Mitochondrial dysfunction in adipocytes: the culprit in type 2 diabetes?

Maassen, J. A.

doi:10.1007/s00125-006-0165-z

Cited by 14 publications

(8 citation statements)

References 14 publications

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“…Obese subjects have also been shown to display elevated levels of BCAAs (Newgard et al, 2009). Moreover, several studies suggest that mitochondrial dysfunction in adipose tissue contributes to metabolic disturbances associated with obesity (De Pauw et al, 2009; Maassen, 2006). It may be that enhanced glucose production in insulin resistant states is further aggravated by factors and metabolic alterations originating from suboptimal mitochondrial function in adipose tissue.…”

Section: Discussionmentioning

confidence: 99%

Altered Mitochondrial Function and Metabolic Inflexibility Associated with Loss of Caveolin-1

et al. 2012

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Caveolin-1 is a major structural component of raft structures within the plasma membrane and has been implicated as a regulator of cellular signal transduction with prominent expression in adipocytes. Here, we embarked on a comprehensive characterization of the metabolic pathways dysregulated in caveolin-1 null mice. We found that these mice display decreased circulating levels of total and high molecular weight adiponectin and a reduced ability to change substrate use in response to feeding/fasting conditions. Caveolin-1 null mice are extremely lean, but retain muscle mass despite lipodystrophy and massive metabolic dysfunction. Hepatic gluconeogenesis is chronically elevated, while hepatic steatosis is reduced. Our data suggest that the complex phenotype of the caveolin-1 null mouse is caused by altered metabolic and mitochondrial function in adipose tissue with a subsequent compensatory response driven mostly by the liver. This mouse model highlights the central contributions of adipose tissue for system-wide preservation of metabolic flexibility.

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Section: Discussionmentioning

confidence: 99%

Altered Mitochondrial Function and Metabolic Inflexibility Associated with Loss of Caveolin-1

et al. 2012

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“…Mitochondrial dysfunction in adipocytes has been associated with obesity [24] and type 2 diabetes [25]. The major advantage of iPSCs over ES cells is that iPSCs can be derived from a patient’s own somatic cells, thereby avoiding immune rejection after transplantation and the ethical concerns raised by ES cells [4,5,26–28].…”

Section: Discussionmentioning

confidence: 99%

Enhanced Differentiation of Three-Gene-Reprogrammed Induced Pluripotent Stem Cells into Adipocytes via Adenoviral-Mediated PGC-1α Overexpression

Huang

Chou

Chang

et al. 2011

IJMS

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Induced pluripotent stem cells formed by the introduction of only three factors, Oct4/Sox2/Klf4 (3-gene iPSCs), may provide a safer option for stem cell-based therapy than iPSCs conventionally introduced with four-gene iPSCs. Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) plays an important role during brown fat development. However, the potential roles of PGC-1α in regulating mitochondrial biogenesis and the differentiation of iPSCs are still unclear. Here, we investigated the effects of adenovirus-mediated PGC-1α overexpression in 3-gene iPSCs. PGC-1α overexpression resulted in increased mitochondrial mass, reactive oxygen species production, and oxygen consumption. Microarray-based bioinformatics showed that the gene expression pattern of PGC-1α-overexpressing 3-gene iPSCs resembled the expression pattern observed in adipocytes. Furthermore, PGC-1α overexpression enhanced adipogenic differentiation and the expression of several brown fat markers, including uncoupling protein-1, cytochrome C, and nuclear respiratory factor-1, whereas it inhibited the expression of the white fat marker uncoupling protein-2. Furthermore, PGC-1α overexpression significantly suppressed osteogenic differentiation. These data demonstrate that PGC-1α directs the differentiation of 3-gene iPSCs into adipocyte-like cells with features of brown fat cells. This may provide a therapeutic strategy for the treatment of mitochondrial disorders and obesity.

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“…NRTI have been associated with mitochondrial toxicity [38,[46][47][48][49]. A decline in oxidative phosphorylation, resulting from mitochondrial dysfunction, could result in accumulation of FFA (metabolites), which, in turn, could have a negative effect on the signalling cascade of insulin [43,44] and may reinforce mitochondrial dysfunction [44,50]. NRTI-induced mitochondrial dysfunction as a cause for insulin insensitivity has been suggested by a recent study in healthy volunteers [38].…”

Section: Discussionmentioning

confidence: 99%

Zidovudine/lamivudine contributes to insulin resistance within 3 months of starting combination antiretroviral therapy

Blümer¹,

Vonderen

Sutinen

et al. 2008

Aids

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Mitochondrial dysfunction in adipocytes: the culprit in type 2 diabetes?

Cited by 14 publications

References 14 publications

Altered Mitochondrial Function and Metabolic Inflexibility Associated with Loss of Caveolin-1

Altered Mitochondrial Function and Metabolic Inflexibility Associated with Loss of Caveolin-1

Enhanced Differentiation of Three-Gene-Reprogrammed Induced Pluripotent Stem Cells into Adipocytes via Adenoviral-Mediated PGC-1α Overexpression

Zidovudine/lamivudine contributes to insulin resistance within 3 months of starting combination antiretroviral therapy

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