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Effects of Lipid Treatment on Intestinal Epithelial Cells

Discuss about the Effect of Lipid Treatment.

Lipid treatment has a great effect on the HT- 29, HCT 116 and Caco-2 epithelial cells. The lipid treatments may include the palmitic acids, Omega 3 and Oleic acid. The short chain fatty acids such as acetate, butyrate and propionate are the major metabolic products of the anaerobic bacteria fermentation, which takes place in intestine. It acts as the fuel of the intestinal epithelial cells. In view of Asarat et al. (2015), propionic acid refers to the three carbon short chain fatty acid. This has various effects on the colonic functions. SCFA can modify effects of lipid induced epithelial cells either lonely or as a mixture. Different concentration of SCFA affects the intestinal epithelial cells.

In this context, the roles of lipid and SCFA are discussed. The assignment focuses on the various effects of lipid treatment on body and the pathways signaling of different lipid activation. In the literature review section, various aspects of the lipid treatment are discussed. 

Ramakers et al. (2007) mentioned that the treatment of lipids has various effects on the HT- 29, HCT 116 and Caco-2 epithelial cells. The short chain fatty acids include the acetate, butyrate and propionate. These have significant role on the physiological function of the colonocytes and epithelial cells. Sukhotnik et al. (2008) stated that SCFA are co cultured with normal intestinal epithelial or the adenocarcinoma derived. On the other hand, Sun et al. (2017) opined that Omega 3 PUFA have inflammatory property, which have different mechanism. However, in the patients with the bowel disease, the transcription factors (NF-kB) and the intercellular expression are involved in the recruitment of leukocytes. This happens to the side of the increased inflammation. The palmitic acid has affects on the early intestinal adaptation incase of rats, who suffer from short bowel syndrome (Beyaz et al. 2016). The gut bacteria metabolize the short chain fatty acid.

On the other hand, as mentioned by Sukhotnik et al. (2008), propionic acid may have effects on the intestinal mucosal wall function. It needs to be mentioned that this barrier functions are rare during the pre weaning. HCT29 and HCT116 are the two human colon epithelial cells. These cells are lined with the FFA4. Vinolo et al. (2011) opined that omega 3 polyunsaturated fatty acid is known as the essential fatty acid that is not absorbed in the human body. In a study, Tang et al. (2011) showed that FFA4 identification as the GPCR for the ling chain PUFAs and FFA4 are reported, which is involved in fatty acid stimulation. The involvement helps to release the cholecystokinin and glucagon like peptide 1. Eicosapentaenoic acid has effects on the expression of the Caco-2 enterocytes as well as the oleic acid (Xia et al. 2017).

SCFA and Lipid Treatment

Investigate how SCFA (butyrate, acetate and propionate) either as mixture or alone can modify the effect of lipid induced epithelial cells alterations. Also, the effects of different concentrations of SCFAs on viability, proliferation and apoptosis responses in intestinal epithelial cell.

The human epithelial cells can contribute to the regulation of the intestinal immune response through various ways like various immune factors production and inflammation. The immune factors production includes the interleukin (IL8) that acts as the chemoattractant for the neutrophils (Zhang et al. 2016). SCFA has effects on the IECs viability and IL-8 in vitro production. SCFA can be co-cultured with the normal intestinal epithelial or it can be co-cultured with the adenocarcinoma derived. Cell proliferation, viability and production of the IL8 and the expression of the IL mRNA can be determined in cell cultures. This can show that 20 mM of the SCFA was the non-cytotoxic and the growth was enhanced (Mobraten et al. 2013). On the other hand, the HT29 growth was inhibited. The SCFAs regulated the LPS stimulated IL 8 secretion. This happens with the various response patterns. However, no positive effects are seen on IL 8 release from the non LPS stimulated cells. Ramakers et al. (2007) mentioned that the SCFA has effects on the LPS stimulated IL 8 release with the mRNA expression of IL 8. This can explain the anti carcinogenic and anti-inflammatory mechanism of the SCFAs.

The fatty acyl co-A contains short chain fatty acid, which can diffuse via the inner mitochondrial membrane (Asarat et al. 2015). The short chain fatty acid activation and the membrane transport is done by the binding to the coenzyme A. when the acetyl CoA enters into the citric acid cycle with the molecule of oxaloacetate, succinyl coA enters as well as the principle (Tan et al. 2014). It is a catabolic process, in which the short chain fatty acids break down. In case of SCFA synthesis lipid metabolism plays significant role.

