Year : 2024 | Volume : | : | Page : –

Pankaj Malhotra,

Taneesha Gupta,

Ankit,

Assistant Professor, Department of Pharmacy, School of Health Sciences, Sushant University, Gurugram, Haryana, India
Research Scholar, Department of Pharmacy, School of Health Sciences, Sushant University, Gurugram, Haryana, India
Research Scholar, Department of Pharmacy, School of Health Sciences, Sushant University, Gurugram, Haryana, India

Abstract

Non-alcoholic fatty liver disorders (NAFLD) are defined by the accumulation of excess fat in the liver that has no other cause, such as drinking alcohol. Pyruvate dehydrogenase has been established as an alternative treatment for this disorder. NAFLD pathogenesis is complex and includes oxidative stress inflammatory processes, and mitochondrial dysfunction. Impaired liver fatty acid oxidation and glucose oxidation are significant individuals in developing NAFLD, and strategies to reverse these defects can help alleviate the condition. A spectrum of liver diseases comprises NAFLD, which is currently referred to as metabolic dysfunction-associated liver disease (MASLD). The significant amount of hepatocytes with minimal to no alcohol use hepatic steatosis disease indicates it. Over the next decade, NAFLD will overtake all other causes of cirrhosis due to its growing incidence, along with increased rates of obesity, metabolic syndromes, and, hence prompting liver T2D transplantation. However, heart disease remains the leading give rise to of death with a negligible proportion developing liver-related problems and fibrosis. To pathology, NAFLD is related to ergastoplasm stress, lipid toxicity, oxidative stress, and lipid depositions. Increased obesity and NAFLD which is distinguished by the buildup of excess fat in the liver without alcohol abuse or other contributing factors like hepatitis C infection are common in the general public as a result of sedentary lifestyles and high-calorie consumption. Further, recent studies have demonstrated that, even while oxidative energy generation plays a minor role in the liver’s total glucose/ pyruvate metabolism, defects in glucose oxidation may potentially be portion of the mitochondrial dysfunction in (NAFLD). Therefore, hepatic steatosis can be reduced and glucose homeostasis can be improved by reducing the defect in glucose oxidation. In this review, we will discuss the data supporting the role of reduced liver glucose oxidation in NAFLD pathogenesis and investigate the possibility of specifically targeting pyruvate dehydrogenase (PDH), the enzyme that limits the rate of glucose oxidation in NAFLD. We will also go over possible MOA for how elevated hepatic PDH activity and consequent glucose oxidation might cure the pathophysiology of obesity-induced NAFLD, as well as ways to target this pathway with therapeutic drugs.

Keywords: Pyruvate dehydrogenase, therapeutic, NAFLD, diabetes mellitus, non-alcoholic fatty liver, oxidation stress.

How to cite this article:
Pankaj Malhotra, Taneesha Gupta, Ankit. The Role of Pyruvate Dehydrogenase in Non-alcoholic Fatty Liver Disease: Therapeutic Insights and Future Directions. Research & Reviews: A Journal of Pharmacology. 2024; ():-.

How to cite this URL:
Pankaj Malhotra, Taneesha Gupta, Ankit. The Role of Pyruvate Dehydrogenase in Non-alcoholic Fatty Liver Disease: Therapeutic Insights and Future Directions. Research & Reviews: A Journal of Pharmacology. 2024; ():-. Available from: https://journals.stmjournals.com/rrjop/article=2024/view=176019

