Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

Petrus, Paul; Lecoutre, Simon; Dollet, Lucile; Wiel, Clotilde; Sulen, André; Gao, Hui; Tavira, Beatriz; Laurencikiene, Jurga; Rooyackers, Olav; Checa, Antonio; Douagi, Iyadh; Wheelock, Craig E.; Arner, Peter; McCarthy, Mark; Bergö, Martin O.; Edgar, Laurienne; Choudhury, Robin P.; Aouadi, Myriam; Krook, Anna

doi:10.1016/j.cmet.2019.11.019

Cited by 170 publications

(141 citation statements)

References 73 publications

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“…A recent in vitro study reported that GLN is the most markedly reduced amino acid in fat tissues obtained from subjects with obesity. Decreased GLN levels in adipose tissues result in increased nuclear O-GlcNAcylation in adipocytes that may consequently activate the transcription of proinflammatory proteins [ 33 ]. Our results are consistent with a report that administration of GLN reduced macrophage infiltration and attenuated expressions of proinflammatory genes and proteins in adipocytes [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Intravenous Glutamine Administration Improves Glucose Tolerance and Attenuates the Inflammatory Response in Diet-Induced Obese Mice after Sleeve Gastrectomy

et al. 2020

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Obesity is a health problem associated with many metabolic disorders. Weight reduction can effectively alleviate obesity-associated complications. Sleeve gastrectomy is a commonly used bariatric surgery and is considered safe and effective for improving outcomes. Glutamine (GLN) is an amino acid with anti-oxidative and anti-inflammatory properties. This study used a mouse model of sleeve gastrectomy to investigate the impacts of intravenous GLN administration on glucose tolerance and adipocyte inflammation short-term after surgery. C57BL6 male mice were divided into normal control (NC) and high-fat diet groups. The high-fat diet provided 60% of energy from fat for 10 weeks to induce obesity. Mice fed the high-fat diet were then assigned to a sham (SH) or sleeve gastrectomy with saline (S) or GLN (G) groups. The S group was intravenously injected with saline, while the G group was administered GLN (0.75 g/kg body weight) via a tail vein postoperatively. Mice in the experimental groups were sacrificed on day 1 or 3 after the surgery. Results showed that obesity resulted in fat accumulation, elevated glucose levels, and adipokines production. Sleeve gastrectomy aggravated expressions of inflammatory cytokine and macrophage infiltration markers, cluster of differentiation 68 (CD68), epidermal growth factor-like module-containing mucin-like hormone receptor-like 1 (EMR-1), and macrophage chemoattractant protein-1, in adipose tissues. Treatment of obese mice with GLN downregulated hepatic proteomic profiles associated with the gluconeogenesis pathway and improved glucose tolerance. Moreover, macrophage infiltration and adipose tissue inflammation were attenuated after the sleeve gastrectomy. These findings imply that postoperative intravenous GLN administration may improve glucose tolerance and attenuate inflammation shortly after the bariatric surgery in subjects with obesity.

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Section: Discussionmentioning

confidence: 99%

Intravenous Glutamine Administration Improves Glucose Tolerance and Attenuates the Inflammatory Response in Diet-Induced Obese Mice after Sleeve Gastrectomy

et al. 2020

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“…Even though both fat tissue and muscle, as well as associated immune cells in these inflamed tissues, can be sources of metabolites, it is unknown how much they can contribute to the pool of circulating metabolites. For example, studies measuring the metabolomics profile in visceral adipose tissue and serum from obese patients found low correlations between serum and adipose tissue metabolites [82]. On the other hand, we can speculate that there might be a competition between inflamed tissues (adipose tissue vs. synovial tissue) for the uptake of circulating anti-inflammatory metabolites.…”

Section: Comorbiditiesmentioning

confidence: 92%

Circulating Pro- and Anti-Inflammatory Metabolites and Its Potential Role in Rheumatoid Arthritis Pathogenesis

Coras

Murillo-Saich

Gumá

2020

Cells

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Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that affects synovial joints, leading to inflammation, joint destruction, loss of function, and disability. Although recent pharmaceutical advances have improved the treatment of RA, patients often inquire about dietary interventions to improve RA symptoms, as they perceive pain and/or swelling after the consumption or avoidance of certain foods. There is evidence that some foods have pro- or anti-inflammatory effects mediated by diet-related metabolites. In addition, recent literature has shown a link between diet-related metabolites and microbiome changes, since the gut microbiome is involved in the metabolism of some dietary ingredients. But diet and the gut microbiome are not the only factors linked to circulating pro- and anti-inflammatory metabolites. Other factors including smoking, associated comorbidities, and therapeutic drugs might also modify the circulating metabolomic profile and play a role in RA pathogenesis. This article summarizes what is known about circulating pro- and anti-inflammatory metabolites in RA. It also emphasizes factors that might be involved in their circulating concentrations and diet-related metabolites with a beneficial effect in RA.

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“…In T cell activation, glutamine deprivation has been shown to alter the activation of naive CD4 + T cells and result in their differentiation into forkhead box P3-positive (Foxp3 + ) regulatory T (T reg ) cells, which have suppressor functions 109 . Recently, glutamine metabolism has been shown to be linked to white adipose tissue (WAT) inflammation in obesity 110 . The researchers discovered that glutamine metabolism is impaired in the obese state, leading to increased chromatin O-GlcNAcylation and activation of genes in proinflammatory pathways.…”

Section: Control Of Epigenetic Changes By Glutaminementioning

confidence: 99%

Glutamine reliance in cell metabolism

et al. 2020

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As knowledge of cell metabolism has advanced, glutamine has been considered an important amino acid that supplies carbon and nitrogen to fuel biosynthesis. A recent study provided a new perspective on mitochondrial glutamine metabolism, offering mechanistic insights into metabolic adaptation during tumor hypoxia, the emergence of drug resistance, and glutaminolysis-induced metabolic reprogramming and presenting metabolic strategies to target glutamine metabolism in cancer cells. In this review, we introduce the various biosynthetic and bioenergetic roles of glutamine based on the compartmentalization of glutamine metabolism to explain why cells exhibit metabolic reliance on glutamine. Additionally, we examined whether glutamine derivatives contribute to epigenetic regulation associated with tumorigenesis. In addition, in discussing glutamine transporters, we propose a metabolic target for therapeutic intervention in cancer.

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Glutamine Links Obesity to Inflammation in Human White Adipose Tissue

Cited by 170 publications

References 73 publications

Intravenous Glutamine Administration Improves Glucose Tolerance and Attenuates the Inflammatory Response in Diet-Induced Obese Mice after Sleeve Gastrectomy

Intravenous Glutamine Administration Improves Glucose Tolerance and Attenuates the Inflammatory Response in Diet-Induced Obese Mice after Sleeve Gastrectomy

Circulating Pro- and Anti-Inflammatory Metabolites and Its Potential Role in Rheumatoid Arthritis Pathogenesis

Glutamine reliance in cell metabolism

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