-
1
-
-
0012473279
-
The nuclear receptor superfamily: The second decade
-
Mangelsdorf DJ, Thummel C, Beato M, Herrlich P, Schutz G, Umesono K, Kastner P, Mark M, Chambon P, Evans RM. The nuclear receptor superfamily: the second decade. Cell. 83:1995;835-839.
-
(1995)
Cell
, vol.83
, pp. 835-839
-
-
Mangelsdorf, D.J.1
Thummel, C.2
Beato, M.3
Herrlich, P.4
Schutz, G.5
Umesono, K.6
Kastner, P.7
Mark, M.8
Chambon, P.9
Evans, R.M.10
-
2
-
-
0031898610
-
PPAR-γ: Adipogenic regulator and thiazolidinedione receptor
-
Spiegelman BM. PPAR-γ: adipogenic regulator and thiazolidinedione receptor. Diabetes. 47:1998;507-514.
-
(1998)
Diabetes
, vol.47
, pp. 507-514
-
-
Spiegelman, B.M.1
-
3
-
-
0031197036
-
Peroxisome proliferator-activated receptor agonists
-
Willson TM, Wahli W. Peroxisome proliferator-activated receptor agonists. Curr Opin Chem Biol. 1:1997;235-241.
-
(1997)
Curr Opin Chem Biol
, vol.1
, pp. 235-241
-
-
Willson, T.M.1
Wahli, W.2
-
4
-
-
15444347751
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Pioglitazone induces in vivo adipocyte differentiation in the obese Zucker fa/fa rat
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of special interest. Treatment of obese Zucker fatty rats with pioglitazone for two weeks induces a marked increase in the number of small adipocytes in the retroperitoneal fat pad accompanied by increases in expression of the GLUT4 gene and decreases in the expression of the ob gene. This study together with that of Okuno [5] indicate that TZDs have effects on adipocyte differentiation in vivo and that adipocyte differentiation can increase glucose disposal.
-
Hallakou S, Doare L, Foufelle F, Kergoat M, Guerre-Millo M, Berthault M-F, Dugail I, Morin J, Auwerx J, Ferre P. Pioglitazone induces in vivo adipocyte differentiation in the obese Zucker fa/fa rat. of special interest Diabetes. 46:1997;1393-1399 Treatment of obese Zucker fatty rats with pioglitazone for two weeks induces a marked increase in the number of small adipocytes in the retroperitoneal fat pad accompanied by increases in expression of the GLUT4 gene and decreases in the expression of the ob gene. This study together with that of Okuno [5] indicate that TZDs have effects on adipocyte differentiation in vivo and that adipocyte differentiation can increase glucose disposal.
-
(1997)
Diabetes
, vol.46
, pp. 1393-1399
-
-
Hallakou, S.1
Doare, L.2
Foufelle, F.3
Kergoat, M.4
Guerre-Millo, M.5
Berthault, M.-F.6
Dugail, I.7
Morin, J.8
Auwerx, J.9
Ferre, P.10
-
5
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0032520921
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Troglitazone increases the number of small adipocytes without the change of white adipose tissue mass in obese Zucker rats
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of special interest. Treatment of obese Zucker fatty rats with troglitazone for 15 days results in a four-fold increase in the number of small adipocytes in both retroperitoneal and subcutaneous adipose tissue with concomitant decreases in the number of large adipocytes via apoptosis. Troglitazone also normalizes the elevated expression levels of TNFα and leptin. Thus, TZD-induced adipocyte differentiation in vivo most likely contributes to the beneficial effects of these drugs on glucose utilization.
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Okuno A, Tamemoto H, Tobe K, Ueki K, Mori Y, Iwamoto K, Umesono K, Akanuma Y, Fujiwara T, Horikoshi H, et al. Troglitazone increases the number of small adipocytes without the change of white adipose tissue mass in obese Zucker rats. of special interest J Clin Invest. 101:1998;1354-1361 Treatment of obese Zucker fatty rats with troglitazone for 15 days results in a four-fold increase in the number of small adipocytes in both retroperitoneal and subcutaneous adipose tissue with concomitant decreases in the number of large adipocytes via apoptosis. Troglitazone also normalizes the elevated expression levels of TNFα and leptin. Thus, TZD-induced adipocyte differentiation in vivo most likely contributes to the beneficial effects of these drugs on glucose utilization.
-
(1998)
J Clin Invest
, vol.101
, pp. 1354-1361
-
-
Okuno, A.1
Tamemoto, H.2
Tobe, K.3
Ueki, K.4
Mori, Y.5
Iwamoto, K.6
Umesono, K.7
Akanuma, Y.8
Fujiwara, T.9
Horikoshi, H.10
-
6
-
-
0028587742
-
Tumor necrosis factor α: A key component of the obesity-diabetes link
-
Hotamisligil GS, Spiegelman BM. Tumor necrosis factor α: a key component of the obesity-diabetes link. Diabetes. 43:1994;1271-1278.
