Robert Noland

Assistant Professor

Pennington Biomedical Research Center

United States

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Robert Noland is an Assistant Professor at Pennington Biomedical Research Center in the United States. His research focuses on metabolic functions and responses to dietary interventions, exercise therapy, and the implications of sleep duration on glucose homeostasis and energy metabolism. Recent publications include studies on glucocorticoid-induced fat accumulation, skeletal muscle glucose disposal, and the effects of voluntary exercise on systemic inflammation and heart failure management.

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Elizabeth Floyd

Associate Professor

Pennington Biomedical Research Center

UNITED STATES

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Eric Ravussin

Professor (Adjunct) Biochemistry and Molecular Biology Division

Louisiana State University

UNITED STATES

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Melissa Linden

Assistant Professor

University of Massachusetts Boston

UNITED STATES

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Robert Noland

Research Interests

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Articles (18)

High-Protein Diet Prevents Glucocorticoid-Induced Fat Mass Accumulation and Hyperglycemia

Impact of Voluntary Exercise on Systemic Inflammation in a 2? Hit Model of Heart Failure With Preserved Ejection Fraction

Male mouse skeletal muscle lacking HuR shows enhanced glucose disposal at a young age.

Pancreatic expression of CPT1A is essential for whole body glucose homeostasis by supporting glucose-stimulated insulin secretion

Exercise Therapy Rescues Skeletal Muscle Dysfunction and Exercise Intolerance in Cardiometabolic HFpEF

Shortened sleep duration impairs adipose tissue adrenergic stimulation of lipolysis in postmenopausal women

Effect of sleep restriction on insulin sensitivity and energy metabolism in postmenopausal women: A randomized crossover trial

Corrigendum to “The RNA binding protein HuR influences skeletal muscle metabolic flexibility in rodents and humans” [Metab. 97 (2019) 40–49, (S0026049519300988), (10.1016/j.metabol.2019.05.010)]

Lysosomal glucose sensing and glycophagy in metabolism

NOD mice have distinct metabolic and immunologic profiles when compared with genetically similar MHC-matched ICR mice

Intact mitochondrial substrate efflux is essential for prevention of tubular injury in a sex-dependent manner

Dynamin-related protein 1 regulates substrate oxidation in skeletal muscle by stabilizing cellular and mitochondrial calcium dynamics.

Rickettsia conorii survival in THP-1 macrophages involves host lipid droplet alterations and active rickettsial protein production.

Female Mice Are Protected from Metabolic Decline Associated with Lack of Skeletal Muscle HuR.

Combined effects of a ketogenic diet and exercise training alter mitochondrial and peroxisomal substrate oxidative capacity in skeletal muscle.

The Ubiquitin Ligase SIAH2 Negatively Regulates Glucocorticoid Receptor Activity and Abundance.

BAM15-mediated mitochondrial uncoupling protects against obesity and improves glycemic control.

Response of Liver Metabolic Pathways to Ketogenic Diet and Exercise Are Not Additive.

Collaborators (8)

Christopher Morrison

Jake Doiron

Jacob Mey

Daria Ilatovskaya

Marie‐Pierre St‐Onge

Elizabeth Floyd

Eric Ravussin

Melissa Linden

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