Modulation of white adipose tissue proteome by aging and calorie restriction

Valle, Adamo; Sastre‐Serra, Jorge; Roca, Pilar; Oliver, Jordi

doi:10.1111/j.1474-9726.2010.00613.x

Cited by 25 publications

(13 citation statements)

References 51 publications

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“…In fact, despite the progeroid phenotype of Zmpste24 Ϫ/Ϫ mice, these animals also display transcriptional alterations in metabolism regulatory genes in the liver and profound changes in circulating glucose and hormone levels indicative of an activated antiaging response (27)(28)(29). In line with these findings, the shift in the expression profile of metabolic proteins found in Zmpste24 Ϫ/Ϫ mice highly resembles that observed in adipose tissue from old rats subjected to calorie restriction (18). Collectively, our proteomic data support the original proposal by Mariñ o et al (27) that a protective metabolic response is triggered in Zmpste24 Ϫ/Ϫ mice in order to attenuate the deleterious consequences associated to partially processed lamin A accumulation.…”

Section: Discussionmentioning

confidence: 53%

“…Because obesity is the most prevalent condition affecting adipose tissue function, the vast majority of the proteomic studies carried out to date have focused on the molecular characterization of adipose tissue from obese human (8,15), mouse (16,17), or rat (18,19) models. Actually, no other pathological states of adipose tissue have been investigated so far using proteomic techniques.…”

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confidence: 99%

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Proteomic Profiling of Adipose Tissue from Zmpste24−/− Mice, a Model of Lipodystrophy and Premature Aging, Reveals Major Changes in Mitochondrial Function and Vimentin Processing

Peinado

Quirós

Pulido

et al. 2011

Molecular & Cellular Proteomics

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Lipodystrophy is a major disease involving severe alterations of adipose tissue distribution and metabolism. Mutations in genes encoding the nuclear envelope protein lamin A or its processing enzyme, the metalloproteinase Zmpste24, cause diverse human progeroid syndromes that are commonly characterized by a selective loss of adipose tissue. Similarly to humans, mice deficient in Zmpste24 accumulate prelamin A and display phenotypic features of accelerated aging, including lipodystrophy. Herein, we report the proteome and phosphoproteome of adipose tissue as well as serum metabolome in lipodystrophy by using Zmpste24 ؊/؊ mice as experimental model. We show that Zmpste24 deficiency enhanced lipolysis, fatty acid biogenesis and ␤-oxidation as well as decreased fatty acid re-esterification, thus pointing to an increased partitioning of fatty acid toward ␤-oxidation and away from storage that likely underlies the observed size reduction of Zmpste24-null adipocytes. Besides the mitochondrial proteins related to lipid metabolism, other protein networks related to mitochondrial function, including those involved in tricarboxylic acid cycle and oxidative phosphorylation, were up-regulated in Zmpste24 ؊/؊ mice. These results, together with the observation of an increased mitochondrial response to oxidative stress, support the relationship between defective prelamin A processing and mitochondrial dysfunction and highlight the relevance of oxidative damage in lipoatrophy and aging. We also show that absence of Zmpste24 profoundly alters the processing of the cytoskeletal protein vimentin and identify a novel protein dysregulated in lipodystrophy, High-Mobility Group Box-1 Protein. Finally, we found several lipid derivates with important roles in energy balance, such as Lysophosphatidylcholine or 2-arachidonoylglycerol, to be dysregulated in Zmpste24

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Section: Discussionmentioning

confidence: 53%

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confidence: 99%

Proteomic Profiling of Adipose Tissue from Zmpste24−/− Mice, a Model of Lipodystrophy and Premature Aging, Reveals Major Changes in Mitochondrial Function and Vimentin Processing

Peinado

Quirós

Pulido

et al. 2011

Molecular & Cellular Proteomics

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“…Genetic manipulation that is aimed at changing the expression of these genes selectively in adipose tissue has been shown to alter the susceptibility to adipose tissue dysfunction and other metabolic derangements (20,21). Moreover, accumulating data from preclinical and clinical studies show that caloric restriction (CR) promotes catabolic pathways and a favorable adipokine expression profile via modulation of molecular pathways that are involved in lifespan extension, with protective metabolic effects on adipocyte and wholebody metabolism (22)(23)(24).…”

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confidence: 99%

Molecular mechanisms underlying metabolic syndrome: the expanding role of the adipocyte

et al. 2017

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The metabolic syndrome (MetS) is defined as a cluster of 3 or more metabolic and cardiovascular risk factors and represents a serious problem for public health. Altered function of adipose tissue has a significant impact on whole-body metabolism and represents a key driver for the development of these metabolic derangements, collectively referred as to MetS. In particular, increased visceral and ectopic fat deposition play a major role in the development of insulin resistance and MetS. A large body of evidence demonstrates that aging and MetS share several metabolic alterations. Of importance, molecular pathways that regulate lifespan affect key processes of adipose tissue physiology, and transgenic mouse models with adipose-specific alterations in these pathways show derangements of adipose tissue and other metabolic features of MetS, which highlights a causal link between dysfunctional adipose tissue and deleterious effects on whole-body homeostasis. This review analyzes adipose tissue-specific dysfunctions, including metabolic alterations that are related to aging, that have a significant impact on the development of MetS.-Armani, A., Berry, A., Cirulli, F., Caprio, M. Molecular mechanisms underlying metabolic syndrome: the expanding role of the adipocyte.

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“…Recently, proteomic profiling was done in aging rat white adipose tissue, and calorie restriction reversed the aging-related protein alteration. Calorie restriction improves the oxidative stress, cellular and energy metabolism, iron storage, and antioxidant affects (Valle et al 2010). The comparison of CR and our regenerated-related genes that reset the aging genes revealed over-representation of genes related to lipid metabolism, cellular growth and proliferation, transcription, cell adhesion, and response to stimulus (Hong et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Induction of cell proliferation in old rat liver can reset certain gene expression levels characteristic of old liver to those associated with young liver

Chishti

Kaya

Binbakheet

et al. 2012

AGE

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During the past decade, it has become increasingly clear that consistent changes in the levels of expression of a small cohort of genes accompany the aging of mammalian tissues. In many cases, these changes have been shown to generate features that are characteristic of the senescent phenotype. Previously, a small pilot study indicated that some of these changes might be reversed in rat liver, if the liver cells became malignant and were proliferating. The present study has tested the hypothesis that inducing proliferation in old rat liver can reset the levels of expression of these age-related genes to that observed in young tissue. A microarray approach was used to identify genes that exhibited the greatest changes in their expression during aging. The levels of expression of these markers were then examined in transcriptomes of both proliferating hepatomas from old animals and old rat liver lobes that had regenerated after partial hepatectomy but were again quiescent. We have found evidence that over 20 % of the aging-related genes had their levels of expression reset to young levels by stimulating proliferation, even in cells that had undergone a limited number of cell cycles and then become quiescent again. Moreover, our network analysis indicated alterations in MAPK/ERK and Jun-N-terminal kinase pathways and the potential important role of PAX3, VCAN, ARRB2, NR1H2, and ITGA5 that may provide insights into mechanisms involved in longevity and regeneration that are distinct from cancer.

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Modulation of white adipose tissue proteome by aging and calorie restriction

Cited by 25 publications

References 51 publications

Proteomic Profiling of Adipose Tissue from Zmpste24−/− Mice, a Model of Lipodystrophy and Premature Aging, Reveals Major Changes in Mitochondrial Function and Vimentin Processing

Proteomic Profiling of Adipose Tissue from Zmpste24−/− Mice, a Model of Lipodystrophy and Premature Aging, Reveals Major Changes in Mitochondrial Function and Vimentin Processing

Molecular mechanisms underlying metabolic syndrome: the expanding role of the adipocyte

Induction of cell proliferation in old rat liver can reset certain gene expression levels characteristic of old liver to those associated with young liver

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