-
(1994)
Diabetes
, vol.43
, pp. 1271-1278
-
-
Hotamisligil, G.S.1
Spiegelman, B.M.2
-
7
-
-
0030885575
-
Thiazolidinediones block tumor necrosis factor-α-induced inhibition of insulin signaling
-
Peraldi P, Xu M, Spiegelman BM. Thiazolidinediones block tumor necrosis factor-α-induced inhibition of insulin signaling. J Clin Invest. 100:1997;1863-1869.
-
(1997)
J Clin Invest
, vol.100
, pp. 1863-1869
-
-
Peraldi, P.1
Xu, M.2
Spiegelman, B.M.3
-
8
-
-
0030661983
-
TNF-α-induced insulin resistance in vivo and its prevention with troglitazone
-
Miles PDG, Romeo OM, Higo K, Cohen A, Rafaat K, Olefsky JM. TNF-α-induced insulin resistance in vivo and its prevention with troglitazone. Diabetes. 46:1997;1678-1683.
-
(1997)
Diabetes
, vol.46
, pp. 1678-1683
-
-
Miles, P.D.G.1
Romeo, O.M.2
Higo, K.3
Cohen, A.4
Rafaat, K.5
Olefsky, J.M.6
-
9
-
-
0029860791
-
Modulation of insulin activities by leptin
-
Cohen B, Novick D, Rubinstein M. Modulation of insulin activities by leptin. Science. 274:1996;1151-1152.
-
(1996)
Science
, vol.274
, pp. 1151-1152
-
-
Cohen, B.1
Novick, D.2
Rubinstein, M.3
-
10
-
-
0040381066
-
Leptin impairs metabolic actions of insulin in isolated rat adipocytes
-
Muller G, Ertl J, Gerl M, Preibisch G. Leptin impairs metabolic actions of insulin in isolated rat adipocytes. J Biol Chem. 272:1997;10585-10593.
-
(1997)
J Biol Chem
, vol.272
, pp. 10585-10593
-
-
Muller, G.1
Ertl, J.2
Gerl, M.3
Preibisch, G.4
-
11
-
-
0030582447
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Induction of uncoupling protein in brown adipose tissue: Synergy between norepinephrine and pioglitazone, an insulin-sensitizing agent
-
Foellmi-Adams LA, Wyse BM, Herron D, Nedergaard J, Kletzien RF. Induction of uncoupling protein in brown adipose tissue: synergy between norepinephrine and pioglitazone, an insulin-sensitizing agent. Biochem Pharm. 52:1996;693-701.
-
(1996)
Biochem Pharm
, vol.52
, pp. 693-701
-
-
Foellmi-Adams, L.A.1
Wyse, B.M.2
Herron, D.3
Nedergaard, J.4
Kletzien, R.F.5
-
12
-
-
10544229796
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Activation of the nuclear receptor PPARγ promotes brown adipocyte differentiation
-
Tai T-A, Jennermann C, Brown KK, Oliver BB, MacGinnitie MA, Wilkison WO, Brown HR, Lehmann JM, Kliewer SA, Morris DC, Graves RA. Activation of the nuclear receptor PPARγ promotes brown adipocyte differentiation. J Biol Chem. 271:1996;29909-29914.
-
(1996)
J Biol Chem
, vol.271
, pp. 29909-29914
-
-
Tai, T.-A.1
Jennermann, C.2
Brown, K.K.3
Oliver, B.B.4
MacGinnitie, M.A.5
Wilkison, W.O.6
Brown, H.R.7
Lehmann, J.M.8
Kliewer, S.A.9
Morris, D.C.10
Graves, R.A.11
-
13
-
-
0031985802
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Thiazolidinedione exposure increases the expression of uncoupling protein 1 in cultured human preadipocytes
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of special interest. Treatment of human adipocytes isolated from omental, subcutaneous, and perirenal fat pads with rosiglitazone results in increased expression levels of the brown adipocyte marker UCP1. UCP1 protein was detected by confocal microscopy in rosiglitazone-treated perirenal preadipocytes. Thus, TZDs can induce the expression of a BAT-specific gene involved in energy consumption in human adipose tissue.
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Digby JE, Montague CT, Sewter CP, Sanders L, Wilkison WO, O'Rahilly S, Prins JB. Thiazolidinedione exposure increases the expression of uncoupling protein 1 in cultured human preadipocytes. of special interest Diabetes. 47:1998;138-141 Treatment of human adipocytes isolated from omental, subcutaneous, and perirenal fat pads with rosiglitazone results in increased expression levels of the brown adipocyte marker UCP1. UCP1 protein was detected by confocal microscopy in rosiglitazone-treated perirenal preadipocytes. Thus, TZDs can induce the expression of a BAT-specific gene involved in energy consumption in human adipose tissue.
-
(1998)
Diabetes
, vol.47
, pp. 138-141
-
-
Digby, J.E.1
Montague, C.T.2
Sewter, C.P.3
Sanders, L.4
Wilkison, W.O.5
O'Rahilly, S.6
Prins, J.B.7
-
14
-
-
0029941669
-
Differentiation dependent expression of the brown adipocyte uncoupling protein gene: Regulation by peroxisome proliferator-activated receptor γ
-
Sears IB, MacGinnitie MA, Kovacs LG, Graves RA. Differentiation dependent expression of the brown adipocyte uncoupling protein gene: regulation by peroxisome proliferator-activated receptor γ Mol Cell Biol. 16:1996;3410-3419.