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References

[1] Cheol Soo Choi, Ghoshal, P., Srinivasan, M., Kim, S., Cline, G., & Patel, M. S. (2010a). Liver-specific pyruvate dehydrogenase complex deficiency regulates lipogenesis in adipose tissue and Improves Peripheral Insulin Sensitivity. Lipids, 45(11), 987–995.
[2] Guan, H., Shao, G., Cheng, F., Ni, P., & Wu, M. (2023). Risk factors of nonalcoholic fatty hepatic disease in healthy women. Medicine, 102(31), e34437–e34437.
[3] Harris, R. A., Bowker-Kinley, M. M., Huang, B., & Wu, P. (2002). Regulation of of the pyruvate dehydrogenase complex’s activity regulation. Developments in Enzyme Management, 42, 249–259.
[4] Holness, M. J., & Sugden, M. C. (2003). Reversible phosphorylation controls the activity of the pyruvate dehydrogenase complex. Transactions of the Biochemical Society, 31(6), 1143–1151.
[5] Hwang, Y.-C., Ahn, H.-Y., Park, S.-W., & Park, C.-Y. (2018). Non-alcoholic Fatty Liver Disease Is Associated with Higher Death Rates from Cancer and Overall Mortality, Cardiovascular Disease, and Liver Disease in Women but Not Men. Clinical Gastroenterology and Hepatology, 16(7), 1131-1137.
[6] Jing, E., O’Neill, B. T., Rardin, M. J., André Kleinridders, Ilkeyeva, O. R., Siegfried Ussar, Bain, J. R., Lee, K. Y., Verdin, E. M., Newgard, C. B., Gibson, B. W., & C. Ronald Kahn. (2013). Sirt3 Regulates Metabolic Flexibility of Skeletal Muscle Through Reversible Enzymatic Deacetylation. Diabetes, 62(10), 3404–3417.
[7] Liu, Y., Zhong, G.-C., Tan, H.-Y., Hao, F.-B., & Hu, J.-J. (2019). Nonalcoholic fatty liver disease and mortality from all causes, cardiovascular disease, and cancer: a meta-analysis. Scientific Reports, 9(1).
[8] Merritt, M. E., Harrison, C., A. Dean Sherry, Malloy, C. R., & Burgess, S. C. (2011). Hyperpolarized pyruvate carboxykinase and hepatic pyruvate carboxylase flux were observed. C magnetic resonance. National Academy of Sciences of the United States of America, 108(47), 19084–19089.
[9] Park, S., Jae Han Jeon, Byong Keol Min, Chae Myeong Ha, Themis Thoudam, Bo Yoon Park, & In Kyu Lee. (2018). Differential Pyruvate Dehydrogenase Complex Functions in Metabolism: The Pyruvate Dehydrogenase Complex’s Role in Metabolic Remodelling
. Diabetes & Metabolism Journal, 42(4), 270–270.
[10] Patel, M. S., & Korotchkina, L. G. (2006). Regulation of the pyruvate dehydrogenase complex. Biochemical Society Transactions, 34(2), 217–217.
[11] Roche, T. E., & Y. Hiromasa. (2007). Pyruvate dehydrogenase kinase regulatory mechanisms and inhibition in treating diabetes, heart ischemia, and cancer. Cellular and Molecular Life Sciences, 64(7-8), 830–849.
[12] Saed, C. T., Seyed Amirhossein Tabatabaei Dakhili, & Ussher, J. R. (2021). Pyruvate Dehydrogenase as a Therapeutic Target for Nonalcoholic Fatty Liver Disease. ACS Pharmacology & Translational Science, 4(2), 582–588.
[13] Samuel, V., & Shulman, G. (2012). Mechanisms for Insulin Resistance: Common Threads and Missing Links. Cell, 148(5), 852–871.
[14] Wang, S., Li, J., & Zhao, Y. (2024). Construction and analysis of a network of exercise-induced mitochondria-related non-coding RNA in the regulation of diabetic cardiomyopathy. 19(3), e0297848–e0297848.
[15] R. Scott Rector, Thyfault, J. P., Uptergrove, G. M., E. Matthew Morris, Naples, S. P., Borengasser, S. J., Mikus, C. R., Laye, M. J., M. Harold Laughlin, Booth, F. W., & Ibdah, J. A. (2010). Mitochondrial dysfunction precedes insulin resistance and hepatic steatosis and contributes to the natural history of non-alcoholic fatty liver disease in an obese rodent model. Journal of Hepatology, 52(5), 727–736.
[16] Wyness, Laura. (2017). Non-alcoholic fatty liver disease (NAFLD): Nutrition and lifestyle advice. Network Health Digest. 37.
[17] Rinella, M. E., & Sanyal, A. J. (2016). Management of NAFLD: a stage-based approach. Nature Reviews. Gastroenterology & Hepatology, 13(4), 196–205.
[18] Matteoni CA, Younossi ZM, Gramlich T, Boparai N, Liu YC, McCullough AJ. Nonalcoholic fatty liver disease: A spectrum of clinical and pathological seventy and Gastroenterology, 116(6), 1413–1419.
