Regulation of lipoprotein lipase mRNA content in 3T3-L1 cells by tumour necrosis factor

Cornelius, Peter; Enerbäck, Sven; Bjursell, Gunnar; Olivecrona, Thomas; Pekala, Phillip H.

doi:10.1042/bj2490765

Cited by 115 publications

(51 citation statements)

References 33 publications

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“…Because TNF-␣ has been previously implicated in the regulation of adipogenesis, insulin resistance, and leptin production, 10,20,21,24,25,33 we sequenced the TNF-␣ gene in SHR and SHR.1N. A total of 26 sequence differences in the TNF-␣ gene were identified between SHR and SHR.1N ( Figure 6).…”

Section: Sequence Analysis Of the Tnf-␣ Gene In Shr And Shr1nmentioning

confidence: 99%

Segment of Rat Chromosome 20 Regulates Diet-Induced Augmentations in Adiposity, Glucose Intolerance, and Blood Pressure

et al. 2003

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Abstract-Previous linkage and association studies have suggested that a region of human chromosome 6 containing the tumor necrosis factor (TNF)-␣ gene is involved in the pathogenesis of obesity and obesity-associated hypertension. The aim of the present investigation was to establish whether a segment of rat chromosome 20 (RNO20), which also contains the TNF-␣ gene, determines diet-induced changes in adiposity and blood pressure (BP). The results showed that a transfer of the RNO20 segment from the normotensive Brown Norway (BN) rat onto the background of the spontaneously hypertensive rat (SHR) is associated with a significantly greater increase in adiposity, glucose intolerance, circulating leptin levels, and BP during 12-week, high-fat-diet feeding. In contrast, the transfer is not associated with significant changes in these variables during 12-week, normal-diet feeding. In addition, sequencing of the TNF-␣ gene revealed differences between SHR and BN in the 5Ј-and 3Ј-regulatory regions of the gene. Subsequent analyses of TNF-␣ gene expression in fat, muscle, and liver, however, did not provide support for the functional involvement of these differences. In summary, the investigated RNO20 segment contains 1 or more gene variants that affect adiposity, glucose tolerance, serum leptin levels, and BP, but only when the animals are exposed to a particular environment, ie, high-fat-diet feeding. Further studies are needed to identify genes mediating these effects. Considering current changes in our lifestyle involving an increased calorie and fat intake, we believe that gene-environment interactions, such as those described here, play an important role in the current epidemic of obesity and obesityassociated hypertension.

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Section: Sequence Analysis Of the Tnf-␣ Gene In Shr And Shr1nmentioning

confidence: 99%

Segment of Rat Chromosome 20 Regulates Diet-Induced Augmentations in Adiposity, Glucose Intolerance, and Blood Pressure

et al. 2003

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“…Thus, TNF-␣ strongly inhibits adipose conversion and even causes a dramatic dedifferentiation of adipocytes in culture (3)(4)(5)(6). Moreover, it is also documented that TNF-␣ decreases the synthesis and activity of several proteins essential for lipogenesis and triglyceride accumulation in adipocytes.…”

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confidence: 99%

“…Moreover, it is also documented that TNF-␣ decreases the synthesis and activity of several proteins essential for lipogenesis and triglyceride accumulation in adipocytes. These include lipoprotein lipase (5,(7)(8)(9), acetyl-coenzyme A carboxylase (4,10,11), acyl-coenzyme A synthetase (12), stearoyl-coenzyme A desaturase (12), and the insulin-sensitive glucose transporter GLUT4 (13,14).…”

mentioning

confidence: 99%

Differential Regulation by Tumor Necrosis Factor-α of β1-, β2-, and β3-Adrenoreceptor Gene Expression in 3T3-F442A Adipocytes

