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Study of Dapagliflozin on Mitochondrial Dysfunction and Impaired Insulin Signaling/Action

Information source: The University of Texas Health Science Center at San Antonio
ClinicalTrials.gov processed this data on August 23, 2015
Link to the current ClinicalTrials.gov record.

Condition(s) targeted: Insulin Sensitivity; Multiple Mitochondrial Dysfunctions Syndrome

Intervention: Dapagliflozin (Drug); Placebo (Drug)

Phase: N/A

Status: Recruiting

Sponsored by: The University of Texas Health Science Center at San Antonio

Official(s) and/or principal investigator(s):
Ralph DeFronzo, MD, Principal Investigator, Affiliation: The University of Texas Health Science Center at San Antonio

Overall contact:
Aurora Merovci, Phone: 210-567 4686

Summary

The purpose of this study is to examine the effect of the chronic treatment of type 2 diabetes (T2DM) with dapagliflozin on: (1) mitochondrial gene function/expression and insulin signaling/action and (2) oral glucose tolerance and beta cell function. Dapagliflozin is a potent, highly specific inhibitor of renal glucose transport [SGLT2].

Clinical Details

Official title: Regulation of Hepatic and Peripheral Glucose Metabolism: Protocol IVA. Effect of Plasma Glucose Reduction by Selective SLGT2 Inhibition on Mitochondrial Dysfunction and Impaired Insulin Signaling/Sensitivity in T2DM

Study design: Allocation: Randomized, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Basic Science

Primary outcome: Change in Insulin Sensitivity

Secondary outcome: Change in Mitochondrial Function

Detailed description: "Glucotoxicity" has been implicated as a cause of insulin resistance and impaired beta cell function in T2DM. Abundant support for the glucotoxicity hypothesis has been provided by in vivo and in vitro studies in animals, but a rigorous test of this hypothesis in man is lacking. The investigators propose to test the glucotoxicity hypothesis by chronically reducing the plasma glucose in type 2 diabetic subjects (T2DM) with an inhibitor of renal glucose transport, dapaglifozin, and examining the effect of restoration of normoglycemia on mitochondrial function and insulin signaling/sensitivity. Lastly, the investigators will test the "glucolipotoxicity" hypothesis, which states that the toxic effects of elevated plasma FFA on insulin sensitive tissues (i. e., muscle) are magnified in the presence of concurrent hyperglycemia. Thus, high glucose levels increase malonyl CoA, which inhibits CPT I, leading to accumulation of FACoA/DAG, which impair mitochondrial function and inhibit insulin action.

Eligibility

Minimum age: 18 Years. Maximum age: 70 Years. Gender(s): Both.

Criteria:

Inclusion Criteria:

- T2DM

- Drug Naive Or On Oral Therapy

Exclusion Criteria:

- Insulin Treatment

- Major Organ Disease

Locations and Contacts

Aurora Merovci, Phone: 210-567 4686

Diabetes Division, UTHSCSA, San Antonio, Texas 78229, United States; Recruiting
Irma, Phone: 210-567-4686
Additional Information

Starting date: March 2011
Last updated: June 10, 2015

Page last updated: August 23, 2015

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