Skeletal muscle energetics are compromised only during high-intensity contractions in the Goto-Kakizaki rat model of type 2 diabetes
Author:
Affiliation:
1. Department of Physiology, Michigan State University, East Lansing, Michigan
2. Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada
3. Department of Radiology, Michigan State University, East Lansing, Michigan
Abstract
Funder
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Gouvernement du Canada | Canadian Institutes of Health Research (Instituts de recherche en santé du Canada)
HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Link
https://www.physiology.org/doi/pdf/10.1152/ajpregu.00127.2019
Reference100 articles.
1. Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus
2. Mitochondrial reactive oxygen species generation in obese non-diabetic and type 2 diabetic participants
3. Muscle buffer capacity estimated from pH changes during rest-to-work transitions
4. Goto-kakizaki Rats: Its Suitability as Non-obese Diabetic Animal Model for Spontaneous Type 2 Diabetes Mellitus
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2. Measuring Mitochondrial Function: From Organelle to Organism;Methods in Molecular Biology;2022
3. Are Alterations in Skeletal Muscle Mitochondria a Cause or Consequence of Insulin Resistance?;International Journal of Molecular Sciences;2020-09-22
4. Mitochondrial Utilization of Competing Fuels Is Altered in Insulin Resistant Skeletal Muscle of Non-obese Rats (Goto-Kakizaki);Frontiers in Physiology;2020-06-16
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