Fatty acid flux in adipocytes: The in's and out's of fat cell lipid trafficking

Thompson, Brian R.; Lobo, Sandra; Bernlohr, David A.

doi:10.1016/j.mce.2009.08.015

Cited by 97 publications

(76 citation statements)

References 121 publications

(126 reference statements)

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“…Indeed, unilammelar phosphatidylcholine (PC) membrane vesicle studies support this fl ip-fl op mechanism for nonionized long-chain fatty acid transport ( 36 ), and the addition of free long-chain fatty acids to these vesicles resulted in a very rapid fl ip-fl op of the fatty acids ( 36,37 ).…”

Section: Fatty Acid Oxidation Accumulation and Remodelingmentioning

confidence: 97%

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Saini-Chohan

Mitchell

Vaz

et al. 2012

Journal of Lipid Research

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Section: Fatty Acid Oxidation Accumulation and Remodelingmentioning

confidence: 97%

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Saini-Chohan

Mitchell

Vaz

et al. 2012

Journal of Lipid Research

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“…Some of these FFAs are shunted to the liver and stored in lipid droplets, while some of them are oxidized in other organs. However, many of them are locally re-esterified in adipocytes (29)(30)(31). Those FFAs that escape reesterification play a critical role in several organs as a primary energy source during prolonged fasting (32).…”

Section: Macrophages Major Constituents Of At and Mediators Of Remodmentioning

confidence: 99%

Adipose tissue remodeling and obesity

Sun¹,

Kusminski²,

Scherer³

2011

J. Clin. Invest.

1,585

1,381

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To fulfill its role as the major energy-storing tissue, adipose has several unique properties that cannot be seen in any other organ, including an almost unlimited capacity to expand in a non-transformed state. As such, the tissue requires potent mechanisms to remodel, acutely and chronically. Adipocytes can rapidly reach the diffusional limit of oxygen during growth; hypoxia is therefore an early determinant that limits healthy expansion. Proper expansion requires a highly coordinated response among many different cell types, including endothelial precursor cells, immune cells, and preadipocytes. There are therefore remarkable similarities between adipose expansion and growth of solid tumors, a phenomenon that presents both an opportunity and a challenge, since pharmacological interventions supporting healthy adipose tissue adaptation can also facilitate tumor growth. IntroductionAdipose tissue (AT) can respond rapidly and dynamically to alterations in nutrient deprivation and excess through adipocyte hypertrophy and hyperplasia, thereby fulfilling its major role in wholebody energy homeostasis. AT remodeling is an ongoing process that is pathologically accelerated in the obese state, and thus, features such as reduced angiogenic remodeling, ECM overproduction, a heightened state of immune cell infiltration and subsequent proinflammatory responses prevail in many obese fat-pads (1). However, not all AT expansion is necessarily associated with pathological changes. The concept of the "metabolically healthy obese" state (2) suggests that some individuals can preserve systemic insulin sensitivity on the basis of "healthy" AT expansion, bypassing all of the aforementioned pathological consequences associated with obesity (3), thereby also avoiding the obesity-associated lipotoxic side effects. Many physiologically relevant processes important for human AT remodeling can be studied in rodent models, with the added advantage that processes related to AT expansion and reduction can occur at an extremely rapid rate. A 24-hour fast in a mouse is associated with a dramatic loss of AT mass and an acute remodeling process that involves rapid infiltration of macrophages; moreover, merely 24 to 48 hours of exposure to a high-fat diet (HFD) can cause a prompt increase in adipocyte size (4). AT is therefore an ideal model system to study rapid alterations in tissue expansion and reduction, as it adapts to a differential nutrient supply. Here, we will focus on key aspects of the intricate dynamics of AT remodeling and subsequent inflammatory consequences that arise from obesity.

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“…It was taken into consideration that FFA rapidly diffused through the phospholipids bilayer in high concentrations. However, the protein-mediated FA transport system produces a marked effect at low substrate concentrations (Chabowski et al, 2006;Thompson et al, 2010). The specific role of each protein within this system is still unclear.…”

Section: Discussionmentioning

confidence: 99%

Changes in fat metabolism of black-bone chickens during early stages of infection with Newcastle disease virus

Chao

Yang

et al. 2012

Animal

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Experiments were conducted to determine the effects of Newcastle disease on chicken fat metabolism. Thirty black-bone chickens were infected intraocularly with the Newcastle disease virus (NDV). Six birds were killed at 0, 12, 24, 48 and 72 h post infection, respectively. Results showed that the NDV infection decreased concentration of high-density lipoprotein cholesterol and increased concentrations of total cholesterol and low-density lipoprotein cholesterol in the plasma. Concentrations of triglycerides and free fatty acid were decreased after their initial increase. NDV infection also dramatically raised the activities of lipoprotein lipase (LPL), hepatic lipase and lipases in the serum. Furthermore, PCR results showed that the incipient infection up-regulated mRNA expression of LPL, adipose triglyceride lipase and nuclear factor peroxisome proliferator-activated receptor alpha (PPARα), but down-regulated them at later stage. Similarly, mRNA expression of fatty acid synthase, acetyl-CoA carboxylase and nuclear factor PPARγ, fatty acid transport protein 1 (FATP1), and 4(FATP4) decreased, whereas fatty acid translocase and fatty acid-binding protein increased initially. Data from Western blotting analysis showed that the changes in protein levels were consistent with mRNA expression. These results indicated that fat metabolism of the chicken was affected by the NDV infection. At the beginning of NDV infection, lipogenesis was inhibited, whereas lipolysis was strengthened. After lipolysis was strengthened, fat metabolism was found to be maximally depressed.

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Fatty acid flux in adipocytes: The in's and out's of fat cell lipid trafficking

Cited by 97 publications

References 121 publications

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Delineating the role of alterations in lipid metabolism to the pathogenesis of inherited skeletal and cardiac muscle disorders

Adipose tissue remodeling and obesity

Changes in fat metabolism of black-bone chickens during early stages of infection with Newcastle disease virus

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