Robert C. Noland
Pennington Biomedical Research Center
Publications 46
#1Susan J. Burke (Pennington Biomedical Research Center)H-Index: 14
#2Heidi M. Batdorf (Pennington Biomedical Research Center)H-Index: 3
Last.J. Jason Collier (Pennington Biomedical Research Center)
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Abstract Clinical glucocorticoid use, and diseases that produce elevated circulating glucocorticoids, promote drastic changes in body composition and reduction in whole body insulin sensitivity. Because steroid-induced diabetes is the most common form of drug-induced hyperglycemia, we investigated mechanisms underlying the recognized phenotypes associated with glucocorticoid excess. Male C57BL/6 J mice were exposed to either 100ug/mL corticosterone (cort) or vehicle in their drinking water. Body...
#1Robert Ross (UM: University of Michigan)H-Index: 51
#2Bret H. Goodpaster (Translational Research Institute)H-Index: 81
Last.Claude Bouchard (Pennington Biomedical Research Center)H-Index: 136
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There is evidence from human twin and family studies as well as mouse and rat selection experiments that there are considerable interindividual differences in the response of cardiorespiratory fitness (CRF) and other cardiometabolic traits to a given exercise programme dose. We developed this consensus statement on exercise response variability following a symposium dedicated to this topic. There is strong evidence from both animal and human studies that exercise training doses lead to variable ...
5 CitationsSource
#1Sujoy Ghosh (Pennington Biomedical Research Center)H-Index: 30
#2Shawna E. Wicks (Pennington Biomedical Research Center)H-Index: 8
Last.Robert C. Noland (Pennington Biomedical Research Center)H-Index: 19
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2 CitationsSource
#1Randall L. Mynatt (LSU: Louisiana State University)H-Index: 30
#2Robert C. Noland (LSU: Louisiana State University)H-Index: 19
Last.Jaycob D. Warfel (LSU: Louisiana State University)H-Index: 4
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Abstract Background Metabolic flexibility can be assessed by changes in respiratory exchange ratio (RER) following feeding. Though metabolic flexibility (difference in RER between fasted and fed state) is often impaired in individuals with obesity or type 2 diabetes, the cellular processes contributing to this impairment are unclear. Materials and methods From several clinical studies we identified the 16 most and 14 least metabolically flexible male and female subjects out of >100 participants ...
1 CitationsSource
ABSTRACTPurposeStudies suggest ketogenic diets (KDs) produce favorable outcomes (health and exercise performance); however, most rodent studies have used a low protein KD, which does not reflect the normal-to-high protein KDs used by humans. Liver has an important role in ketoadaptation due to its i
#1Scott E. Fuller (University of Louisiana at Lafayette)
#2Tai-Yu Huang (Pennington Biomedical Research Center)
Last.Robert C. Noland (Pennington Biomedical Research Center)H-Index: 19
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Effects of low-intensity exercise on substrate metabolism pathways were tested in liver and skeletal muscle of healthy mice. This is the first study to describe exercise-induced adaptations in pero...
Last.John P. KirwanH-Index: 55
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Introduction: Mitochondria are organelles that routinely undergo fission and fusion in a process known as mitochondrial dynamics. Increased mitochondrial fission is implicated in the pathogenesis of obesity, type 2 diabetes, and metabolic disease. DRP1 has been identified as a key regulator of mitochondrial fission. We and others have demonstrated that loss of DRP1 is associated with improvements in glucose homeostasis, however, the role of DRP1 in mitochondrial fatty acid oxidation is unknown. ...
#1Claudia Kruger (Pennington Biomedical Research Center)H-Index: 10
#2Trang-Tiffany Nguyen (Pennington Biomedical Research Center)H-Index: 1
Last.Krisztian Stadler (Pennington Biomedical Research Center)H-Index: 21
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Proximal tubular epithelial cells are highly energy demanding. Their energy need is covered mostly from mitochondrial fatty acid oxidation. Whether derailments in fatty acid metabolism and mitochondrial dysfunction are forerunners of tubular damage has been suggested but is not entirely clear. Here we modeled mitochondrial overload by creating mice lacking the enzyme carnitine acetyltransferase (CrAT) in the proximal tubules, thus limiting a primary mechanism to export carbons under conditions o...
1 CitationsSource
#1Susan J. BurkeH-Index: 14
#2Heidi M. BatdorfH-Index: 3
Last.J. Jason CollierH-Index: 18
view all 9 authors...
1 CitationsSource