Metabolic regulation by secreted phospholipase A2

Sato, Hiroyasu; Taketomi, Yoshitaka; Murakami, Makoto

doi:10.1186/s41232-016-0012-7

Cited by 53 publications

(38 citation statements)

References 52 publications

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“…Previously, PLA2G2A was investigated for its involvement in the development and progression of inflammation and atherosclerosis (18,28). Its role in metabolism has not been studied, however, which is significant given the emerging information that several sPLA 2 s have roles in the regulation of obesity, hepatic steatosis, hyperlipidemia, and insulin signaling (29). Our previous findings showed that acute treatment with T 3 inhibits PLA2G2A gene expression in the livers of rats and mice (30).…”

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confidence: 99%

Secretory phospholipase A₂ group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

et al. 2018

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Secretory phospholipase A group IIA (PLA2G2A) is a phospholipase which has a role in inflammation, atherogenesis, and host defense. Previously, we found that PLA2G2A protects mice on high-fat diets from weight gain and insulin resistance. Here, we examined the regulation of PLA2G2A and the metabolic changes that occur in response to variations in thyroid status. In particular, the impact of PLA2G2A on the brown adipose tissue (BAT) thermogenic gene expression was explored. We induced hypothyroidism in C57BL/6 and PLA2G2A-overexpressing (IIA+) mice over a 10 wk period or treated them with thyroid hormone (T) for 5 wk. There were no significant changes in PLA2G2A abundance in response to thyroid status. The energy expenditure of hypothyroid IIA+ mice did not increase; however, the energy expenditure, substrate utilization, insulin sensitivity, and glucose tolerance were all elevated in the IIA+ mice given T. Moreover, white adipocytes from IIA+ mice were much more prone to "beiging," including increased expression of brown adipose thermogenic markers such as uncoupling protein 1 (UCP1), PR domain containing 16, and early B cell factor 2. Finally, the BAT of IIA+ mice had increased UCP1 and other proteins indicative of mitochondrial uncoupling and nonshivering adaptive thermogenesis. These data reveal a novel role for PLA2G2A on adipose tissue thermogenesis depending on thyroid status.-Kuefner, M. S., Deng, X., Stephenson, E. J., Pham, K., Park, E. A. Secretory phospholipase A group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone.

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confidence: 99%

Secretory phospholipase A₂ group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

et al. 2018

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“…The stimuli that can initiate adipose tissue inflammation are complex and numerous [33,34] and include fibrosis and alterations in extracellular matrix components and stiffness [83,[92][93][94][95][96], apoptosis and necrosis of hypertrophic adipocytes [97], hypoxia from defective angiogenesis [24,98], free fatty acids (lipotoxicity) [21], and exogenous, as well as gut microbiota-derived LPS [36]. The GOterms for this cluster of Biological Processes are presented in Figure 7, and there are two genes of particular interest PLA2G16 and MAPK1.PLA2G16-phospholipase 2A-a lipolytic enzyme made in hypertrophic adipocytes that produces FFAs and induces hyperlipidemia [99,100]. Coregulation between PLA2G16 and F13A1 could thus imply a link to FFAs.…”

Section: Discussionmentioning

confidence: 99%

Transglutaminases and Obesity in Humans: Association of F13A1 to Adipocyte Hypertrophy and Adipose Tissue Immune Response

Kaartinen

Arora

Heinonen

et al. 2020

IJMS

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Transglutaminases TG2 and FXIII-A have recently been linked to adipose tissue biology and obesity, however, human studies for TG family members in adipocytes have not been conducted. In this study, we investigated the association of TGM family members to acquired weight gain in a rare set of monozygotic (MZ) twins discordant for body weight, i.e., heavy–lean twin pairs. We report that F13A1 is the only TGM family member showing significantly altered, higher expression in adipose tissue of the heavier twin. Our previous work linked adipocyte F13A1 to increased weight, body fat mass, adipocyte size, and pro-inflammatory pathways. Here, we explored further the link of F13A1 to adipocyte size in the MZ twins via a previously conducted TWA study that was further mined for genes that specifically associate to hypertrophic adipocytes. We report that differential expression of F13A1 (ΔHeavy–Lean) associated with 47 genes which were linked via gene enrichment analysis to immune response, leucocyte and neutrophil activation, as well as cytokine response and signaling. Our work brings further support to the role of F13A1 in the human adipose tissue pathology, suggesting a role in the cascade that links hypertrophic adipocytes with inflammation.

