about
Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivityExercise training increases mitochondrial content and ex vivo mitochondrial function similarly in patients with type 2 diabetes and in control individualsCardiac lipid content is unresponsive to a physical activity training intervention in type 2 diabetic patients, despite improved ejection fraction.Modulation of myocellular fat stores: lipid droplet dynamics in health and disease.High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistanceLower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients.Stimulation of human whole-body energy expenditure by salsalate is fueled by higher lipid oxidation under fasting conditions and by higher oxidative glucose disposal under insulin-stimulated conditions.The use of statins potentiates the insulin-sensitizing effect of exercise training in obese males with and without Type 2 diabetes.Improved ejection fraction after exercise training in obesity is accompanied by reduced cardiac lipid content.Distinct lipid droplet characteristics and distribution unmask the apparent contradiction of the athlete's paradoxCardiac lipid content is reduced after twelve weeks of endurance and strength training in overweight subjectsLipotoxicity plays a key role in the development of both insulin resistance and muscle atrophy in patients with type 2 diabetes
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description
academisch docent
@nl
researcher at Maastricht University
@en
name
Ruth Meex
@ast
Ruth Meex
@en
Ruth Meex
@es
Ruth Meex
@nl
type
label
Ruth Meex
@ast
Ruth Meex
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Ruth Meex
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Ruth Meex
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R. Meex
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R.C.R. Meex
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Ruth C. R. Meex
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Ruth Meex
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Ruth Meex
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Ruth Meex
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Ruth Meex
@nl
P1006
P214
P1006
P106
P21
P213
0000 0003 9687 9824
P214
P31
P496
0000-0002-7247-9191
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PRS1341743
P7859
viaf-291948567