[19] Wong, R. J., Cheung, R., & Ahmed, A. (2014). Nonalcoholic steatohepatitis is the most rapidly growing indication for liver transplantation in patients with hepatocellular carcinoma in the U.S. Hepatology, 59(6), 2188–2195.
[20] Pais, R., Charlotte, F., Fedchuk, L., Bedossa, P., Pascal Lebray, Thierry Poynard, & Vlad Ratziu. (2013). Patients with non-alcoholic fatty liver show disease progression, according to a comprehensive assessment of follow-up biopsies.. Journal of Hepatology, 59(3), 550–556.
[21] McPherson, S., Hardy, T., Henderson, E., Burt, A. D., Day, C. P., & Anstee, Q. M. (2015). Pairing biopsies provide evidence of NAFLD development from steatosis to fibrosing-steatohepatitis: implications for clinical treatment and prognosis. Journal of Hepatology, 62(5), 1148–1155.
[22] McPherson, S., Hardy, T., Henderson, E., Burt, A. D., Day, C. P., & Anstee, Q. M. (2015). Evidence of NAFLD progression from steatosis to fibrosing-steatohepatitis using paired biopsies: Implications for prognosis and clinical management. Journal of Hepatology, 62(5), 1140 – 1145.
[23] Friedman, S. L., Neuschwander-Tetri, B. A., Rinella, M., & Sanyal, A. J. (2018). Mechanisms of NAFLD development and therapeutic strategies. Nature Medicine, 24(7), 908–922.
[24] Francque, S. M., Marchesini, Shlomo Vinker, Mehmet Ungan, Mendive, J. M., & Christos Lionis. (2021). Non-alcoholic fatty liver disease: A patient guideline. JHEP Reports, 3(5), 100322–100322.
[25] Huang, D. Q., El-Serag, H. B., & Rohit Loomba. (2020). Global epidemiology of NAFLD-related HCC: trends, predictions, risk factors and prevention. Nature Reviews. Gastroenterology & Hepatology, 18(4), 223–238.
[26] Baratta, F., Pastori, D., Polimeni, L., Bucci, T., Ceci, F., Calabrese, C., Ernesti, I., Gaetano Pannitteri, Violi, F., Angelico, F., & Maria Del Ben. (2017). Non-Alcoholic Fatty Liver Disease: Effect on Insulin Resistance. the American Journal of Gastroenterology, 112(12), 1832–1839.
[27] Adams, L. A., Feldstein, A., Lindor, K. D., & Angulo, P. (2004). Nonalcoholic fatty liver disease among patients with hypothalamic and pituitary dysfunction. gastroenterology, 39(4), 909–914.
[28] P Mofrad. (2003). Clinical and histologic spectrum of nonalcoholic fatty liver disease associated with normal ALT values. Hepatology, 37(6), 1286–1292.
[29] Kim, D., W. Ray Kim, Hwa Jung Kim, & Therneau, T. M. (2013). Association between non-invasive fibrosis markers and mortality among adults with nonalcoholic fatty liver disease in the United States. Hepatology, 57(4), 1357–1365.
[30] Lim, Y.-S., & W Ray Kim. (2008). The Global Impact of Hepatic Fibrosis and End-Stage Liver Disease. Clinics in Liver Disease, 12(4), 733–746.
[31] Saed, C. T., Seyed Amirhossein Tabatabaei Dakhili, & Ussher, J. R. (2021). Pyruvate Dehydrogenase as a remedy Target for Nonalcoholic Fatty Liver Disease. ACS Pharmacology & Translational Science, 4(2), 582–588.
[32] Savic, D., Hodson, L., Neubauer, S., & Pavlides, M. (2020). The Importance of the Fatty Acid Transporter L-Carnitine in NAFLD. Nutrients, 12(8), 2178–2178.
[33] Younossi, Z. M., Marchesini, G., Pinto-Cortez, H., & Petta, S. (2019). Epidemiology of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis: Implications for Liver Transplantation. Transplantation, 103(1), 22–27.
[34] Petersen, M. C., & Shulman, G. I. (2018). Mechanisms of Insulin Action and Insulin Resistance. Physiological Reviews, 98(4), 2133–2223.
[35] Samuel, V., & Shulman, G. (2012). Mechanisms for Insulin Resistance: Common Threads and Missing Links. Cell, 148(5), 852–871.
[36] E. Dale Abel, Peroni, O., Kim, J. K., Kim, Y.-B., Boss, O., Hadro, E., Timo Minnemann, Shulman, G. I., & Kahn, B. B. (2001). Adipose-selective targeting of the GLUT4 gene impairs insulin action in muscle and liver. Nature, 409(6821), 729–733.
[37] Angulo, P., Kleiner, D. E., Sanne Dam-Larsen, Adams, L. A., P. R., Keach, J. C., Lafferty, H. D., Stahler, A., (2015). Liver Fibrosis, but No Other Histologic Features, Is Associated With Long-term Outcomes in Patients With Nonalcoholic Fatty Liver Disease. Gastroenterology, 149(2), 389-397.e10.
[38] Arkan, M. C., Hevener, A. L., Greten, F. R., Maeda, S., Li, Z.-W., Long, J. M., Wynshaw-Boris, A., Poli, G., Olefsky, J., & Karin, M. (2005). IKK-β links inflammation to obesity-induced insulin resistance. Nature Medicine, 11(2), 191–198.
