Next Article in Journal
Suppression of GHS-R in AgRP Neurons Mitigates Diet-Induced Obesity by Activating Thermogenesis
Next Article in Special Issue
NutrimiRAging: Micromanaging Nutrient Sensing Pathways through Nutrition to Promote Healthy Aging
Previous Article in Journal
Can Early Rehabilitation Prevent Posttraumatic Osteoarthritis in the Patellofemoral Joint after Anterior Cruciate Ligament Rupture? Understanding the Pathological Features
Previous Article in Special Issue
Gene-Diet Interaction and Precision Nutrition in Obesity
Article Menu
Issue 4 (April) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2017, 18(4), 831; doi:10.3390/ijms18040831

Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes

Department of Nutrition Science, Purdue University, West Lafayette, IN 47907, USA
Author to whom correspondence should be addressed.
Academic Editors: Lynnette Ferguson and Virginia R. Parslow
Received: 28 February 2017 / Revised: 1 April 2017 / Accepted: 8 April 2017 / Published: 14 April 2017
(This article belongs to the Special Issue Gene-Diet Interactions in Chronic Diseases)
View Full-Text   |   Download PDF [800 KB, uploaded 14 April 2017]   |  


Skeletal muscle mitochondrial dysfunction, evidenced by incomplete beta oxidation and accumulation of fatty acid intermediates in the form of long and medium chain acylcarnitines, may contribute to ectopic lipid deposition and insulin resistance during high fat diet (HFD)-induced obesity. The present review discusses the roles of anterograde and retrograde communication in nucleo-mitochondrial crosstalk that determines skeletal muscle mitochondrial adaptations, specifically alterations in mitochondrial number and function in relation to obesity and insulin resistance. Special emphasis is placed on the effects of high fat diet (HFD) feeding on expression of nuclear-encoded mitochondrial genes (NEMGs) nuclear receptor factor 1 (NRF-1) and 2 (NRF-2) and peroxisome proliferator receptor gamma coactivator 1 alpha (PGC-1α) in the onset and progression of insulin resistance during obesity and how HFD-induced alterations in NEMG expression affect skeletal muscle mitochondrial adaptations in relation to beta oxidation of fatty acids. Finally, the potential ability of acylcarnitines or fatty acid intermediates resulting from mitochondrial beta oxidation to act as retrograde signals in nucleo-mitochondrial crosstalk is reviewed and discussed. View Full-Text
Keywords: mitochondria; skeletal muscle; obesity; insulin resistance; high fat diet; PGC1α; NRF-1; NRF-2; TFAM; acylcarnitine; metabolomics mitochondria; skeletal muscle; obesity; insulin resistance; high fat diet; PGC1α; NRF-1; NRF-2; TFAM; acylcarnitine; metabolomics

Figure 1

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

Devarshi, P.P.; McNabney, S.M.; Henagan, T.M. Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes. Int. J. Mol. Sci. 2017, 18, 831.

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



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top