Effects of Acipimox on Mitochondrial Function in Obesity
The purpose of the study is to examine whether a medication called acipimox can improve your body's mitochondria. Mitochondria are the "power house" of the cell and make energy for your body.
Obesity is associated with increased risk for developing diabetes. However, the investigators do not know how obesity leads to diabetes. Previous studies have shown levels of fat in the blood (free fatty acids or FFA) are higher in obesity, and elevated FFA can affect how our body uses glucose and responds to insulin. Recent studies have shown that changes in mitochondria may be involved in the development of diabetes and may be affected by FFA. The investigators propose to improve the function of mitochondria in obese people with pre-diabetes by treating with acipimox, a medication which decreases FFA. The investigators will use state of the art techniques to evaluate the mitochondria, including a new magnetic resonance imaging (MRI) technique to measure function of mitochondria in muscle.
|Study Design:||Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
|Official Title:||The Effects of Short Term Acipimox Treatment on Skeletal Muscle Phosphocreatine Recovery in Obesity|
- Change from Baseline in Phosphocreatine recovery at 6-months [ Time Frame: Change from Baseline to 6-months Visit ] [ Designated as safety issue: No ]The rate of recovery of phosphocreatine concentration after depletion by exercise is considered a measurement of mitochondrial function. Change in phosphocreatine recovery from baseline to 6 months will therefore give a measurement of change in mitochondrial function.
- Change from Baseline in insulin sensitivity at 6-months [ Time Frame: Change from Baseline to 6-months visit ] [ Designated as safety issue: No ]Change in insulin resistance assessed by 2-step hyperinsulinemic-euglycemic clamp study at Baseline and at 6-months.
- Change from Baseline in mitochondrial gene expression at 6-months [ Time Frame: Change from Baseline to 6-months ] [ Designated as safety issue: No ]Muscle biopsies will be performed and small pieces of muscle tissue will be used to measure expression of genes involved in mitochondrial function and biogenesis at Baseline and at 6-months
- Change from Baseline in mitochondrial number and morphology at 6-months [ Time Frame: Change from Baseline to 6-months ] [ Designated as safety issue: No ]Muscle tissue obtained from biopsy will be used to assess mitochondrial number and morphology by microscopes at Baseline and at 6-months
- Change from Baseline in intramyocellular lipid content at 6-months [ Time Frame: Change from Baseline to 6-months ] [ Designated as safety issue: No ]
- Change from Baseline in lipid profile at 3-months and 6-months [ Time Frame: Change from Baseline to 3-months and 6-months ] [ Designated as safety issue: No ]
|Study Start Date:||May 2012|
|Estimated Study Completion Date:||June 2017|
|Estimated Primary Completion Date:||June 2016 (Final data collection date for primary outcome measure)|
Treatment with the study drug Acipimox
250 mg by mouth (PO) three times daily
Placebo Comparator: Placebo
Treatment with Placebo control.
0 mg by mouth (PO) three times daily
Please refer to this study by its ClinicalTrials.gov identifier: NCT01488409
|Contact: Hideo Makimura, MD, PhDemail@example.com|
|United States, Massachusetts|
|Massachusetts General Hospital||Recruiting|
|Boston, Massachusetts, United States, 02114|
|Contact: Hideo Makimura, MD, PhD 617-726-8277 firstname.lastname@example.org|
|Principal Investigator: Hideo Makimura, MD, PhD|
|Principal Investigator:||Hideo Makimura, MD, PhD||Massachusetts General Hospital|