Discuss what the lipids and SCFAs activate in the cells. What pathways signaling are activated (PPAR delta, PPAR gamma, wnt β- catenin genes, GPR). Use diagrams to explain them more.

Den Besten et al. (2013) mentioned that the GRP is a glycosylated, G-protein and – transmembrane that coupled the receptors to activate the phospholipase C signaling pathway. The receptor is expressed in the numerous cancers such as lung, prostate and colon cancer. However, GRP is a protein-coding gene that activates the ligands of gastrin-releasing peptide (Sun et al.  2017). The function of the pathway is to help in the breathing properly.

Pathways Signaling Activated by Lipids and SCFAs

The peroxisome proliferator activated receptor gamma is a member of nuclear receptor. PPAR- γ activators are the diverse group of the agents, which ranges from the endogenous fatty acids. PPAR gamma binds with the retinoid X receptor α and signal antiproliferative antiangiogenic pathways (Koh et al. 2016).

The Wnt pathway causes the accumulation of the β catenin in cytoplasm. Kasubuchi et al. (2015) stated that the nucleus acts as the transcriptional coactivator that belongs to either TCF or LEF family. This pathway plays significant role in the mutation, which leads type 2 diabetes, breast and prostate cancer and giloblastoma.

In view of Kasubuchi et al. (2015), PPAR- ? function as the integrator of the transcription repression as well as the nuclear receptor signaling. This mainly activates the transcription of the various genes that binds to the specific DNA substances. The target genes include ANGPTL4, CD36 and PDK4. These expressions of genes help to elevate the colorectal cancer cells. APC can repress the elevated expression that is involved in the PPAR- ? signaling pathway (Beyaz et al. 2016). Lipid lowered drug targets the PPAR- ?. In case of obesity, PPAR- ? plays significant role to regulate the metabolic dysfunction and reduce the health issues regarding obesity.

Mentioned the additional questions that remaining to be explored in this area, what is still unknown about this topic. There are several facts that are unknown to be explored in this context.

Based on the above discussion, it can be concluded that sodium Butyrate helps to treat the HCT- 116 and the HT- 29 cells with the indicated concentration. From the findings, it can be highlighted that PPAR- ?, which is diet modulated can alter the function of the intestinal stem as well as the progenitor cell function. However, the DHA, AA and EPA elicit similar signaling events (Tang et al. 2011). SCFA are co cultured with normal intestinal epithelial or the adenocarcinoma derived. With the various kinetics and the efficiency via GRP120 in the Caco- 2 cells are also elicited. This will help to understand the dietary PUFAs, which influence the inflammatory processes relevant to decline the PUFAs effect in treatment of IBD. The effects of the Caco- 2 dees not affect the PPARγ activation (Sukhotnik et al. 2008). Early exposure to the high palmitic acid both accelerates and augments the structural bowel adaptation in the rat model of the SBS. The responsible factors are the lowered cell apoptosis and the increased cell proliferation. HFD affects the progenitor cells and PPAR- ? pharmacological activation. SCFA has effects on the LPS stimulated IL 8 release with the mRNA expression of IL 8. Non stimulated ICAM- 1expression and the cytokine can stimulate the Caco- 2 cells that is cultured for twenty two days with the arachidonic acid.

Additional Questions to be Explored

References:

Asarat, M., Vasiljevic, T., Apostolopoulos, V. and Donkor, O., 2015. Short-chain fatty acids regulate secretion of IL-8 from human intestinal epithelial cell lines in vitro. Immunological investigations, 44(7), pp.678-693.

Bentley?Hewitt, K.L., De Guzman, C.E., Ansell, J., Mandimika, T., Narbad, A. and Lund, E.K., 2014. Polyunsaturated fatty acids modify expression of TGF?β in a co?culture model ultilising human colorectal cells and human peripheral blood mononuclear cells exposed to Lactobacillus gasseri, Escherichia coli and Staphylococcus aureus. European Journal of Lipid Science and Technology, 116(5), pp.505-513.

