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Dietary Advanced Glycation End Products as Mediators of Obesity: Cellular and Molecular Mechanisms of Action

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Cellular and Biochemical Mechanisms of Obesity

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 23))

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Abstract

Obesity, a disorder of body weight regulatory systems that is characterized by the accumulation of excess body fat is increasingly becoming a global pandemic. Despite several approaches that have been applied to mitigate obesity, they have not been able to totally reverse the obesity and its mediated complication . Advanced glycation end products (AGEs) refer to a group of prooxidant heterogenous compounds whose formation results from nonenzymatic reactions between reactive sugars and proteins, lipids and nucleic acids. While supporting evidence has suggested that AGEs may have contributory roles in the pathogenesis of obesity, there are indications that increased consumption of dietary AGEs increases the circulating AGEs levels and their deposition in the tissues including the adipose tissue, increasing the risk of development of obesity and its comorbidities. Identification of the underlying mechanism may provide an important strategy for novel therapeutic approaches against obesity. This chapter therefore provided novel insights into the role of dietary AGEs in the pathogenesis of obesity and the purported mechanisms of action.

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Abbreviations

Akt:

Protein kinase B

ALI:

Arginine-lysine imidazole

BMI:

Body mass index

IRS-1:

Insulin receptor substrate 1

IRS-2:

Insulin receptor substrate 2

PI3K:

Phosphatidylinositol 3-kinase

RAGE:

Receptor for Advanced Glycation End products

ROS:

Reactive Oxygen Species

sRAGE:

Soluble receptors for advanced glycation end products

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Author information

Authors and Affiliations

  1. Department of Physiology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia

    Chinedum Ogbonnaya Eleazu & Mahaneem Mohamed

  2. Department of Chemistry, Biochemistry and Molecular Biology, Alex Ekwueme Federal University, Ebonyi State, Ndufu-Alike, Ikwo, Nigeria

    Chinedum Ogbonnaya Eleazu

  3. Department of Physiology, College of Medical Sciences, University of Calabar, Cross River State, P.M.B 1115, Calabar, Nigeria

    Victor Udo Nna

  4. Department of Science Laboratory Technology, Akanu Ibiam Federal Polytechnic, Ebonyi State, Unwana, Nigeria

    Joseph Bagi Suleiman

  5. Unit of Integrative Medicine, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia

    Mahaneem Mohamed

Authors
  1. Chinedum Ogbonnaya Eleazu
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  2. Victor Udo Nna
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  3. Joseph Bagi Suleiman
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  4. Mahaneem Mohamed
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Corresponding author

Correspondence to Mahaneem Mohamed .

Editor information

Editors and Affiliations

  1. St. Boniface Hospital Research, Asper Clinical Research Institute, Winnipeg, MB, Canada

    Paramjit S. Tappia

  2. Asper Clinical Research Institute, St. Boniface Hospital, Winnipeg, MB, Canada

    Bram Ramjiawan

  3. St. Boniface Hospital Research, Institute of Cardiovascular Science, Winnipeg, MB, Canada

    Naranjan S. Dhalla

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Eleazu, C.O., Nna, V.U., Suleiman, J.B., Mohamed, M. (2021). Dietary Advanced Glycation End Products as Mediators of Obesity: Cellular and Molecular Mechanisms of Action. In: Tappia, P.S., Ramjiawan, B., Dhalla, N.S. (eds) Cellular and Biochemical Mechanisms of Obesity. Advances in Biochemistry in Health and Disease, vol 23. Springer, Cham. https://doi.org/10.1007/978-3-030-84763-0_9

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