-
(1996)
Mol Cell Biol
, vol.16
, pp. 3410-3419
-
-
Sears, I.B.1
MacGinnitie, M.A.2
Kovacs, L.G.3
Graves, R.A.4
-
15
-
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0030341454
-
Cloning and identification of mouse steroid receptor coactivator-1 (mSRC-1) as a coactivator of peroxisome proliferator-activated receptor γ
-
Zhu Y, Calandra C, Rao MS, Reddy J. Cloning and identification of mouse steroid receptor coactivator-1 (mSRC-1) as a coactivator of peroxisome proliferator-activated receptor γ Gene Expression. 6:1996;185-195.
-
(1996)
Gene Expression
, vol.6
, pp. 185-195
-
-
Zhu, Y.1
Calandra, C.2
Rao, M.S.3
Reddy, J.4
-
16
-
-
0031558788
-
The antidiabetic agent thiazolidinedione stimulates the interaction between PPARγ and CBP
-
Mizukami J, Taniguchi T. The antidiabetic agent thiazolidinedione stimulates the interaction between PPARγ and CBP. Biochem Biophys Res Commun. 240:1997;61-64.
-
(1997)
Biochem Biophys Res Commun
, vol.240
, pp. 61-64
-
-
Mizukami, J.1
Taniguchi, T.2
-
17
-
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0030771856
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Isolation and characterization of PBP, a protein that interacts with peroxisome proliferator-activated receptor
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Zhu Y, Qi C, Jain S, Rao MS, Reddy JK. Isolation and characterization of PBP, a protein that interacts with peroxisome proliferator-activated receptor. J Biol Chem. 272:1997;25500-25506.
-
(1997)
J Biol Chem
, vol.272
, pp. 25500-25506
-
-
Zhu, Y.1
Qi, C.2
Jain, S.3
Rao, M.S.4
Reddy, J.K.5
-
18
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0032549811
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A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis
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of outstanding interest. PGC-1 is identified as a PPARγ-interacting protein that is expressed in BAT but not WAT. PGC-1 expression levels are increased dramatically in BAT animals exposed to cold, a stimulus known to induce BAT-mediated thermogenesis. PGC-1 significantly increases the transcriptional activity of PPARγ on the UCP1 gene promoter and ectopic expression of PPARγ in white adipose cells results in changes in the expression of genes involved in adaptive thermogenesis. This study implicates PGC-1 as a key regulator of BAT-mediated thermogenesis.
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Puigserver P, Wu Z, Park CW, Graves R, Wright M, Spiegelman BM. A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis. of outstanding interest Cell. 92:1998;829-839 PGC-1 is identified as a PPARγ-interacting protein that is expressed in BAT but not WAT. PGC-1 expression levels are increased dramatically in BAT animals exposed to cold, a stimulus known to induce BAT-mediated thermogenesis. PGC-1 significantly increases the transcriptional activity of PPARγ on the UCP1 gene promoter and ectopic expression of PPARγ in white adipose cells results in changes in the expression of genes involved in adaptive thermogenesis. This study implicates PGC-1 as a key regulator of BAT-mediated thermogenesis.
-
(1998)
Cell
, vol.92
, pp. 829-839
-
-
Puigserver, P.1
Wu, Z.2
Park, C.W.3
Graves, R.4
Wright, M.5
Spiegelman, B.M.6
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19
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0031441286
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Troglitazone action is independent of adipose tissue
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of outstanding interest. Troglitazone treatment reduces elevated glucose, insulin, and lipid levels and normalizes glucose tolerance in aP2/DTA mice whose adipose tissue was selectively ablated through fat-specific expression of diptheria toxin A chain. This study provides strong evidence that activation of PPARγ in tissues other than adipose is important for the actions of TZDs. Interestingly, marked increases are seen in hepatic triglyceride and glycogen content and PPARγ expression levels are significantly increased in the livers of a P2/DTA mice, suggesting a compensatory role for the liver in the maintenance of energy homeostasis in animals lacking fat.
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Burant CF, Sreenan S, Hirano K-i, Tai-T-AC, Lohmiller J, Lukens J, Davidson NO, Ross S, Graves RA. Troglitazone action is independent of adipose tissue. of outstanding interest J Clin Invest. 100:1997;2900-2908 Troglitazone treatment reduces elevated glucose, insulin, and lipid levels and normalizes glucose tolerance in aP2/DTA mice whose adipose tissue was selectively ablated through fat-specific expression of diptheria toxin A chain. This study provides strong evidence that activation of PPARγ in tissues other than adipose is important for the actions of TZDs. Interestingly, marked increases are seen in hepatic triglyceride and glycogen content and PPARγ expression levels are significantly increased in the livers of a P2/DTA mice, suggesting a compensatory role for the liver in the maintenance of energy homeostasis in animals lacking fat.
