18. Role of EFAs/PUFAs in Brain Growth and Development and Pathophysiology of the Metabolic Syndrome

  1. Undurti N. Das MD, PhD, FAMS President CEO Editor-in-Chief1,2

Published Online: 15 JAN 2010

DOI: 10.1002/9780813820637.ch18

Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids

Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids

How to Cite

Das, U. N. (2010) Role of EFAs/PUFAs in Brain Growth and Development and Pathophysiology of the Metabolic Syndrome, in Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids, Wiley-Blackwell, Oxford, UK. doi: 10.1002/9780813820637.ch18

Author Information

  1. 1

    UND Life Sciences, Ohio, USA

  2. 2

    Lipids in Health and Disease, USA

Publication History

  1. Published Online: 15 JAN 2010
  2. Published Print: 19 FEB 2010

ISBN Information

Print ISBN: 9780813815534

Online ISBN: 9780813820637

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Keywords:

  • EFAs/PUFAs in brain growth and metabolic syndrome pathophysiology;
  • brain, rich in arachidonic acid (AA), EPA and docosahexaenoic acid (DHA);
  • PUFAs in brain growth and development;
  • retinoic acid (RA) and nuclear retinoic acid receptor (RAR);
  • EPA/DHA - altering gene expression in developing brain;
  • β-Catenin-Wnt signaling and PUFAs;
  • leptin, potent feeding suppressant - absence, leading to morbid obesity;
  • PUFAs and insulin resistance;
  • Roux-en-Y gastric bypass (RYGB) - US abdominal surgical procedures for obesity;
  • gene expression for eNOS in RYGB

Summary

This chapter contains sections titled:

  • PUFAs in Brain Growth and Development

  • RAR-RXR Nuclear Receptors, PUFAs, and Neuronal Growth

  • Interaction among TNF-α, AA/EPA/DHA, and Insulin and Their Role in Neuronal Growth and Synapse Formation

  • PUFAs and Catenin, wnt, and Hedgehog Signaling Pathway in Brain Growth and Development

  • β-Catenin-Wnt Signaling and PUFAs

  • Modulation of the Secretion and Function of NMDA, γ-Aminobutyric Acid (GABA), Serotonin, and Dopamine by PUFAs

  • Leptin Regulates NPY/AgRP and POMC/CART Neurons and Programs Hypothalamic “Body Weight/Appetite/Satiety Set Point”

  • PUFAs Regulate Leptin, NPY/AgRP, and POMC/CART Neurons and Participate in Programming Hypothalamic “Body Weight/Appetite/Satiety Set Point”

  • PUFAs, Insulin, and Acetylcholine Not Only Interact among Themselves but Are Also Neuroprotective in Nature

  • PUFAs and Insulin Resistance

  • Maternal Diet Influences δΔ6 and δΔ5 Desaturases and Leptin Levels

  • Interaction(s) among Hypothalamic Neuropeptides, Gut, Adipose Tissue, Insulin, Cytokines, and Free Radicals and Its Relevance to the Pathophysiology of the Metabolic Syndrome

  • Hypothalamic Gene Expression Profile in the RYGB Animal Model

  • Increased Phospholipase A2 Expression after RYGB Surgery and Its Relevance to Suppression of Low-grade Systemic Inflammation in the Obese and Formation of Anti-inflammatory Lipids

  • Expression of Gene for eNOS in RYGB

  • RYGB-induced Weight Loss Is Due to Changes in the Levels of Hypothalamic Neuropeptides and Monoamines

  • What Are the Diagnostic and Prognostic Implications of This Knowledge?

  • Therapeutic Implications

  • PUFAs and Endocannabinoids

  • PUFAs and Type 2 Diabetes Mellitus

  • Hypothalamic PUFAs Regulate Insulin Secretion and Glucose Homeostasis by Influencing ATP-sensitive K+ Channels

  • Vagus as the Communicator between Gut, Liver, and Hypothalamus

  • References