Dynamics of Muscle Mitochondria in Type 2 Diabetes Exercise
DYNAMMO-T2DEX
DYNAMMO-T2DEX
Sponsor study identifier
interventional
24
1 country
1
Study Start
November 2016
Actual (reported)Primary Completion
September 2023
Actual (reported)Study Completion
January 2025
Actual (reported)Insulin promotes the clearance of sugars from the blood into skeletal muscle and fat cells for use as energy; it also promotes storage of excess nutrients as fat. Type 2 diabetes occurs when the cells of the body become resistant to the effects of insulin, and this causes high blood sugar and contributes to a build-up of fat in muscle, pancreas, liver, and the heart. Understanding how insulin resistance occurs will pave the way for new therapies aimed at preventing and treating type 2 diabetes. Mitochondria are cellular structures that are responsible for turning nutrients from food, into the energy that our cells run on. As a result, mitochondria are known as "the powerhouse of the cell." Mitochondria are dynamic organelles that can move within a cell to the areas where they are needed, and can fuse together to form large, string-like, tubular networks or divide into small spherical structures. The name of this process is "mitochondrial dynamics" and the process keeps the cells healthy. However, when more food is consumed compared to the amount of energy burned, mitochondria may become overloaded and dysfunctional resulting in a leak of partially metabolized nutrients that can interfere with the ability of insulin to communicate within the cell. This may be a way for the cells to prevent further uptake of nutrients until the current supply has been exhausted. However, long term overload of the mitochondria may cause blood sugar levels to rise and lead to the development of type 2 diabetes. This study will provide information about the relationship between mitochondrial dynamics, insulin resistance and type 2 diabetes.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
January 2025
Actual (reported)Click on a node to explore related trials.
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Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
November 2016
Actual (reported)November 28, 2016
Actual (reported)November 30, 2016
Actual (reported)September 2023
Actual (reported)January 2025
Actual (reported)Effects of exercise on mitochondrial dynamics
Dynamics will be assessed from quantitative measures of dynamin-related protein-1.
5 years
Effects of exercise on mitochondrial function
5 years
Insulin sensitivity
5 years
12 week exercise program, 5 days/week, 60 min/day
12 week standard of care recommendations
Registry-reported names are shown in full. Names without a link have not yet been matched to a Syfrah profile.
Pennington Biomedical Research Center
Baton Rouge, Louisiana, 70808, United States
Heintz EC, Dantas WS, Taylor AL, Zunica ERM, Belmont KP, Slone JM, Mey JT, Beyl R, Vandanmagsar B, Parry HA, Ajayi P, Glancy B, Axelrod CL, Kirwan JP. Miro1 mediates skeletal muscle insulin resistance in type 2 diabetes. Nat Commun. 2026 Oct 19;17(1):10702. doi: 10.1038/s41467-026-77278-6.
John Kirwan, PhD
Pennington Biomedical Research Center
24 participants (actual enrollment reported by the registry).
First Submitted
November 28, 2016
First Posted
November 30, 2016
Study Start
November 2016
Actual (reported)Individual Variability to Aerobic Exercise Training
Contact the study team to confirm eligibility.
Primary Completion
September 2023
Actual (reported)Study Completion
January 2025
Actual (reported)Last Updated
April 29, 2025
Record last verified: 2025-04
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Source: ClinicalTrials.gov.
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