[39] Taneesha Gupta, Pankaj Malhotra “A Comprehensive Study on Interactions between Protein Molecules and Their Importance in Drug Discovery,” Research & Reviews: A Journal of Drug Formulation, Development and Production 10, no. 03 (July 4, 2024): 1–10,
[40] Savage, D. B., Kitt Falk Petersen, & Shulman, G. I. (2007). Disordered Lipid Metabolism and the Pathogenesis of Insulin Resistance. Physiological Reviews, 87(2), 507–520.
[41] Day, E. A., Ford, R. J., & Steinberg, G. R. (2017). AMPK as a Therapeutic Objective in the Management of Metabolic Disorders. Endocrinology and Metabolism Trends, 28(8), 545–560.
[42] Seyed Amirhossein Tabatabaei Dakhili, Greenwell, A. A., & Ussher, J. R. (2023). Pyruvate Dehydrogenase Complex and Glucose Oxidation as a Therapeutic Target in Diabetic Heart Disease. Journal of Lipid and Atherosclerosis, 12(1), 47–47.
[43] Scherer, P. E., & Hill, J. A. (2016). Obesity, Diabetes, and Cardiovascular Diseases. Circulation Research, 118(11), 1703–1705.
[44] Haffner, S. M., Lehto, S., Laakso, M. (1998). Mortality from Coronary Heart Disease in Subjects with Type 2 Diabetes and in Nondiabetic Subjects with and without Prior Myocardial Infarction. Journal of Medicine, 339(4), 229–234.
[45] Petersen, M. C., D. F., & Shulman, G. I. (2017). Regulation of hepatic glucose metabolism in health and disease. Nature Reviews. Endocrinology, 13(10), 572–587.
[46] Seyed Amirhossein Tabatabaei Dakhili, Greenwell, A., & Ussher, J. (2023). Pyruvate Dehydrogenase Complex and Glucose Oxidation as a Therapeutic Target in Diabetic Heart Disease. ResearchGate; Korean Society of Lipidology and Atherosclerosis, 14(10), 423-543.
[47] Seyed Amirhossein Tabatabaei Dakhili, Greenwell, A. A., & Ussher, J. R. (2023). Pyruvate Dehydrogenase Complex and Glucose Oxidation as a Therapeutic Target in Diabetic Heart Disease. Journal of Lipid and Atherosclerosis, 12(1), 47–47.
[48] Ussher, J. R., Koves, T. R., Jaswal, J. S., Zhang, L., Ilkayeva, O., (2009). Insulin-Stimulated Cardiac Glucose Oxidation Is Increased in High-Fat Diet–Induced Obese Mice Lacking Malonyl CoA Decarboxylase. Diabetes, 58(8), 1766–1775.
[49] Watt, M. J., Dzamko, N., Thomas, W. G., Rose-John, S., Ernst, M., Carling, D., Kemp, B. E., Febbraio, M. A., & Steinberg, G. R. (2006). CNTF reverses obesity-induced insulin resistance by activating skeletal muscle AMPK. Nature Medicine, 12(5), 541–548.
[50] Kang, H.-J., Min, B.-K., Choi, W.-I., Jeon, J.-H., Dong Wook Kim, Park, S., Lee, Y.-K., . (2021). Pyruvate dehydrogenase kinase 1 and 2 deficiency reduces high-fat diet-induced hypertrophic obesity and inhibits the differentiation of preadipocytes into mature adipocytes. Experimental and Molecular Medicine/Experimental and Molecular Medicine, 53(9), 1390–1401.
[51] Lee, I.-K. (2014). The Role of Pyruvate Dehydrogenase Kinase in Diabetes and Obesity. Diabetes & Metabolism Journal, 38(3), 181–181.
[52] Lee, I.-K. (2014). The Role of Pyruvate Dehydrogenase Kinase in Diabetes and Obesity. Diabetes & Metabolism Journal, 38(3), 181–181.
[53] Wang, X., Shen, X., Yan, Y., & Li, H. (2021). Pyruvate dehydrogenase kinases (PDKs): an overview toward clinical applications. Bioscience Reports, 41(4).
[54] Huang, B., Wu, P., Bowker-Kinley, M. M., & Harris, R. A. (2002). Regulation of Pyruvate Dehydrogenase Kinase Expression by Peroxisome Proliferator–Activated Receptor-α Ligands, Glucocorticoids, and Insulin. Diabetes, 51(2), 276–283.
[55] Wang, X., Shen, X., Yan, Y., & Li, H. (2021). Pyruvate dehydrogenase kinases (PDKs): an overview toward clinical applications. Bioscience Reports, 41(4).
[56] Keller, H., Dreyer, C., Medin, J., A Mahfoudi, K Ozato, & W Wahli. (1993). By activating peroxisome proliferator-activated receptor-retinoid X receptor heterodimers, fatty acids and retinoids regulate lipid metabolism. Proceedings of the National Academy of Sciences of the United States of America, 90(6), 2160–2164.
[58] Malhotra, P., Neha Minocha, Pandey, P., Kaushik, D., & Neelam Vashist. (2024). A Review on History, Chemical Constituents, Phytochemistry, Pharmacological Activities, and Recent Patents of Valerian. the Natural Products Journal, 14(2).

