FABP4 Dynamics in Obesity: Discrepancies in Adipose Tissue and Liver Expression Regarding Circulating Plasma Levels

Queipo-Ortuño, María Isabel; Escoté, Xavier; Ceperuelo-Mallafré, Victòria; Garrido‐Sánchez, Lourdes; Miranda, Merce; Clemente‐Postigo, Mercedes; Pérez-Pérez, Rafael; Peral, Belén; Cardona, Fernando; Fernández-Real, José Manuel; Tinahones, Francisco J.; Vendrell, Joan

doi:10.1371/journal.pone.0048605

Cited by 69 publications

(60 citation statements)

References 43 publications

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“…Supporting these assumptions, we did not observe significant differences between groups in mRNA level of markers of nonadipocyte cells, suggesting no interference of other cell types with the DNA quantification procedure. Furthermore, the decreased Fabp4 expression in mice receiving the HF-D diet is in agreement with an IR state, fat cell hypertrophy, and changes in body composition as described in humans (25,26).…”

Section: Figsupporting

confidence: 82%

EPA prevents fat mass expansion and metabolic disturbances in mice fed with a Western diet

Pinel

Pitois

Rigaudière

et al. 2016

Journal of Lipid Research

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The authors acknowledge the staff from Auvergne University Experimental Animal Laboratory and Christophe Del’Homme, Philippe Denis, Anne Terisse-Lottier and Alexandre Teynie from the Experimental Animal Facility of the Human Nutrition Unit (INRA of Clermont-Ferrand) for their assistance throughout the animal protocol. We thank Celine Bobby for her help for TaqMan gene expression assays. We gratefully acknowledge financial support and doctoral fellowship (to A.P.) fromLesieur and AvrilImpact of ALA, EPA and DHA on obesity and metabolic complications were studied in mice fed a high-fat high-sucrose diet (HF). HF diets were supplemented with ALA, EPA or DHA (1%w/w) and given to C57BL/6J mice for 16 weeks and to Ob/Ob mice for 6 weeks. In C57BL/6J mice, EPA reduced plasma cholesterol (-20%), limited fat mass accumulation (-23%), adipose cell hypertrophy (-50%), and reduced plasma leptin concentration (-60%), compared to HF fed mice. Furthermore, mice supplemented with EPA exhibited a higher insulin sensitivity (+24%) and glucose tolerance (+20%) compared to HF fed mice. Similar effects were observed in EPA supplemented Ob/Ob mice, although fat mass accumulation was not prevented. By contrast in comparison to HF fed mice, DHA did not prevent fat mass accumulation, increased plasma leptin concentration (+128%) in C57BL/6J mice and did not improve glucose homeostasis in C57BL/6J and Ob/Ob mice. In 3T3-L1 adipocytes, DHA stimulated leptin expression whereas EPA induced adiponectin expression, suggesting that improved leptin / adiponectin balance may contribute to the protective effect of EPA. In conclusion, supplementation with EPA, but not ALA and DHA, could preserve glucose homeostasis in an obesogenic environment and limit fat mass accumulation in the early stage of weight gain

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Section: Figsupporting

confidence: 82%

EPA prevents fat mass expansion and metabolic disturbances in mice fed with a Western diet

Pinel

Pitois

Rigaudière

et al. 2016

Journal of Lipid Research

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“…FABP4 is one of the most abundant proteins in mature adipocytes and is also detected at high concentrations in human serum. Although the biological role of FABP4 is not fully understood, it has been linked to insulin sensitivity, lipid metabolism, and inflammation [46]. Previously, we have shown that FABP4 levels are elevated in obese and diabetic individuals, and such increased levels are closely correlated with adverse lipid profiles, insulin resistance, and vascular smooth muscle cell proliferation [47,48,49,50].…”

Section: Discussionmentioning

confidence: 99%

Differential Protein Expression in White Adipose Tissue from Obesity-Prone and Obesity-Resistant Mice in Response to High Fat Diet and Anti-Obesity Herbal Medicines

Kim

Park²,

Choi³

et al. 2015

Cell Physiol Biochem

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Background: One of the most interesting issues in obesity research is why certain humans are obesity-prone (OP) while others are obesity-resistant (OR) upon exposure to a high-calorie diet. However, the pathways responsible for these phenotypic differences are still largely unknown. Methods: In order to discover marker molecules determining susceptibility and/or resistance to obesity in response to high fat diet (HFD) or anti-obesity herbal medicine (TH), we conducted comparative proteomic analysis of white adipose tissue (WAT) from OP, OR, as well as TH-treated mice. Results: OP mice fed HFD gained approximately 33% more body weight than OR mice, and TH significantly reduced body weight gain in HFD-fed mice by 30%. These mice were further subjected to proteomic analysis using two-dimensional electrophoresis (2-DE) combined with matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS). Proteomic data revealed 59 spots that were differentially regulated from a total of 1,045 matched spots, and 57 spots of these were identified as altered WAT proteins between OP and OR mice by peptide mass finger printing. Interestingly, 45 proteins were similarly regulated in OR mice in response to TH treatment. Of these, 10 proteins have already been recognized in the context of obesity; however, other proteins involved in obesity susceptibility or resistance were identified for the first time in the present study. Conclusion: Our results suggest that TH actively contributed to body weight reduction in HFD-fed obese mice by altering protein regulation in WAT, and it was also found that TH-responsive proteins can be used as potent molecules for obesity treatment.

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“…However, in the insulin-resistant state, which is a condition often associated with central obesity, adipocyte lipolysis increases regardless of nutritional fluctuations, leading to the release of abundant FFAs into the blood [12]. In the liver, several membrane-bound proteins are responsible for transporting circulating FFAs into hepatocytes, including fatty acid transporter protein (FATP)-2 [15], FATP-5 [16], fatty acid translocase (FAT/CD36) [17][18][19], caveolins [20,21], fatty acid binding proteins (FABP)-1, FABP-4, and FABP-5 [22,23]. Upregulation of several FFA transporters is associated with increased insulin resistance and hepatic steatosis in NAFLD patients [24][25][26][27].…”

Section: Increased Hepatic Fatty Acid Uptakementioning

confidence: 99%

Molecular mechanisms of fatty liver in obesity

Xiang

Xie

2015

Front. Med.

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Nonalcoholic fatty liver disease (NAFLD) covers a spectrum of liver disorders ranging from simple steatosis to advanced pathologies, including nonalcoholic steatohepatitis and cirrhosis. NAFLD significantly contributes to morbidity and mortality in developed societies. Insulin resistance associated with central obesity is the major cause of hepatic steatosis, which is characterized by excessive accumulation of triglyceride-rich lipid droplets in the liver. Accumulating evidence supports that dysregulation of adipose lipolysis and liver de novo lipogenesis (DNL) plays a key role in driving hepatic steatosis. In this work, we reviewed the molecular mechanisms responsible for enhanced adipose lipolysis and increased hepatic DNL that lead to hepatic lipid accumulation in the context of obesity. Delineation of these mechanisms holds promise for developing novel avenues against NAFLD.

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FABP4 Dynamics in Obesity: Discrepancies in Adipose Tissue and Liver Expression Regarding Circulating Plasma Levels

Cited by 69 publications

References 43 publications

EPA prevents fat mass expansion and metabolic disturbances in mice fed with a Western diet

EPA prevents fat mass expansion and metabolic disturbances in mice fed with a Western diet

Differential Protein Expression in White Adipose Tissue from Obesity-Prone and Obesity-Resistant Mice in Response to High Fat Diet and Anti-Obesity Herbal Medicines

Molecular mechanisms of fatty liver in obesity

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