Resistance training recovers attenuated APPL1 expression and improves insulin-induced Akt signal activation in skeletal muscle of type 2 diabetic rats
Published 2018 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Resistance training recovers attenuated APPL1 expression and improves insulin-induced Akt signal activation in skeletal muscle of type 2 diabetic rats
Authors
Keywords
-
Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 314, Issue 6, Pages E564-E571
Publisher
American Physiological Society
Online
2018-02-07
DOI
10.1152/ajpendo.00362.2017
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Dioscorea esculenta–induced increase in muscle sex steroid hormones is associated with enhanced insulin sensitivity in a type 2 diabetes rat model
- (2017) Koji Sato et al. FASEB JOURNAL
- Metabolic and hormonal response to intermittent high-intensity and continuous moderate intensity exercise in individuals with type 1 diabetes: a randomised crossover study
- (2016) Lia Bally et al. DIABETOLOGIA
- Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men
- (2016) Robert W. Morton et al. JOURNAL OF APPLIED PHYSIOLOGY
- Panaxatriol derived from ginseng augments resistance exercised–induced protein synthesis via mTORC1 signaling in rat skeletal muscle
- (2016) Yusuke Takamura et al. NUTRITION RESEARCH
- The role of mTOR signalling in the regulation of skeletal muscle mass in a rodent model of resistance exercise
- (2016) Riki Ogasawara et al. Scientific Reports
- Differential Role of Insulin/IGF-1 Receptor Signaling in Muscle Growth and Glucose Homeostasis
- (2015) Brian T. O’Neill et al. Cell Reports
- Human Muscle Fiber Type–Specific Insulin Signaling: Impact of Obesity and Type 2 Diabetes
- (2014) Peter H. Albers et al. DIABETES
- mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle
- (2013) Riki Ogasawara et al. JOURNAL OF APPLIED PHYSIOLOGY
- APPL1 potentiates insulin secretion in pancreatic cells by enhancing protein kinase Akt-dependent expression of SNARE proteins in mice
- (2012) K. K. Y. Cheng et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Physical Activity Advice Only or Structured Exercise Training and Association With HbA1cLevels in Type 2 Diabetes
- (2011) Daniel Umpierre JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
- Endurance exercise training increases APPL1 expression and improves insulin signaling in the hepatic tissue of diet-induced obese mice, independently of weight loss
- (2011) R. Marinho et al. JOURNAL OF CELLULAR PHYSIOLOGY
- The adaptor protein APPL1 increases glycogen accumulation in rat skeletal muscle through activation of the PI3-kinase signalling pathway
- (2011) M E Cleasby et al. JOURNAL OF ENDOCRINOLOGY
- APPL1 Potentiates Insulin-Mediated Inhibition of Hepatic Glucose Production and Alleviates Diabetes via Akt Activation in Mice
- (2009) Kenneth K.Y. Cheng et al. Cell Metabolism
- Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes
- (2009) R. A. DeFronzo et al. DIABETES CARE
- Yin-Yang Regulation of Adiponectin Signaling by APPL Isoforms in Muscle Cells
- (2009) Changhua Wang et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Exercise and adrenaline increase PGC-1α mRNA expression in rat adipose tissue
- (2009) Lindsey N. Sutherland et al. JOURNAL OF PHYSIOLOGY-LONDON
- Resistance exercise increases human skeletal muscle AS160/TBC1D4 phosphorylation in association with enhanced leg glucose uptake during postexercise recovery
- (2008) Hans C. Dreyer et al. JOURNAL OF APPLIED PHYSIOLOGY
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExploreAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started