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“…Regarding LPCs, which are produced when phospholipids such as PCs or PEs are hydrolyzed by phospholipase A 2 (PLA 2 ) [31], results from published studies vary. In harmony with the findings of this study, lower levels of some LPC species including LPC (18:2) were associated with a higher risk of metabolic dysfunction [32,33].…”

Section: Discussionmentioning

confidence: 99%

“…While observed differences in the relationship of LPCs with metabolic disease could be due to the fatty acid side chain, PLA 2 isoforms could also play a role. For example, to protect from adipose tissue inflammation during obesity, hyperlipidemic LDL is hydrolyzed by PLA 2 -V to release unsaturated fatty acids which aid saturated adipocytes-released fatty acids to initiate the polarization of macrophages [31].…”

Section: Discussionmentioning

confidence: 99%

A lipidome-wide association study of the lipoprotein insulin resistance index

et al. 2020

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Background: The lipoprotein insulin resistance (LPIR) score was shown to predict insulin resistance (IR) and type 2 diabetes (T2D) in healthy adults. However, the molecular basis underlying the LPIR utility for classification remains unclear. Objective: To identify small molecule lipids associated with variation in the LPIR score, a weighted index of lipoproteins measured by nuclear magnetic resonance, in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study (n = 980). Methods: Linear mixed effects models were used to test the association between the LPIR score and 413 lipid species and their principal component analysis-derived groups. Significant associations were tested for replication with homeostatic model assessment-IR (HOMA-IR), a phenotype correlated with the LPIR score (r = 0.48, p < 0.001), in the Heredity and Phenotype Intervention (HAPI) Heart Study (n = 590). Results: In GOLDN, 319 lipids were associated with the LPIR score (false discovery rate-adjusted p-values ranging from 4.59 × 10 − 161 to 49.50 × 10 − 3). Factors 1 (triglycerides and diglycerides/storage lipids) and 3 (mixed lipids) were positively (β = 0.025, p = 4.52 × 10 − 71 and β = 0.021, p = 5.84 × 10 − 41 , respectively) and factor 2 (phospholipids/ non-storage lipids) was inversely (β = − 0.013, p = 2.28 × 10 − 18) associated with the LPIR score. These findings were replicated for HOMA-IR in the HAPI Heart Study (β = 0.10, p = 1.21 × 10 − 02 for storage, β = − 0.13, p = 3.14 × 10 − 04 for non-storage, and β = 0.19, p = 8.40 × 10 − 07 for mixed lipids). Conclusions: Non-storage lipidomics species show a significant inverse association with the LPIR metabolic dysfunction score and present a promising focus for future therapeutic and prevention studies.

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Metabolic regulation by secreted phospholipase A2

Cited by 53 publications

References 52 publications

Secretory phospholipase A₂ group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

Secretory phospholipase A₂ group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

Transglutaminases and Obesity in Humans: Association of F13A1 to Adipocyte Hypertrophy and Adipose Tissue Immune Response

A lipidome-wide association study of the lipoprotein insulin resistance index

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Metabolic regulation by secreted phospholipase A2

Cited by 53 publications

References 52 publications

Secretory phospholipase A2 group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

Secretory phospholipase A2 group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

Transglutaminases and Obesity in Humans: Association of F13A1 to Adipocyte Hypertrophy and Adipose Tissue Immune Response

A lipidome-wide association study of the lipoprotein insulin resistance index

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Secretory phospholipase A₂ group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone

Secretory phospholipase A₂ group IIA enhances the metabolic rate and increases glucose utilization in response to thyroid hormone