-
(1997)
J Clin Invest
, vol.100
, pp. 2900-2908
-
-
Burant, C.F.1
Sreenan, S.2
Hirano, K.-I.3
Tai, -T-A.C.4
Lohmiller, J.5
Lukens, J.6
Davidson, N.O.7
Ross, S.8
Graves, R.A.9
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20
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0030000088
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Regulation of PPARγ gene expression by nutrition and obesity in rodents
-
Vidal-Puig A, Jimenez-Linan M, Lowell BB, Hamann A, Hu E, Spiegelman B, Flier JS, Moller DE. Regulation of PPARγ gene expression by nutrition and obesity in rodents. J Clin Invest. 97:1996;2553-2561.
-
(1996)
J Clin Invest
, vol.97
, pp. 2553-2561
-
-
Vidal-Puig, A.1
Jimenez-Linan, M.2
Lowell, B.B.3
Hamann, A.4
Hu, E.5
Spiegelman, B.6
Flier, J.S.7
Moller, D.E.8
-
21
-
-
0030977450
-
Peroxisome proliferator-activated receptor gene expression in human tissues: Effects of obesity, weight loss, and regulation by insulin and glucocorticoids
-
Vidal-Puig AJ, Considine RV, Jimenez-Linan M, Werman A, Pories WJ, Caro JF, Flier JS. Peroxisome proliferator-activated receptor gene expression in human tissues: effects of obesity, weight loss, and regulation by insulin and glucocorticoids. J Clin Invest. 99:1997;2416-2422.
-
(1997)
J Clin Invest
, vol.99
, pp. 2416-2422
-
-
Vidal-Puig, A.J.1
Considine, R.V.2
Jimenez-Linan, M.3
Werman, A.4
Pories, W.J.5
Caro, J.F.6
Flier, J.S.7
-
22
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0030951143
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Identification, characterization, and tissue distribution of human peroxisome proliferator-activated receptor (PPAR) isoforms PPARγ2 versus PPARγ1 and activation with retinoid X receptor agaonists and antagonists
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Mukherjee R, Jow L, Croston GE, Paterniti JR Jr. Identification, characterization, and tissue distribution of human peroxisome proliferator-activated receptor (PPAR) isoforms PPARγ2 versus PPARγ1 and activation with retinoid X receptor agaonists and antagonists. J Biol Chem. 272:1997;8071-8076.
-
(1997)
J Biol Chem
, vol.272
, pp. 8071-8076
-
-
Mukherjee, R.1
Jow, L.2
Croston, G.E.3
Paterniti J.R., Jr.4
-
23
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-
0032006547
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Skeletal muscle peroxisome proliferator-activated receptor-γ expression in obesity and non-insulin-dependent diabetes mellitus
-
Kruszynska YT, Mukherjee R, Jow L, Dana S, Paterniti JR Jr, Olefsky JM. Skeletal muscle peroxisome proliferator-activated receptor-γ expression in obesity and non-insulin-dependent diabetes mellitus. J Clin Invest. 101:1998;543-548.
-
(1998)
J Clin Invest
, vol.101
, pp. 543-548
-
-
Kruszynska, Y.T.1
Mukherjee, R.2
Jow, L.3
Dana, S.4
Paterniti J.R., Jr.5
Olefsky, J.M.6
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24
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0004473133
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PPAR-γ gene expression is elevated in skeletal muscle of obese and type II diabetic subjects
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Park KS, Ciaraldi TP, Abrams-Carter L, Mudaliar S, Nikoulina SE, Henry RR. PPAR-γ gene expression is elevated in skeletal muscle of obese and type II diabetic subjects. Diabetes. 46:1997;1230-1234.
-
(1997)
Diabetes
, vol.46
, pp. 1230-1234
-
-
Park, K.S.1
Ciaraldi, T.P.2
Abrams-Carter, L.3
Mudaliar, S.4
Nikoulina, S.E.5
Henry, R.R.6
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25
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0030747895
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Tissue distribution and quantification of the expression of mRNAs of peroxisome proliferator-activated receptors and liver X receptor-α in humans: No alteration in adipose tissue of obese and NIDDM patients
-
Auboeuf D, Rieusset J, Fajas L, Vallier P, Frering V, Riou JP, Staels B, Auwerx J, Laville M, Vidal H. Tissue distribution and quantification of the expression of mRNAs of peroxisome proliferator-activated receptors and liver X receptor-α in humans: no alteration in adipose tissue of obese and NIDDM patients. Diabetes. 46:1997;1319-1327.
-
(1997)
Diabetes
, vol.46
, pp. 1319-1327
-
-
Auboeuf, D.1
Rieusset, J.2
Fajas, L.3
Vallier, P.4
Frering, V.5
Riou, J.P.6
Staels, B.7
Auwerx, J.8
Laville, M.9
Vidal, H.10
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26
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0031019249
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Uncoupling protein-2: A novel gene linked to obesity and hyperinsulinemia
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Fleury C, Neverova M, Collins S, Raimbault S, Champigny O, Levi-Meyruis C, Bouillard F, Seldin MF, Surwit RS, Ricquier D, Warden CH. Uncoupling protein-2: a novel gene linked to obesity and hyperinsulinemia. Nat Genet. 15:1997;269-272.