[59] Rolf Kristian Berge, Asle Aarsland, Harald Kryvi, Bremer, J., & Niels Aarsaether. (1989). Alkylthioacetic acid (3-thia fatty acids) — a new group of non-β-oxidizable, peroxisome-inducing fatty acid analogues. I. A study on the structural requirements for proliferation of peroxisomes and mitochondria in rat liver. Biochimica et Biophysica Acta. Lipids and Lipid Metabolism/Biochimica et Biophysica Acta. L, Lipids and Lipid Metabolism, 1004(3), 345–356.
[60] Kang, H.-J., Min, B.-K., Choi, W.-I., Jeon, J.-H., Dong Wook Kim, Park, S., Lee, Y.-K., Kim, H., Ju-Eun Byeon, Go, Y., Hye Jin Ham, Yong Hyun Jeon, Kim, M.-J., Jung Yi Lee, Wende, A. R., Sung Hee Choi, Harris, R. A., & Lee, I.-K. (2021). Pyruvate dehydrogenase kinase 1 and 2 deficiency reduces high-fat diet-induced hypertrophic obesity and inhibits the differentiation of preadipocytes into mature adipocytes. Experimental and Molecular Medicine/Experimental and Molecular Medicine, 53(9), 1390–1401.
[60] He, Q., Gao, Z., Yin, J., Zhang, J., Yun, Z., & Ye, J. (2011). Regulation of HIF-1α activity in adipose tissue by obesity-associated factors: adipogenesis, insulin, and hypoxia. Endocrinology and Metabolism/American Journal of Physiology: Endocrinology and Metabolism, 300(5), E877–E885.
[61] McCommis, K. S., & Finck, B. N. (2019). Treating Hepatic Steatosis and Fibrosis by Modulating Mitochondrial Pyruvate Metabolism. CMGH, 7(2), 275–284.
[62] Zhang, M., Zhao, Y., Li, Z., & Wang, C. (2018). Pyruvate dehydrogenase kinase 4 mediates lipogenesis and contributes to the pathogenesis of nonalcoholic steatohepatitis. Biochemical and Biophysical Research Communications, 495(1), 582–586.
[63] Saed, C. T., Seyed Amirhossein Tabatabaei Dakhili, & Ussher, J. R. (2021). Pyruvate Dehydrogenase as a Therapeutic Target for Nonalcoholic Fatty Liver Disease. ACS Pharmacology & Translational Science, 4(2), 582–588.
[64] Haas, J. T., Sven Francque, & Staels, B. (2016). Pathophysiology and Mechanisms of Nonalcoholic Fatty Liver Disease. Annual Review of Physiology, 78(1), 181–205.
[65] Seto, W.-K., & Yuen, M.-F. (2016). Nonalcoholic fatty liver disease in Asia: emerging perspectives. Journal of Gastroenterology, 52(2), 164–174.
[66] Asrih, M., & Jornayvaz, F. R. (2015). Metabolic syndrome and nonalcoholic fatty liver disease: Is insulin resistance the link? Molecular and Cellular Endocrinology, 418, 55–65.

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Research & Reviews: A Journal of Pharmacology

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Received	02/09/2024
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