Hadri

Courtalon

Gauthereau

et al. 1997

Journal of Biological Chemistry

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Modulation of ␤-adrenoreceptor expression by tumor necrosis factor-␣ (TNF-␣) was investigated in murine 3T3-F442A adipocytes. TNF-␣ treatment of mature adipocytes decreased ␤ 3 -adrenoreceptor mRNA content in a time-and concentration-dependent manner, with a 8.5-fold decrease observed after a 6-h exposure to 300 pM TNF-␣. ␤ 1 -Adrenoreceptor mRNA abundance was slightly decreased by TNF-␣ treatment, while ␤ 2 -adrenoreceptor mRNA levels were potently induced (6-fold increase at 6 h). (؊)-[ 125 I]Iodocyanopindolol saturation and competition binding experiments indicated that TNF-␣ induced a 2-fold decrease in ␤ 3 -adrenoreceptor number, a nonsignificant reduction in ␤ 1 -subtype population, and a ϳ4.5-fold increase in ␤ 2 -adrenoreceptor density. This correlated with a lower EC 50 value measured for epinephrine in stimulating adenylyl cyclase, whereas the EC 50 value for norepinephrine increased. Nuclear run-on assays on isolated nuclei and mRNA stability measurements showed that TNF-␣ increased both ␤ 2 -adrenoreceptor gene transcription and ␤ 2 -adrenoreceptor mRNA half-life, while ␤ 1 -and ␤ 3 -adrenoreceptor gene expression was modulated only at the transcriptional level by the cytokine. These findings demonstrate a differential modulation by TNF-␣ of the three ␤-adrenoreceptor subtypes in adipocytes, which may contribute to metabolic disorders induced by the cytokine in the adipocyte.Tumor necrosis factor-␣ (TNF-␣) 1 is a multifunctional cytokine that was originally identified as a tumoricidal protein (1). Subsequent investigations have shown that TNF-␣ was fundamentally involved in control of the growth, differentiation, and metabolism in several normal cells and tissues.A sum of work has been focused on the role of TNF-␣ in the regulation of adipocyte development and metabolism (1, 2). Thus, TNF-␣ strongly inhibits adipose conversion and even causes a dramatic dedifferentiation of adipocytes in culture (3-6). Moreover, it is also documented that TNF-␣ decreases the synthesis and activity of several proteins essential for lipogenesis and triglyceride accumulation in adipocytes. These include lipoprotein lipase (5, 7-9), acetyl-coenzyme A carboxylase (4, 10, 11), acyl-coenzyme A synthetase (12), stearoyl-coenzyme A desaturase (12), and the insulin-sensitive glucose transporter GLUT4 (13,14).In addition to the above effects on adipogenesis and reduction of de novo fatty acid synthesis, TNF-␣ also depletes triglycerides from adipocytes by directly increasing lipolysis (15-17). So far, the molecular mechanism by which the cytokine potentiates lipolysis remains unclear (17).Through activation of three ␤-AR subtypes, catecholamines exert a key role in the regulation of lipid metabolism in adipocytes. They modulate cAMP-dependent processes such as lipolysis and the genetic control of the lipogenic and thermogenic pathways. As regards the pleiotropic effects of TNF-␣ on several metabolic pathways in adipocytes, and to the key role of the ␤-AR system in lipid mobilization, it is possible that an interplay between TNF...

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“…Treatment of preadipocytes with TNFα inhibits adipogenic conversion [71,81] and treatment of adipocytes results in what has been termed "dedifferentiation" [70,71,75]. Exposure of adipocytes to TNF α has long been known to promote adipocyte lipolysis [66,70]; this can be partly attributed to TNFα-mediated inhibition of LPL activity, which was first noted two decades ago [1,8,51]. The dedifferentiated phenotype that results from TNFα treatment has been ascribed, at least in part, to the TNFα-mediated transcriptional downregulation of the master adipocyte transcription factor PPARγ and thus the subsequent loss of PPARγ-mediated transactivation of select adipocyte genes [81].…”

Section: Adhfe1 Transcript Expression In 3t3-l1 Adipocytes Is Refractmentioning

confidence: 99%

Differentiation-dependent expression of Adhfe1 in adipogenesis

Kim¹,

Tillison²,

Zhou³

et al. 2007

Archives of Biochemistry and Biophysics

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We have determined that adipocytes are a major site of expression of the transcript for the novel alcohol dehydrogenase (ADH), Adhfe1. Adhfe1 is unique in that the sequence of its encoded protein places it among the iron-activated ADHs. Western blot analysis reveals Adhfe1 encodes a 50 kDa cytoplasmic protein and immunocytochemical staining indicates mitochondrial localization. Adhfe1 transcript exhibits differentiation-dependent expression during in vitro brown and white adipogenesis. Unlike many adipocyte-enriched genes, however, Adhfe1 transcript expression in adipocytes is refractory to TNFα-mediated downregulation. However, use of pharmacological inhibitors reveals PI 3-kinase-mediated signals maintain the basal level of Adhfe1 transcript in 3T3-L1 adipocytes. Tissue profiling studies show Adhfe1 transcript is restricted to white and brown adipose tissues, liver, and kidney. In comparison to C57BL/6 mice, Adhfe1 transcript is downregulated 40% in white adipose tissue of ob/ob obese mice. Further characterization of Adhfe1 should yield new insights into adipocyte function and energy metabolism.

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Regulation of lipoprotein lipase mRNA content in 3T3-L1 cells by tumour necrosis factor

Cited by 115 publications

References 33 publications

Segment of Rat Chromosome 20 Regulates Diet-Induced Augmentations in Adiposity, Glucose Intolerance, and Blood Pressure

Segment of Rat Chromosome 20 Regulates Diet-Induced Augmentations in Adiposity, Glucose Intolerance, and Blood Pressure

Differential Regulation by Tumor Necrosis Factor-α of β1-, β2-, and β3-Adrenoreceptor Gene Expression in 3T3-F442A Adipocytes

Differentiation-dependent expression of Adhfe1 in adipogenesis

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