-
(1997)
Nat Genet
, vol.15
, pp. 269-272
-
-
Fleury, C.1
Neverova, M.2
Collins, S.3
Raimbault, S.4
Champigny, O.5
Levi-Meyruis, C.6
Bouillard, F.7
Seldin, M.F.8
Surwit, R.S.9
Ricquier, D.10
Warden, C.H.11
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27
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0031577549
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Up-regulation of UCP-2 gene expression by PPAR agonists in preadipose and adipose cells
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of special interest. Rosiglitazone treatment of differentiated Ob1771 adipocytes resulted in significant increases in UCP2 gene expression. These data together with those of Camirand [28] suggest that PPARγ regulates energy dissipation through the enhancement of thermogenesis.
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Aubert J, Champigny O, Saint-Marc P, Negrel R, Collins S, Ricquier D, Ailhaud G. Up-regulation of UCP-2 gene expression by PPAR agonists in preadipose and adipose cells. of special interest Biochem Biophys Res Commun. 238:1997;606-611 Rosiglitazone treatment of differentiated Ob1771 adipocytes resulted in significant increases in UCP2 gene expression. These data together with those of Camirand [28] suggest that PPARγ regulates energy dissipation through the enhancement of thermogenesis.
-
(1997)
Biochem Biophys Res Commun
, vol.238
, pp. 606-611
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Aubert, J.1
Champigny, O.2
Saint-Marc, P.3
Negrel, R.4
Collins, S.5
Ricquier, D.6
Ailhaud, G.7
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28
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85011477288
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Thiazolidinediones stimulate uncoupling protein-2 expression in cell lines representing white and brown adipose tissues and skeletal muscle
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of special interest. Treatment of cell lines derived from WAT (3T3-L1 and 3T3-F442A), BAT (HIB-1B), and muscle (L6) with the TZD darglitazone resulted in 5 to 10-fold increases in the expression levels of UCP2, indicating a role for PPARγ in the regulation of this gene.
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Camirand A, Marie V, Rabelo R, Silva JE. Thiazolidinediones stimulate uncoupling protein-2 expression in cell lines representing white and brown adipose tissues and skeletal muscle. of special interest Endocrinology. 139:1998;428-431 Treatment of cell lines derived from WAT (3T3-L1 and 3T3-F442A), BAT (HIB-1B), and muscle (L6) with the TZD darglitazone resulted in 5 to 10-fold increases in the expression levels of UCP2, indicating a role for PPARγ in the regulation of this gene.
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(1998)
Endocrinology
, vol.139
, pp. 428-431
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Camirand, A.1
Marie, V.2
Rabelo, R.3
Silva, J.E.4
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29
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0030612740
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PPARγ-induces cell cycle withdrawal: Inhibition of E2F/DP DNA-binding activity via down-regulation of PP2A
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of outstanding interest. Pioglitazone treatment of either HIB-1B cells that endogenously express PPARγ or NIH-3T3 cells in which PPARγ was ectopically expressed results in growth arrest. Under the same conditions, NIH-3T3 cells lacking PPARγ or expressing PPARγ proteins mutated in either the DNA or ligand-binding domains failed to arrest growth. Cell-cycle withdrawal was traced to decreased levels of the PP2A phosphatase with concomitant reductions in the DNA-binding activity of E2F/DP transcription complexes, known regulators of cell-cycle progression. This study indicates that PPARγ regulates cell-cycle withdrawal via a novel mechanism.
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Altiok S, Xu M, Spiegelman BM. PPARγ-induces cell cycle withdrawal: inhibition of E2F/DP DNA-binding activity via down-regulation of PP2A. of outstanding interest Genes Dev. 11:1997;1987-1998 Pioglitazone treatment of either HIB-1B cells that endogenously express PPARγ or NIH-3T3 cells in which PPARγ was ectopically expressed results in growth arrest. Under the same conditions, NIH-3T3 cells lacking PPARγ or expressing PPARγ proteins mutated in either the DNA or ligand-binding domains failed to arrest growth. Cell-cycle withdrawal was traced to decreased levels of the PP2A phosphatase with concomitant reductions in the DNA-binding activity of E2F/DP transcription complexes, known regulators of cell-cycle progression. This study indicates that PPARγ regulates cell-cycle withdrawal via a novel mechanism.
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(1997)
Genes Dev
, vol.11
, pp. 1987-1998
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Altiok, S.1
Xu, M.2
Spiegelman, B.M.3
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30
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12644265334
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Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor γ and the retinoid X receptor
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of special interest. PPARγ is expressed at high levels in the major histologic types of human liposarcoma. Primary human liposarcoma cells were induced to differentiate and withdraw from the cell-cycle upon treatment with pioglitazone as measured by expression of adipocyte-specific genes, oil red O staining, and BrdUrd labeling. Pioglitazone-induced differentiation was enhanced by co-treatment with an RXR-selective retinoid. These data provide the first evidence that PPARγ ligands might have a utility in the differentiation treatment of cancer.
