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Skeletal muscle MIRO1 Mediates Insulin Resistance and Muscular Complications in Type 2 Diabetes

Award Number: F31DK146724
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/30/2026
PERIOD OF PERFORMANCE END DATE: 09/29/2027

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Skeletal muscle MIRO1 Mediates Insulin Resistance and Muscular Complications in Type 2 Diabetes - ABSTRACT Type 2 diabetes (T2D) affects over 500 million individuals globally, presenting a significant public health challenge. Current treatment strategies are expensive, burdensome, and fail to target the underlying molecular mechanisms of disease progression. There is a critical need to identify novel physiological regulators of T2D to support the development of more effective and individualized therapies, which is an area aligned with the mission of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Skeletal muscle is the primary site of insulin-stimulated glucose uptake, accounting for ~80% of whole-body glucose disposal. Skeletal muscle insulin resistance is a principal hallmark of T2D. However, the mechanisms linking skeletal muscle insulin resistance to impairments in glucose homeostasis and muscle function remain incompletely understood. Mitochondria play a crucial role in muscle energy metabolism, and recent evidence suggests that mitochondrial membrane dynamics are key to maintaining metabolic health. Mitochondrial Rho-GTPase 1 (MIRO1; RHOT1) is a GTPase located on the outer mitochondrial membrane involved in mitochondrial trafficking and calcium regulation. While MIRO1 has been studied extensively in neurodegenerative diseases, its role in peripheral tissues, such as skeletal muscle, is entirely unexplored. The central hypothesis of this proposal is that MIRO1 accumulation contributes to skeletal muscle insulin resistance and impaired muscle function through dysregulation of intracellular calcium handling. This F31 fellowship will support my research training as I pursue two specific aims: (1) to determine whether MIRO1 is a causal driver of insulin resistance using cellular and animal genetic models, and (2) to define the role of MIRO1 in skeletal muscle function and glucose metabolism. These studies will use cutting-edge molecular, physiological, and imaging techniques to uncover novel MIRO1- dependent mechanisms of metabolic dysfunction. Successful completion of this project will enhance our understanding of T2D pathophysiology and potentially identify MIRO1 as a new therapeutic target for skeletal muscle insulin resistance. This research will also provide me with rigorous scientific training in metabolism, mitochondrial biology, and translational approaches to disease, consistent with the goals of the NIDDK to support the development of the next generation of physician-scientists and biomedical researchers.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $50,114 )
2026	2026	UNIVERSITY OF OKLAHOMA	865 RESEARCH PKWY STE 560	OKLAHOMA CITY	OK	73104	OKLAHOMA	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	8/10/2026	NEW	$50,114
														Subtotal = $50,114

Grand Total All Awards = $50,114

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Skeletal muscle MIRO1 Mediates Insulin Resistance and Muscular Complications in Type 2 Diabetes

Award Number: F31DK146724

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/30/2026

PERIOD OF PERFORMANCE END DATE: 09/29/2027

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