August 5, 2008DiabetesOpen Access

Type 1 Diabetic Akita Mouse Hearts Are Insulin Sensitive but Manifest Structurally Abnormal Mitochondria That Remain Coupled Despite Increased Uncoupling Protein 3

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Population

Type 1 diabetic Akita mouse model

Design

Preclinical

Authors

HBHeiko BuggerMedical University of Graz SBSihem BoudinaGeneral Cardiology XHXiao Xuan HuXiamen University

Discussion

Member takes

Implication

No support for UCP3-mediated uncoupling in this T1D model; leaves open distinct mitochondrial mechanisms versus T2D requiring human validation.

Structured PICO

Population

Type 1 diabetic Akita mouse model

Intervention

Observation of cardiac and mitochondrial function (including perfusion of isolated hearts with 1 mmol/l palmitate)

Outcome

Cardiac function, substrate utilization, mitochondrial function and coupling, proton leak kinetics, and oxidative stresssurrogate

Insulin-deficient type 1 diabetic Akita mouse hearts do not exhibit fatty acid-induced mitochondrial uncoupling despite increased UCP3, highlighting mechanistic differences in mitochondrial dysfunction compared to type 2 diabetes.

Cite This Study

Bugger et al. (2008) studied this question.

synapsesocial.com/papers/6a6f5dcbe71d69abee07fb4d https://doi.org/10.2337/db08-0079

Topics

Echocardiography

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Implication

No support for UCP3-mediated uncoupling in this T1D model; leaves open distinct mitochondrial mechanisms versus T2D requiring human validation.

Type 1 Diabetic Akita Mouse Hearts Are Insulin Sensitive but Manifest Structurally Abnormal Mitochondria That Remain Coupled Despite Increased Uncoupling Protein 3

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Type 1 Diabetic Akita Mouse Hearts Are Insulin Sensitive but Manifest Structurally Abnormal Mitochondria That Remain Coupled Despite Increased Uncoupling Protein 3

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider