Loss of Malat1 does not modify age- or diet-induced adipose tissue accretion and insulin resistance in mice

Several studies have suggested that signals emerging from white adipose tissue can contribute to the control of longevity. In turn, aging is associated with perturbed regulation and partitioning of fat depots and insulin resistance. However, the exact mechanisms involved in these relationships remai...

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Bibliographic Details
Published in:PloS one 2018-05, Vol.13 (5), p.e0196603-e0196603
Main Authors: Carter, Sophie, Miard, Stéphanie, Boivin, Louise, Sallé-Lefort, Sandrine, Picard, Frédéric
Format: Article
Language:English
Subjects:
Accretion
Adipose tissue
Age
Age (Biology)
Aging
Animal models
Biology and Life Sciences
Body fat
Cancer
Deposition
Diet
Food consumption
Food intake
Glucose
Glucose tolerance
Health aspects
High fat diet
Hypoxia
Insulin
Insulin resistance
Intolerance
Laboratory animals
Lipids
Medicine and Health Sciences
Metabolism
Metastasis
Mice
Non-coding RNA
Obesity
Oxygen
Oxygen consumption
Pharmacy
Polymerase chain reaction
Proteins
Ribonucleic acid
RNA
Rodents
Sucrose
Sugar
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Summary:Several studies have suggested that signals emerging from white adipose tissue can contribute to the control of longevity. In turn, aging is associated with perturbed regulation and partitioning of fat depots and insulin resistance. However, the exact mechanisms involved in these relationships remain undetermined. Using RAP-PCR on adipose tissue of young and old male mice coupled with qPCR validation, we have uncovered the long non-coding RNA Malat1 as a gene robustly downregulated in visceral white adipose tissue (vWAT) during normal aging in male mice and men. Reductions in Malat1 expression in subcutaneous WAT (scWAT) were also observed in genetic (ob and db) as well as diet-induced models of obesity. Based on these findings, Malat1+/+ and Malat1-/- mouse littermates were thus probed to detect whether loss of Malat1 would impact age or diet-induced gain in fat mass and development of glucose intolerance. Contrary to this hypothesis, male and female Malat1-deficient mice gained as much weight, and developed insulin resistance to a similar extent as their Malat1+/+ littermates when studied up to eight months old on regular chow or a high-fat, high-sucrose diet. Moreover, we observed no marked difference in oxygen consumption, food intake, or lipid profiles between Malat1+/+ and Malat1-/- mice. Therefore, we conclude that the overall metabolic impact of the absence of Malat1 on adipose tissue accretion and glucose intolerance is either physiologically not relevant upon aging and obesity, or that it is masked by as yet unknown compensatory mechanisms.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0196603