Low‐intensity exercise increases skeletal muscle protein expression of PPARδ and UCP3 in type 2 diabetic patients

Fritz, Tomas; Krämer, David Kitz; Karlsson, Håkan K.R.; Galuska, Dana; Engfeldt, Peter; Zierath, Juleen R.; Krook, Anna

doi:10.1002/dmrr.656

Cited by 106 publications

(105 citation statements)

References 37 publications

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“…These results are in agreement with another study showing that changes in plasma glucose concentration and HbA 1c , induced by increased physical activity and weight-loss, were significantly associated with increased mitochondrial content [27]. Interestingly, it has been suggested that insulin-resistant participants may have a lower response to physical training [28]. Recently it was shown that the response to acute exercise in terms of expression and protein content of genes coding for mitochondrial biogenesis was lower in insulin-resistant non-diabetic participants than in lean control participants [29].…”

Section: Introductionsupporting

confidence: 92%

Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes

et al. 2010

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Aim/hypothesis Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. Methods Type 2 diabetic men (n=13) and control (n=14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre-and posttraining muscle biopsies were obtained before a euglycaemichyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. Results Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. Conclusions/interpretation Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.

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Section: Introductionsupporting

confidence: 92%

Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes

et al. 2010

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“…ES for each of the controlled trials was interpreted according to the method of Cohen [16]. from 18 studies including 3 randomized controlled trials reported in 9 publications [17][18][19][20][21][22][23][24][25] (2 trials reported in 8 publications with resistance training [17][18][19][20][21][22][23][24] and 1 with aerobic training [25]), 2 non-randomized controlled trials [26,27] (with aerobic training [26,27]) and 13 uncontrolled trials reported in 15 publications [28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] (11 trials reported in 13 publications with aerobic training [28,[30][31][32][33][34][35][36][37][38]…”

Section: Discussionmentioning

confidence: 99%

“…The study quality was performed for three randomized controlled trials reported in nine publications [17][18][19][20][21][22][23][24][25] and two nonrandomized controlled trials [26,27]. In general, the study quality was moderate, and none of the studies met all of the Delphi list quality criteria.…”

Section: Study Quality Assessmentmentioning

confidence: 99%

“…All studies specified their inclusion criteria, and reported groups or subjects were similar at baseline regarding important prognostic valuables. Four studies published in ten papers reported dropouts with rates ranging from 0-9.1% [17][18][19][20][21][22][23][24]26,27]. One study published in four papers reported exercise compliance [17][18][19][20].…”

Section: Study Quality Assessmentmentioning

confidence: 99%

“…Only one study published in four papers reported blinding of outcome assessors [17][18][19][20]. The participants from four studies reported in ten publications performed their training intervention under complete supervision [17][18][19][20][21][22][23][24][25][26]; in the other studies, instructions were given on how to increase the physical activities and the exercise sessions were recorded [27]. One study published in four papers employed an intention-to-treat (ITT) analysis with imputation of missing data [17][18][19][20] (60 out of 62 subjects completed the study, method of imputation not reported); one study published in four papers [21][22][23][24] planned an intention-to-treat analysis but had no dropouts.…”

Section: Study Quality Assessmentmentioning

confidence: 99%

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Adaptations to exercise training within skeletal muscle in adults with type 2 diabetes or impaired glucose tolerance: a systematic review

Wang

Simar

Singh

2009

Diabetes Metabolism Res

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SummaryThe aim of this investigation was to review morphological and metabolic adaptations within skeletal muscle to exercise training in adults with type 2 diabetes mellitus (T2DM) or impaired glucose tolerance (IGT). A comprehensive, systematic database search for manuscripts was performed from 1966 to March 2008 using computerized databases, including Medline, Premedline, CINAHL, AMED, EMBASE and SportDiscus. Three reviewers independently assessed studies for potential inclusion (exposure to exercise training, T2DM or IGT, muscle biopsy performed). A total of 18 exercise training studies were reviewed. All morphological and metabolic outcomes from muscle biopsies were collected. The metabolic outcomes were divided into six domains: glycogen, glucose facilitated transporter 4 (GLUT4) and insulin signalling, enzymes, markers of inflammation, lipids metabolism and so on. Beneficial adaptations to exercise were seen primarily in muscle fiber area and capillary density, glycogen, glycogen synthase and GLUT4 protein expressions. Few randomized controlled trials including muscle biopsy data existed, with a small number of subjects involved. More trials, especially robustly designed exercise training studies, are needed in this field. Future research should focus on the insulin signalling pathway to better understand the mechanism of the improvements in insulin sensitivity and glucose homeostasis in response to various modalities and doses of exercise in this cohort.

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Myristic acid selectively augments β‐tubulin levels in C2C12 myotubes via diacylglycerol kinase δ

et al. 2022

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Effective amelioration of type II diabetes requires therapies that increase both glucose uptake activity per cell and skeletal muscle mass. Myristic acid (14:0) increases diacylglycerol kinase (DGK) δ protein levels and enhances glucose uptake in myotubes in a DGKδ‐dependent manner. However, it is still unclear whether myristic acid treatment affects skeletal muscle mass. In this study, we found that myristic acid treatment increased the protein level of β‐tubulin, which constitutes microtubules and is closely related to muscle mass, in C2C12 myotubes but not in the proliferation stage in C2C12 myoblasts. However, lauric (12:0), palmitic (16:0) and oleic (18:1) acids failed to affect DGKδ and β‐tubulin protein levels in C2C12 myotubes. Moreover, knockdown of DGKδ by siRNA significantly inhibited the increased protein level of β‐tubulin in the presence of myristic acid, suggesting that the increase in β‐tubulin protein by myristic acid depends on DGKδ. These results indicate that myristic acid selectively affects β‐tubulin protein levels in C2C12 myotubes via DGKδ, suggesting that this fatty acid improves skeletal muscle mass in addition to increasing glucose uptake activity per cell.

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Low‐intensity exercise increases skeletal muscle protein expression of PPARδ and UCP3 in type 2 diabetic patients

Cited by 106 publications

References 37 publications

Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes

Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes

Adaptations to exercise training within skeletal muscle in adults with type 2 diabetes or impaired glucose tolerance: a systematic review

Myristic acid selectively augments β‐tubulin levels in C2C12 myotubes via diacylglycerol kinase δ

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