◽  
Liver Collagen

Interesterified fats are being widely used by the food industry in an attempt to replace trans fatty acids. The effect of interesterified fats containing palmitic or stearic acids on lipid metabolism and inflammatory signaling pathways in adipose and hepatic tissues was evaluated. Male LDLr-KO mice were fed a high-fat diet containing polyunsaturated (PUFA), palmitic (PALM), palmitic interesterified (PALM INTER), stearic (STEAR), or stearic interesterified (STEAR INTER) fats for 16 weeks. The expression of genes and protein levels involved in lipid metabolism and inflammatory processes in liver and white adipose tissue was determined by quantitative RT-PCR and by Western blot, respectively. The infiltration of inflammatory cells in hepatic and adipose tissues was determined by eosin and hematoxylin, while liver collagen content was determined by Sirius Red staining. Both interesterified fats increased liver collagen content and JNK phosphorylation. Additionally, the STEAR INTER group developed nonalcoholic steatohepatitis (NASH) associated with higher neutrophil infiltration. PALM INTER induced adipose tissue expansion and enlargement of adipocytes. Furthermore, PALM INTER triggered increased IKK phosphorylation and TNFα protein content, conditions associated with the upstream activation of the NFkB signaling pathway. STEAR INTER induced NASH, while PALM INTER triggered hepatic fibrosis and adipocyte hypertrophy with inflammatory response in LDLr-KO mice.

scholarly journals Adipose depot-specific upregulation of Ucp1 or mitochondrial oxidative complex proteins are early consequences of genetic insulin reduction in mice

2020 ◽  
Vol 319 (3) ◽  
pp. E529-E539
Author(s):  
Jose Diego Botezelli ◽  
Peter Overby ◽  
Lorenzo Lindo ◽  
Su Wang ◽  
Obélia Haïda ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Tissue Expansion ◽  
Inhibitory Effect ◽  
Protein Levels ◽  
Low Fat Diet ◽  
Specific Effects ◽  
Brown Adipose

Hyperinsulinemia plays a causal role in adipose tissue expansion. Mice with reduced insulin have increased energy expenditure, but the mechanisms remained unclear. Here we investigated the effects of genetically reducing insulin production on uncoupling and oxidative mitochondrial proteins in liver, skeletal muscle, white adipose tissue (WAT), and brown adipose tissue (BAT). Male Ins1+/+ or Ins1+/− littermates were fed either a low-fat diet (LFD) or a high-fat diet (HFD) for 4 wk, starting at 8 wk of age. Replicating our previous observations, HFD increased fasting hyperinsulinemia, and Ins1+/− mice had significantly lower circulating insulin compared with Ins1+/+ littermates. Fasting glucose and body weight were not different between genotypes. We did not observe robust significant differences in liver or skeletal muscle. In mesenteric WAT, Ins1+/− mice had reduced Ndufb8 and Sdhb, while Ucp1 was increased in the context of HFD. HFD alone had a dramatic inhibitory effect on Pparg abundance. In inguinal WAT, Ins1+/− mice exhibited significant increases in oxidative complex proteins, independent of diet, without affecting Ucp1, Pparg, or Prdm16:Pparg association. In BAT, lowered insulin increased Sdhb protein levels that had been reduced by HFD. Ucp1 protein, Prdm16:Pparg association, and Sirt3 abundance were all increased in the absence of diet-induced hyperinsulinemia. Our data show that reducing insulin upregulates oxidative proteins in inguinal WAT without affecting Ucp1, whereas in mesenteric WAT and BAT, reducing insulin upregulates Ucp1 in the context of HFD. Preventing hyperinsulinemia has early depot-specific effects on adipose tissue metabolism and helps explain the increased energy expenditure previously reported in Ins1+/− mice.

scholarly journals Coordinated and Interactive Expression of Genes of Lipid Metabolism and Inflammation in Adipose Tissue and Liver during Metabolic Overload

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e75290 ◽  
Author(s):  
Wen Liang ◽  
Giulia Tonini ◽  
Petra Mulder ◽  
Thomas Kelder ◽  
Marjan van Erk ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Expression Of Genes

scholarly journals The Effects of New Selective PPARα Agonist CP775146 on Systematic Lipid Metabolism in Obese Mice and Its Potential Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shengjie Tang ◽  
Fang Wu ◽  
Xihua Lin ◽  
Weiwei Gui ◽  
Fenping Zheng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Uncoupling Protein ◽  
Density Lipoprotein ◽  
Hormone Sensitive Lipase ◽  
Lipoprotein Cholesterol ◽  
Obese Mice ◽  
Liver Fatty Acid ◽  
Expression Of Genes

