Next Article in Journal
Challenges in Implementing the Integrated Community-Based Outpatient Therapeutic Program for Severely Malnourished Children in Rural Southern Ethiopia
Previous Article in Journal
The Octyl Ester of Ginsenoside Rh2 Induces Lysosomal Membrane Permeabilization via Bax Translocation
Previous Article in Special Issue
Altered Skeletal Muscle Fatty Acid Handling in Subjects with Impaired Glucose Tolerance as Compared to Impaired Fasting Glucose
Article Menu

Export Article

Open AccessReview
Nutrients 2016, 8(5), 247; doi:10.3390/nu8050247

Metabolic Inflammation-Differential Modulation by Dietary Constituents

Nutrigenomics Research Group, UCD Conway Institute of Biomolecular and Biomedical Research and UCD Institute of Food and Health, University College Dublin, Belfield, Dublin 4, Ireland
*
Author to whom correspondence should be addressed.
Received: 3 February 2016 / Revised: 8 April 2016 / Accepted: 21 April 2016 / Published: 27 April 2016
(This article belongs to the Special Issue Fatty Acids in Obesity and Type 2 Diabetes)
View Full-Text   |   Download PDF [1463 KB, uploaded 27 April 2016]   |  

Abstract

Obesity arises from a sustained positive energy balance which triggers a pro-inflammatory response, a key contributor to metabolic diseases such as T2D. Recent studies, focused on the emerging area of metabolic-inflammation, highlight that specific metabolites can modulate the functional nature and inflammatory phenotype of immune cells. In obesity, expanding adipose tissue attracts immune cells, creating an inflammatory environment within this fatty acid storage organ. Resident immune cells undergo both a pro-inflammatory and metabolic switch in their function. Inflammatory mediators, such as TNF-α and IL-1β, are induced by saturated fatty acids and disrupt insulin signaling. Conversely, monounsaturated and polyunsaturated fatty acids do not interrupt metabolism and inflammation to the same extent. AMPK links inflammation, metabolism and T2D, with roles to play in all and is influenced negatively by obesity. Lipid spillover results in hepatic lipotoxicity and steatosis. Also in skeletal muscle, excessive FFA can impede insulin’s action and promote inflammation. Ectopic fat can also affect pancreatic β-cell function, thereby contributing to insulin resistance. Therapeutics, lifestyle changes, supplements and dietary manipulation are all possible avenues to combat metabolic inflammation and the subsequent insulin resistant state which will be explored in the current review. View Full-Text
Keywords: nutrition; metabolic-inflammation; diet; insulin resistance; fatty acids; adipose tissue; liver; muscle; pancreas nutrition; metabolic-inflammation; diet; insulin resistance; fatty acids; adipose tissue; liver; muscle; pancreas
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Lyons, C.L.; Kennedy, E.B.; Roche, H.M. Metabolic Inflammation-Differential Modulation by Dietary Constituents. Nutrients 2016, 8, 247.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Nutrients EISSN 2072-6643 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top