Apolipoprotein CIII Reduction Protects White Adipose Tissues against Obesity-Induced Inflammation and Insulin Resistance in Mice

Recio-López, Patricia; Valladolid‐Acebes, Ismael; Berggren, Per‐Olof; Juntti‐Berggren, Lisa

doi:10.3390/ijms23010062

Cited by 4 publications

(2 citation statements)

References 28 publications

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“…The proinflammatory agent Apolipoprotein C-III ( Apoc3 ), down-regulated in white adipose tissue and the kidney, is associated with T2D, heart, and kidney diseases. Apoc3 reduction in mice was recently demonstrated to protect white adipose tissues against obesity-induced inflammation and insulin resistance 72 . Overall, these results support a high concordance of our rat-based data with human studies and their relevance to human disease.…”

Section: Resultsmentioning

confidence: 99%

Temporal dynamics of the multi-omic response to endurance exercise training across tissues

Amar

Gay

Beltran

et al. 2022

Preprint

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Regular exercise promotes whole-body health and prevents disease, yet the underlying molecular mechanisms throughout a whole organism are incompletely understood. Here, the Molecular Transducers of Physical Activity Consortium (MoTrPAC) profiled the temporal transcriptome, proteome, metabolome, lipidome, phosphoproteome, acetylproteome, ubiquitylproteome, epigenome, and immunome in whole blood, plasma, and 18 solid tissues in Rattus norvegicus over 8 weeks of endurance exercise training. The resulting data compendium encompasses 9466 assays across 19 tissues, 25 molecular platforms, and 4 training time points in young adult male and female rats. We identified thousands of shared and tissue- and sex- specific molecular alterations. Temporal multi-omic and multi-tissue analyses demonstrated distinct patterns of tissue remodeling, with widespread regulation of immune, metabolism, heat shock stress response, and mitochondrial pathways. These patterns provide biological insights into the adaptive responses to endurance training over time. For example, exercise training induced heart remodeling via altered activity of the Mef2 family of transcription factors and tyrosine kinases. Translational analyses revealed changes that are consistent with human endurance training data and negatively correlated with disease, including increased phospholipids and decreased triacylglycerols in the liver. Sex differences in training adaptation were widespread, including those in the brain, adrenal gland, lung, and adipose tissue. Integrative analyses generated novel hypotheses of disease relevance, including candidate mechanisms that link training adaptation to non-alcoholic fatty liver disease, inflammatory bowel disease, cardiovascular health, and tissue injury and recovery. The data and analysis results presented in this study will serve as valuable resources for the broader community and will be provided in an easily accessible public repository (https://motrpac-data.org/).

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Section: Resultsmentioning

confidence: 99%

Temporal dynamics of the multi-omic response to endurance exercise training across tissues

Amar

Gay

Beltran

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…In particular, decreasing ApoC-III ameliorates insulin sensitivity and triglyceride levels [65]. In a very recent study focused on subcutaneous (SAT) and visceral (VAT) white adipose tissue (WAT), Recio-Lopez et al have found that lowering ApoC-III determines improvements of metabolic status, decreases inflammation and size of adipocytes in WAT, and enhances the expression of genes related to thermogenesis and functions of SAT [66].…”

Section: Apoc-iii: Obesity and Lipodystrophymentioning

confidence: 99%

APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism

Giammanco

Spina

Cefalù

et al. 2023

Curr Atheroscler Rep

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Purpose of Review Apolipoprotein C-III (ApoC-III) is a widely known player in triglyceride metabolism, and it has been recently recognized as a polyhedric factor which may regulate several pathways beyond lipid metabolism by influencing cardiovascular, metabolic, and neurological disease risk. This review summarizes the different functions of ApoC-III and underlines the recent findings related to its multifaceted pathophysiological role. Recent Findings The role of ApoC-III has been implicated in HDL metabolism and in the development of atherosclerosis, inflammation, and ER stress in endothelial cells. ApoC-III has been recently considered an important player in insulin resistance mechanisms, lipodystrophy, diabetic dyslipidemia, and postprandial hypertriglyceridemia (PPT). The emerging evidence of the involvement of ApoC-III in the in the pathogenesis of Alzheimer’s disease open the way to further study if modification of ApoC-III level slows disease progression. Furthermore, ApoC-III is clearly linked to cardiovascular disease (CVD) risk, and progression of coronary artery disease (CAD) as well as the calcification of aortic valve and recent clinical trials has pointed out the inhibition of ApoC-III as a promising approach to manage hypertriglyceridemia and prevent CVD. Summary Several evidences highlight the role of ApoC-III not only in triglyceride metabolism but also in several cardio-metabolic pathways. Results from recent clinical trials underline that the inhibition of ApoC-III is a promising therapeutical strategy for the management of severe hypertriglyceridemia and in CVD prevention.

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Hypolipidemic and Anti‐Obesity Effect of Anserine on Mice Orally Administered with High‐Fat Diet via Regulating SREBP‐1, NLRP3, and UCP‐1

Luo,

Chen,

et al. 2024

Molecular Nutrition Food Res

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To investigate the efficacy of anserine on antiobesity, C57BL/6 mice are orally administered with a high‐fat diet (HFD) and different doses of anserine (60, 120, and 240 mg/kg/day) for 16 weeks. Body weight, lipid, and epididymal fat content in mice are measured, and their liver damage is observed. The results display that the body weight, epididymal fat content, and low‐density lipoprotein cholesterol (LDL‐C) content in anserine groups are decreased by 4.36–18.71%, 7.57–35.12%, and 24.32–44.40%, respectively. To further investigate the antiobesity mechanism of anserine, the expression of SREBP‐1, NLRP3, NF‐κB p65 (p65), and p‐NF‐κB p65 (p‐p65) proteins in the liver and peroxisome proliferator‐activated receptor gamma coactivator 1α (PGC1‐α) and UCP‐1 proteins in brown adipose tissue (BAT) is analyzed by Western blot. Results show that anserine can significantly decrease the expression of the NLRP3, p65, p‐p65, and the SREBP‐1 proteins and increase the expression of the PGC1‐α and UCP‐1 proteins. This study demonstrates that anserine lowered blood lipids and prevented obesity; its antiobesity mechanism may be related to the activation of brown fat by inflammation.

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Apolipoprotein CIII Reduction Protects White Adipose Tissues against Obesity-Induced Inflammation and Insulin Resistance in Mice

Cited by 4 publications

References 28 publications

Temporal dynamics of the multi-omic response to endurance exercise training across tissues

Temporal dynamics of the multi-omic response to endurance exercise training across tissues

APOC-III: a Gatekeeper in Controlling Triglyceride Metabolism

Hypolipidemic and Anti‐Obesity Effect of Anserine on Mice Orally Administered with High‐Fat Diet via Regulating SREBP‐1, NLRP3, and UCP‐1

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