Purpose. Peroxisome proliferator-activated receptor α (PPARα) plays a crucial role in the control of lipid homeostasis. Here, we investigated the effects of CP775146, a new selective PPARα agonist, on lipid metabolism in diet-induced obese mice and its possible mechanism. Methods. C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity and then received CP775146 via intraperitoneal injection for 3 days. The content/morphology of the liver, serum lipid, and liver function was measured. The expression of genes related to lipolysis and synthesis in liver was detected by quantitative real-time PCR (qRT-PCR). Results. The safe dose of CP775146 was <0.3 mg/kg. CP775146 reduced the serum levels of liver enzymes, such as alanine aminotransferase (ALT) and glutamic-oxaloacetic transaminase (AST) and lipid metabolism-related biomarkers, including triglycerides (TGs) and low-density lipoprotein cholesterol (LDL-c), non-high-density lipoprotein cholesterol (non-HDL-c), and hepatic TG content, at a dosage of 0.1 mg/kg. HFD-induced pathological liver changes improved after CP775146 treatment. The expression of genes involved in liver fatty acid oxidation (acyl-coenzyme A dehydrogenase, long chain (Acadl), acyl-CoA oxidase 1 (Acox-1), carnitine palmitoyltransferase-1 (CPT-1), and enoyl-CoA, hydratase/3-hydroxyacyl CoA dehydrogenase (Ehhadh)) was upregulated in CP775146-treated mice. Furthermore, CP775146 induced the expression of thermogenesis genes (cell death-inducing DFFA-like effector a (Cidea), uncoupling protein 1 (Ucp1)) and lipolysis genes (hormone-sensitive lipase (Hsl), adipose tissue triglyceride lipase (Atgl)) in epididymal white adipose tissue (eWAT), activating browning and thermogenesis. Conclusion. CP775146 efficiently alleviates obesity-induced liver damage, prevents lipid accumulation by activating the liver fatty acid β-oxidation pathway, and regulates the expression of genes that control brown fat-like pathway in eWAT.

scholarly journals A Mix of Natural Bioactive Compounds Reduces Fat Accumulation and Modulates Gene Expression in the Adipose Tissue of Obese Rats Fed a Cafeteria Diet

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3251
Author(s):  
Albert Gibert-Ramos ◽  
Miguel Z. Martín-González ◽  
Anna Crescenti ◽  
M. Josepa Salvadó
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Fat Oxidation ◽  
Grape Seed ◽  
Protein Levels ◽  
Expression Of Genes ◽  
Brown Adipose ◽  
Obese Rats ◽  
The Individual

Scientists are focusing on bioactive ingredients to counteract obesity. We evaluated whether a mix containing grape seed proanthocyanidin extract (GSPE), anthocyanins, conjugated linoleic acid (CLA), and chicken feet hydrolysate (CFH) could reduce body fat mass and also determined which mechanisms in the white adipose tissue (WAT) and the brown adipose tissue (BAT) were affected by the treatment. The mix or vehicle (VH) were administered for three weeks to obese rats fed a cafeteria (CAF) diet. Biometric measures, indirect calorimetry, and gene expression in WAT and BAT were analyzed as was the histology of the inguinal WAT (IWAT). The individual compounds were also tested in the 3T3-L1 cell line. The mix treatment resulted in a significant 15% reduction in fat (25.01 ± 0.91 g) compared to VH treatment (21.19 ± 1.59 g), and the calorimetry results indicated a significant increase in energy expenditure and fat oxidation. We observed a significant downregulation of Fasn mRNA and an upregulation of Atgl and Hsl mRNA in adipose depots in the group treated with the mix. The IWAT showed a tendency of reduction in the number of adipocytes, although no differences in the total adipocyte area were found. GSPE and anthocyanins modulated the lipid content and downregulated the gene and protein levels of Fasn compared to the untreated group in 3T3-L1 cells. In conclusion, this mix is a promising treatment against obesity, reducing the WAT of obese rats fed a CAF diet, increasing energy expenditure and fat oxidation, and modifying the expression of genes involved in lipid metabolism of the adipose tissue.

scholarly journals Regulation of ABCA1 and ABCG1 gene expression in the intraabdominal adipose tissue

2016 ◽  
Vol 62 (3) ◽  
pp. 283-289 ◽  
Author(s):  
V.V. Miroshnikova ◽  
A.A. Panteleeva ◽  
E.A. Bazhenova ◽  
E.P. Demina ◽  
T.S. Usenko ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Cholesterol Metabolism ◽  
Nuclear Factor ◽  
Specific Expression ◽  
Protein Levels ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
And Control

Tissue specific expression of genes encoding cholesterol transporters ABCA1 and ABCG1 as well as genes encoding the most important transcriptional regulators of adipogenesis – LXRa, LXRb, PPARg and RORa has been investigated in intraabdominal adipose tissue (IAT) samples.A direct correlation between the content of ABCA1 and ABCG1 proteins with RORa protein level (r=0.480, p<0.05; r=0.435, p<0.05, respectively) suggests the role of the transcription factor RORa in the regulation of IAT ABCA1 and ABCG1 protein levels. ABCA1 and ABCG1 gene expression positively correlated with obesity indicators such as body mass index (BMI) (r=0.522, p=0.004; r=0.594, p=0.001, respectively) and waist circumference (r=0.403, p=0.033; r=0.474, p=0.013, respectively). The development of obesity is associated with decreased IAT levels of RORa and LXRb mRNA (p=0.016 and p=0.002, respectively). These data suggest that the nuclear factor RORa can play a significant role in the regulation of cholesterol metabolism and control IAT expression of ABCA1 and ABCG1, while the level of IAT LXRb gene expression may be an important factor associated with the development of obesity.

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