Physical Activity Is the Key Determinant of Skeletal Muscle Mitochondrial Function in Type 2 Diabetes

Tienen, F.H.J. van; Praet, Stephan; Feyter, H.M.M.L. de; Broek, Nicole M. A. van den; Lindsey, Patrick; Schoonderwoerd, Kees; Coo, I.F.M. de; Nicolay, Klaas; Prompers, Jeanine J.; Smeets, Hubert J.M.; Loon, Luc J. C. van

doi:10.1210/jc.2011-3454

Cited by 96 publications

(82 citation statements)

References 39 publications

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“…Recent studies show that mitochondrial dysfunction of diabetic subjects is closely related to lifestyle factors, including diet, physical activity, sleep, and stress. 53,54) Prolonged exercise and diet intervention can reverse, at least partly, the mitochondrial deficiency and improve the metabolic flexibility and insulin sensitivity in patients with T2DM. 54,55) Recently, dietary PQQ supplementation has been revealed to enhance mitochondrial function and biogenesis and improve metabolic homeostasis in mice and rats.…”

Section: Anti-diabetic Effectsmentioning

confidence: 99%

Recent progress in studies on the health benefits of pyrroloquinoline quinone

Akagawa

Nakano

Ikemoto

2016

Bioscience, Biotechnology, and Biochemistry

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Pyrroloquinoline quinone (PQQ), an aromatic tricyclic o-quinone, was identified initially as a redox cofactor for bacterial dehydrogenases. Although PQQ is not biosynthesized in mammals, trace amounts of PQQ have been found in human and rat tissues because of its wide distribution in dietary sources. Importantly, nutritional studies in rodents have revealed that PQQ deficiency exhibits diverse systemic responses, including growth impairment, immune dysfunction, and abnormal reproductive performance. Although PQQ is not currently classified as a vitamin, PQQ has been implicated as an important nutrient in mammals. In recent years, PQQ has been receiving much attention owing to its physiological importance and pharmacological effects. In this article, we review the potential health benefits of PQQ with a focus on its growth-promoting activity, anti-diabetic effect, anti-oxidative action, and neuroprotective function. Additionally, we provide an update of its basic pharmacokinetics and safety information in oral ingestion.

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Section: Anti-diabetic Effectsmentioning

confidence: 99%

Recent progress in studies on the health benefits of pyrroloquinoline quinone

Akagawa

Nakano

Ikemoto

2016

Bioscience, Biotechnology, and Biochemistry

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“…Conversely, two separate lines of muscle-specific Pgc1a (Ppargc1a) transgenic mice displayed a significant enhancement in the markers of mitochondrial content and yet were insulin resistant due to excessive FA delivery and reduced GLUT4 (SLC2A4) expression in muscle (Miura et al 2003, Choi et al 2008. A growing number of studies in humans have also reported intact mitochondrial function in various insulin-resistant populations (De Feyter et al 2008, Trenell et al 2008, Lefort et al 2010, van Tienen et al 2012, Fisher-Wellman et al 2013. Collectively, these studies suggest that mitochondrial dysfunction in muscle is not an obligatory factor required for the accumulation of intramuscular lipids and the development of insulin resistance.…”

Section: Mitochondrial Dysfunction Reactive Oxygen Species and Insulmentioning

confidence: 99%

Fatty acid metabolism, energy expenditure and insulin resistance in muscle

Turner¹,

Cooney²,

Kraegen³

et al. 2013

Journal of Endocrinology

161

120

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Fatty acids (FAs) are essential elements of all cells and have significant roles as energy substrates, components of cellular structure and signalling molecules. The storage of excess energy intake as fat in adipose tissue is an evolutionary advantage aimed at protecting against starvation, but in much of today's world, humans are faced with an unlimited availability of food, and the excessive accumulation of fat is now a major risk for human health, especially the development of type 2 diabetes (T2D). Since the first recognition of the association between fat accumulation, reduced insulin action and increased risk of T2D, several mechanisms have been proposed to link excess FA availability to reduced insulin action, with some of them being competing or contradictory. This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. It also outlines potential problems with models and measurements that may hinder as well as help improve our understanding of the links between FAs and insulin action. (C:18:0), oleic acid (C18:1n-9), linoleic acid (C18:2n-6) and, particularly in smaller mammals, arachidonic acid (20:4n-6) and docosahexaenoic acid (22:6n-3). These FAs are the major components of storage triglycerides and cellular membranes, and although C16-C18 FAs are also components of some of the FA-derived signalling molecules (diacylglycerols (DAGs) and ceramides), many of the major lipid signalling molecules (prostaglandins and leukotrienes) are synthesised from very-long-chain, unsaturated FAs (e.g. arachidonic and docosahexaenoic acids) ( Kruger et al. 2010).In the context of the links between excessive lipid storage (obesity) and reduced insulin action (insulin Journal of EndocrinologyThematic Review N TURNER and others Fatty acids and insulin action 220:2 T61-T79

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“…In line with the microarray studies noted above, mRNA levels for a variety of mitochondrial genes have been shown to be reduced in muscle biopsies obtained from various insulin resistant populations, including lean insulin-resistant offspring of patients with T2D [80], obese subjects [81], patients with polycystic ovarian syndrome [82] and subjects with estab-lished T2DM [83,84]. The level of mtDNA was also shown to be lower in both obese, insulin resistant subjects and obese subjects with T2D [85,86].…”

Section: Mitochondrial Dysfunction In Muscle and Its Association Withmentioning

confidence: 72%

“…A similar finding was reported in a separate population where post-exercise phosphocreatine recovery indicated similar mitochondrial function between obese patients in either the early or advanced stages of T2D and normoglycemic controls matched for age, body composition and habitual physical activity levels [187]. A further study from the same group also recently reported similar in vivo mitochondrial function with MRS in prediabetic subjects compared with age, BMI and activity-matched controls, despite the presence of insulin resistance (by HOMA-IR and OGTT) [83]. In young lean men born with low birth-weight, mitochondrial function by MRS and mitochondrial gene expression are intact, despite these subjects displaying several pre-diabetic characteristics [188].…”

Section: Human Studiesmentioning

confidence: 77%

Mitochondrial Metabolism and Insulin Action

Turner¹

2013

Type 2 Diabetes

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Physical Activity Is the Key Determinant of Skeletal Muscle Mitochondrial Function in Type 2 Diabetes

Cited by 96 publications

References 39 publications

Recent progress in studies on the health benefits of pyrroloquinoline quinone

Recent progress in studies on the health benefits of pyrroloquinoline quinone

Fatty acid metabolism, energy expenditure and insulin resistance in muscle

Mitochondrial Metabolism and Insulin Action

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