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Tontonoz P, Singer S, Forman BM, Sarraf P, Fletcher JA, Fletcher CDM, Brun RP, Mueller E, Altiok S, Oppenheim H, et al. Terminal differentiation of human liposarcoma cells induced by ligands for peroxisome proliferator-activated receptor γ and the retinoid X receptor. of special interest Proc Natl Acad Sci USA. 94:1997;237-241 PPARγ is expressed at high levels in the major histologic types of human liposarcoma. Primary human liposarcoma cells were induced to differentiate and withdraw from the cell-cycle upon treatment with pioglitazone as measured by expression of adipocyte-specific genes, oil red O staining, and BrdUrd labeling. Pioglitazone-induced differentiation was enhanced by co-treatment with an RXR-selective retinoid. These data provide the first evidence that PPARγ ligands might have a utility in the differentiation treatment of cancer.
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(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 237-241
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Tontonoz, P.1
Singer, S.2
Forman, B.M.3
Sarraf, P.4
Fletcher, J.A.5
Fletcher, C.D.M.6
Brun, R.P.7
Mueller, E.8
Altiok, S.9
Oppenheim, H.10
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31
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0031993322
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Terminal differentiation of human breast cancer through PPARγ
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of special interest. PPARγ is shown by immunohistochemistry to be present in the epithelial cells lining the mammary ducts and adipose cells of normal breast and in metastatic breast adenocarcinoma cells. PPARγ is also expressed in several human breast cancer cell lines derived from either primary tumors or metastases. Treatment of these cell lines with troglitazone caused differentiation as measured by lipid accumulation, the expression of genes associated with a more differentiated and reductions in the growth rates and clonogenic capacities of the cells. These data suggest that PPARγ may have a utility in the treatment of breast cancer.
-
Mueller E, Sarraf P, Tontonoz P, Evans RM, Martin KJ, Zhang M, Fletcher C, Singer S, Spiegelman BM. Terminal differentiation of human breast cancer through PPARγ of special interest Mol Cell. 1:1998;465-470 PPARγ is shown by immunohistochemistry to be present in the epithelial cells lining the mammary ducts and adipose cells of normal breast and in metastatic breast adenocarcinoma cells. PPARγ is also expressed in several human breast cancer cell lines derived from either primary tumors or metastases. Treatment of these cell lines with troglitazone caused differentiation as measured by lipid accumulation, the expression of genes associated with a more differentiated and reductions in the growth rates and clonogenic capacities of the cells. These data suggest that PPARγ may have a utility in the treatment of breast cancer.
-
(1998)
Mol Cell
, vol.1
, pp. 465-470
-
-
Mueller, E.1
Sarraf, P.2
Tontonoz, P.3
Evans, R.M.4
Martin, K.J.5
Zhang, M.6
Fletcher, C.7
Singer, S.8
Spiegelman, B.M.9
-
32
-
-
0032006028
-
Beyond Tamoxifen - The retinoid X receptor-selective ligand LG1069 (targetin) causes complete regression of mammary carcinoma
-
Bischoff ED, Gottardis MM, Moon TE, Heyman RA, Lamph WW. Beyond Tamoxifen - the retinoid X receptor-selective ligand LG1069 (targetin) causes complete regression of mammary carcinoma. Cancer Res. 58:1998;479-484.
-
(1998)
Cancer Res
, vol.58
, pp. 479-484
-
-
Bischoff, E.D.1
Gottardis, M.M.2
Moon, T.E.3
Heyman, R.A.4
Lamph, W.W.5
-
33
-
-
0031844535
-
The nuclear eicosanoid receptor, PPARγ, is aberrantly expressed in colonic cancers
-
Dubois RN, Gupta R, Brockman J, Reddy BS, Krakow SL, Lazar MA. The nuclear eicosanoid receptor, PPARγ, is aberrantly expressed in colonic cancers. Carcinogenesis. 19:1998;49-53.
-
(1998)
Carcinogenesis
, vol.19
, pp. 49-53
-
-
Dubois, R.N.1
Gupta, R.2
Brockman, J.3
Reddy, B.S.4
Krakow, S.L.5
Lazar, M.A.6
-
34
-
-
0028321529
-
Differential expression and activation of a family of murine peroxisome proliferator-activated receptors
-
Kliewer SA, Forman BM, Blumber B, Ong ES, Borgmeyer U, Mangelsdorf DJ, Umesono K, Evans RM. Differential expression and activation of a family of murine peroxisome proliferator-activated receptors. Proc Natl Acad Sci USA. 91:1994;7355-7359.
-
(1994)
Proc Natl Acad Sci USA
, vol.91
, pp. 7355-7359
-
-
Kliewer, S.A.1
Forman, B.M.2
Blumber, B.3
Ong, E.S.4
Borgmeyer, U.5
Mangelsdorf, D.J.6
Umesono, K.7
Evans, R.M.8
-
35
-
-
0029152375
-
Isolation of the human peroxisome proliferator activated receptor γ cDNA: Expression in hematopoietic cells and chromosomal mapping
-
Greene ME, Blumberg B, McBride OW, Yi HF, Kronquist K, Kwan K, Hsieh L, Greene G, Nimer SD. Isolation of the human peroxisome proliferator activated receptor γ cDNA: expression in hematopoietic cells and chromosomal mapping. Gene Expression. 4:1995;281-299.
-
(1995)
Gene Expression
, vol.4
, pp. 281-299
-
-
Greene, M.E.1
Blumberg, B.2
McBride, O.W.3
Yi, H.F.4
Kronquist, K.5
Kwan, K.6
Hsieh, L.7
Greene, G.8
Nimer, S.D.9
-
36
-
-
0031886864
-
The peroxisome proliferator-activated receptor-γ is a negative regulator of macrophage activation
-
2 results in increased expression levels of PPARγ and decreased expression of genes expressed in activated macrophages, such as inducible nitric oxide synthase and gelatinase B. These effects are mediated in part through antagonism of the activities of the transcription factors AP-1, STAT, and NF-κB. These data together with those of Jiang [37] are the first to suggest that PPARγ ligands might have a utility in the treatment of inflammatory diseases.
-
2 results in increased expression levels of PPARγ and decreased expression of genes expressed in activated macrophages, such as inducible nitric oxide synthase and gelatinase B. These effects are mediated in part through antagonism of the activities of the transcription factors AP-1, STAT, and NF-κB. These data together with those of Jiang [37] are the first to suggest that PPARγ ligands might have a utility in the treatment of inflammatory diseases.
-
(1998)
Nature
, vol.391
, pp. 79-82
-
-
Ricote, M.1
Li, A.C.2
Willson, T.M.3
Kelly, C.J.4
Glass, C.K.5
-
37
-
-
0031888958
-
PPAR-γ agonists inhibit production of monocyte inflammatory cytokines
-
2, and high concentrations of certain NSAIDs suppress monocyte elaboration of inflammatory cytokines including TNFα, IL-1β, and IL-6. These findings may explain the increased therapeutic utility of high concentrations of NSAIDS on rheumatoid arthritis.
-
2, and high concentrations of certain NSAIDs suppress monocyte elaboration of inflammatory cytokines including TNFα, IL-1β, and IL-6. These findings may explain the increased therapeutic utility of high concentrations of NSAIDS on rheumatoid arthritis.
-
(1998)
Nature
, vol.391
, pp. 82-86
-
-
Jiang, C.1
Ting, A.T.2
Seed, B.3
-
38
-
-
0032540012
-
PPARγ promotes monocyte/macrophage differentiation and uptake of oxidized LDL
-
of special interest. of outstanding interest. Activation of the PPARγ/RXR heterodimer promotes the differentiation of various myelomonocytic cell lines and induces the uptake of oxLDL in THP-1 cells via increased expression of the CD36 scavenger receptor. Moreover, oxLDL induces the expression of PPARγ, suggesting the existence of an autoregulatory loop. These findings were particularly interesting as PPARγ was expressed abundantly in foam cells of atherosclerotic plaques. This study, together with that of Nagy [39] are the first to suggest that PPARγ agonists might contribute to atherosclerosis.
-
of special interest Tontonoz P, Nagy L, Alvarez JGA, Thomazy VA, Evans RM. PPARγ promotes monocyte/macrophage differentiation and uptake of oxidized LDL. of outstanding interest Cell. 93:1998;241-252 Activation of the PPARγ/RXR heterodimer promotes the differentiation of various myelomonocytic cell lines and induces the uptake of oxLDL in THP-1 cells via increased expression of the CD36 scavenger receptor. Moreover, oxLDL induces the expression of PPARγ, suggesting the existence of an autoregulatory loop. These findings were particularly interesting as PPARγ was expressed abundantly in foam cells of atherosclerotic plaques. This study, together with that of Nagy [39] are the first to suggest that PPARγ agonists might contribute to atherosclerosis.
-
(1998)
Cell
, vol.93
, pp. 241-252
-
-
Tontonoz, P.1
Nagy, L.2
Alvarez, J.G.A.3
Thomazy, V.A.4
Evans, R.M.5
-
39
-
-
0032540325
-
Oxidized LDL regulates macrophage gene expression through ligand activation of PPARγ
-
of special interest. oxLDL particles activate PPARγ-dependent transcription. Two components of oxLDL, 9-HODE and 13-HODE, function as PPARγ ligands. These oxidized linoleic acid derivatives mimick the effects of oxLDL in inducing monocyte differentiation and CD36 gene expression. This study provides evidence that PPARγ ligands can be introduced into the cell as components of oxLDL via a receptor-mediated mechanism.
-
Nagy L, Tontonoz P, Alvarez JGA, Chen H, Evans RM. Oxidized LDL regulates macrophage gene expression through ligand activation of PPARγ of special interest Cell. 93:1998;229-240 oxLDL particles activate PPARγ-dependent transcription. Two components of oxLDL, 9-HODE and 13-HODE, function as PPARγ ligands. These oxidized linoleic acid derivatives mimick the effects of oxLDL in inducing monocyte differentiation and CD36 gene expression. This study provides evidence that PPARγ ligands can be introduced into the cell as components of oxLDL via a receptor-mediated mechanism.
-
(1998)
Cell
, vol.93
, pp. 229-240
-
-
Nagy, L.1
Tontonoz, P.2
Alvarez, J.G.A.3
Chen, H.4
Evans, R.M.5
-
40
-
-
0031764885
-
Another potential use of troglitazone in noninsulin-dependent diabetes mellitus
-
Minamikawa J, Yamauchi M, Inoue D, Koshiyama H. Another potential use of troglitazone in noninsulin-dependent diabetes mellitus. J Clinic Endo Met. 83:1998;1041.
-
(1998)
J Clinic Endo Met
, vol.83
, pp. 1041
-
-
Minamikawa, J.1
Yamauchi, M.2
Inoue, D.3
Koshiyama, H.4
-
43
-
-
0006132932
-
Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors α and γ
-
Kliewer SA, Sundseth SS, Jones SA, Brown PJ, Wisely GB, Koble CS, Devchand P, Wahli W, Willson TM, Lenhard JM, Lehmann JM. Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors α and γ Proc Natl Acad Sci USA. 94:1997;4318-4323.
-
(1997)
Proc Natl Acad Sci USA
, vol.94
, pp. 4318-4323
-
-
Kliewer, S.A.1
Sundseth, S.S.2
Jones, S.A.3
Brown, P.J.4
Wisely, G.B.5
Koble, C.S.6
Devchand, P.7
Wahli, W.8
Willson, T.M.9
Lenhard, J.M.10
Lehmann, J.M.11
-
44
-
-
0030985318
-
Fatty acids eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay
-
Krey G, Braissant O, L'Horset F, Kalkhoven E, Perroud M, Parker MG, Wahli W. Fatty acids eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol Endocrinol. 11:1997;779-791.
-
(1997)
Mol Endocrinol
, vol.11
, pp. 779-791
-
-
Krey, G.1
Braissant, O.2
L'Horset, F.3
Kalkhoven, E.4
Perroud, M.5
Parker, M.G.6
Wahli, W.7
-
45
-
-
0023240831
-
Fish oil prevents insulin resistance induced by high-fat feeding in rats
-
Storlien LH, Kraegen EW, Chisholm DJ, Ford GL, Bruce DG, Pascoe WS. Fish oil prevents insulin resistance induced by high-fat feeding in rats. Science. 237:1987;885-888.
-
(1987)
Science
, vol.237
, pp. 885-888
-
-
Storlien, L.H.1
Kraegen, E.W.2
Chisholm, D.J.3
Ford, G.L.4
Bruce, D.G.5
Pascoe, W.S.6
-
46
-
-
0032571089
-
Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat
-
Houseknecht KL, Heuvel JPV, Moya-Camarena SY, Portocarrero CP, Peck LW, Nickel KP, Belury MA. Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat. Biochem Biophys Res Commun. 244:1998;678-682.
-
(1998)
Biochem Biophys Res Commun
, vol.244
, pp. 678-682
-
-
Houseknecht, K.L.1
Heuvel, J.P.V.2
Moya-Camarena, S.Y.3
Portocarrero, C.P.4
Peck, L.W.5
Nickel, K.P.6
Belury, M.A.7
-
47
-
-
0030867111
-
Fatty acids, triglycerides and syndromes of insulin resistance
-
Storlien LH, Kriketos AD, Calvert GD, Baur LA, Jenkins AB. Fatty acids, triglycerides and syndromes of insulin resistance. Prost Leuk Ess Fatty Acids. 57:1997;379-385.
-
(1997)
Prost Leuk Ess Fatty Acids
, vol.57
, pp. 379-385
-
-
Storlien, L.H.1
Kriketos, A.D.2
Calvert, G.D.3
Baur, L.A.4
Jenkins, A.B.5
-
48
-
-
0030007427
-
ADD1/SREBP1 promotes adipocyte differentiation and gene expression linked to fatty acid metabolism
-
Kim JB, Spiegelman BM. ADD1/SREBP1 promotes adipocyte differentiation and gene expression linked to fatty acid metabolism. Genes Dev. 10:1996;1096-1107.
-
(1996)
Genes Dev
, vol.10
, pp. 1096-1107
-
-
Kim, J.B.1
Spiegelman, B.M.2
-
50
-
-
0027240176
-
Cloning of a rat adipocyte membrane protein implicated in binding or transport of long-chain fatty acids that is induced during preadipocyte differentiation
-
Abumrad NA, El-Maghrabi MR, Amri E-Z, Lopez E, Grimaldi PA. Cloning of a rat adipocyte membrane protein implicated in binding or transport of long-chain fatty acids that is induced during preadipocyte differentiation. J Biol Chem. 268:1993;17665-17668.
-
(1993)
J Biol Chem
, vol.268
, pp. 17665-17668
-
-
Abumrad, N.A.1
El-Maghrabi, M.R.2
Amri, E.-Z.3
Lopez, E.4
Grimaldi, P.A.5
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