Beyaz, S., Mana, M.D., Roper, J., Kedrin, D., Saadatpour, A., Hong, S.J., Bauer-Rowe, K.E., Xifaras, M.E., Akkad, A., Arias, E. and Pinello, L., 2016. High-fat diet enhances stemness and tumorigenicity of intestinal progenitors. Nature, 531(7592), pp.53-58.

Den Besten, G., van Eunen, K., Groen, A.K., Venema, K., Reijngoud, D.J. and Bakker, B.M., 2013. The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. Journal of lipid research, 54(9), pp.2325-2340.

Kasubuchi, M., Hasegawa, S., Hiramatsu, T., Ichimura, A. and Kimura, I., 2015. Dietary gut microbial metabolites, short-chain fatty acids, and host metabolic regulation. Nutrients, 7(4), pp.2839-2849.

Koh, A., De Vadder, F., Kovatcheva-Datchary, P. and Bäckhed, F., 2016. From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites. Cell, 165(6), pp.1332-1345.

Lou, H., Lu, J., Choi, E.B., Oh, M.H., Jeong, M., Barmettler, S., Zhu, Z. and Zheng, T., 2017. Expression of IL-22 in the skin causes Th2-biased immunity, epidermal barrier dysfunction, and pruritus via stimulating epithelial Th2 cytokines and the GRP pathway. The Journal of Immunology, 198(7), pp.2543-2555.

Mobraten, K., Haug, T.M., Kleiveland, C.R. and Lea, T., 2013. Omega-3 and omega-6 PUFAs induce the same GPR120-mediated signalling events, but with different kinetics and intensity in Caco-2 cells. Lipids in health and disease, 12(1), p.101.

Nagaraj, A.B., Joseph, P., Kovalenko, O., Singh, S., Armstrong, A., Redline, R., Resnick, K., Zanotti, K., Waggoner, S. and DiFeo, A., 2015. Critical role of Wnt/β-catenin signaling in driving epithelial ovarian cancer platinum resistance. Oncotarget, 6(27), p.23720.

Ramakers, J.D., Mensink, R.P., Schaart, G. and Plat, J., 2007. Arachidonic acid but not eicosapentaenoic acid (EPA) and oleic acid activates NF-κB and elevates ICAM-1 expression in Caco-2 cells. Lipids, 42(8), pp.687-698.

Sukhotnik, I., Hayari, L., Bashenko, Y., Chemodanov, E., Mogilner, J., Shamir, R., Yosef, F.B., Shaoul, R. and Coran, A.G., 2008. Dietary palmitic acid modulates intestinal re-growth after massive small bowel resection in a rat. Pediatric surgery international, 24(12), p.1313.

Sun, M., Wu, W., Liu, Z. and Cong, Y., 2017. Microbiota metabolite short chain fatty acids, GPCR, and inflammatory bowel diseases. Journal of Gastroenterology, 52(1), pp.1-8.

Tan, J., McKenzie, C., Potamitis, M., Thorburn, A.N., Mackay, C.R. and Macia, L., 2014. The role of short-chain fatty acids in health and disease. Adv Immunol, 121(91), p.e119.

Tang, Y., Chen, Y., Jiang, H., Robbins, G.T. and Nie, D., 2011. G?protein?coupled receptor for short?chain fatty acids suppresses colon cancer. International journal of cancer, 128(4), pp.847-856.

Vinolo, M.A., Rodrigues, H.G., Nachbar, R.T. and Curi, R., 2011. Regulation of inflammation by short chain fatty acids. Nutrients, 3(10), pp.858-876.

Wei, J., Li, Z. and Yuan, F., 2014. Evodiamine might inhibit TGF?beta1?induced epithelial–mesenchymal transition in NRK52E cells via Smad and PPAR?gamma pathway. Cell biology international, 38(7), pp.875-880.

Xia, Z., Han, Y., Wang, K., Guo, S., Wu, D., Huang, X., Li, Z. and Zhu, L., 2017. Oral administration of propionic acid during lactation enhances the colonic barrier function. Lipids in Health and Disease, 16(1), p.62.

Zhang, J., Yi, M., Zha, L., Chen, S., Li, Z., Li, C., Gong, M., Deng, H., Chu, X., Chen, J. and Zhang, Z., 2016. Sodium butyrate induces endoplasmic reticulum stress and autophagy in colorectal cells: implications for apoptosis. PloS one, 11(1), p.e0147218.

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