-
1
-
-
0021359902
-
Risk factors for worsening to diabetes in subjects with impaired glucose tolerance
-
Kadowaki, T., et al. 1984. Risk factors for worsening to diabetes in subjects with impaired glucose tolerance. Diabetologia. 26:44-49.
-
(1984)
Diabetologia
, vol.26
, pp. 44-49
-
-
Kadowaki, T.1
-
2
-
-
0028229508
-
Insulin resistance or insulin deficiency: Which is the primary cause of NIDDM?
-
Taylor, S.I., Accili, D., and Imai, Y. 1994. Insulin resistance or insulin deficiency: which is the primary cause of NIDDM? Diabetes. 43:735-740.
-
(1994)
Diabetes
, vol.43
, pp. 735-740
-
-
Taylor, S.I.1
Accili, D.2
Imai, Y.3
-
3
-
-
0028567063
-
Transgenic approaches to the pathogenesis of NIDDM
-
Moller, D.E. 1994. Transgenic approaches to the pathogenesis of NIDDM. Diabetes. 43:1394-1401.
-
(1994)
Diabetes
, vol.43
, pp. 1394-1401
-
-
Moller, D.E.1
-
4
-
-
0029807339
-
Conditional gene targeting
-
Rajewsky, K., et al. 1996. Conditional gene targeting. J. Clin. Invest. 98:600-603.
-
(1996)
J. Clin. Invest.
, vol.98
, pp. 600-603
-
-
Rajewsky, K.1
-
5
-
-
13344277357
-
Early neonatal death in mice homozygous for a null allele of the insulin receptor gene
-
Accili, D., et al. 1996. Early neonatal death in mice homozygous for a null allele of the insulin receptor gene. Nat. Genet. 12:106-109.
-
(1996)
Nat. Genet.
, vol.12
, pp. 106-109
-
-
Accili, D.1
-
6
-
-
0029879127
-
Targeted disruption of the insulin receptor gene in the mouse results in neonatal lethality
-
Joshi, R.L., et al. 1996. Targeted disruption of the insulin receptor gene in the mouse results in neonatal lethality. EMBO J. 15:1542-1547.
-
(1996)
EMBO J.
, vol.15
, pp. 1542-1547
-
-
Joshi, R.L.1
-
7
-
-
0031888649
-
Lack of insulin receptors affects the formation of white adipose tissue in mice. A morphometric and ultrastructural analysis
-
Cinti, S., Eberbach, S., Castellucci, M., and Accili, D. 1998. Lack of insulin receptors affects the formation of white adipose tissue in mice. A morphometric and ultrastructural analysis. Diabetologia. 41:171-177.
-
(1998)
Diabetologia
, vol.41
, pp. 171-177
-
-
Cinti, S.1
Eberbach, S.2
Castellucci, M.3
Accili, D.4
-
8
-
-
0038155702
-
Development of a novel polygenic model of NIDDM in mice heterozygous for IR and IRS-1 null alleles
-
Brüning, J.C., et al. 1997. Development of a novel polygenic model of NIDDM in mice heterozygous for IR and IRS-1 null alleles. Cell. 88:561-572.
-
(1997)
Cell.
, vol.88
, pp. 561-572
-
-
Brüning, J.C.1
-
9
-
-
0032214652
-
A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance
-
Brüning, J.C., et al. 1998. A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol. Cell. 2:559-569.
-
(1998)
Mol. Cell.
, vol.2
, pp. 559-569
-
-
Brüning, J.C.1
-
10
-
-
0032697037
-
Exercise modulates postreceptor insulin signaling and glucose transport in muscle-specific insulin receptor knockout mice
-
Wojtaszewski, J.F., et al. 1999. Exercise modulates postreceptor insulin signaling and glucose transport in muscle-specific insulin receptor knockout mice. J. Clin. Invest. 104:1257-1254.
-
(1999)
J. Clin. Invest.
, vol.104
, pp. 1257-11254
-
-
Wojtaszewski, J.F.1
-
11
-
-
0033524937
-
Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes
-
Kulkarni, R.N., et al. 1999. Tissue-specific knockout of the insulin receptor in pancreatic beta cells creates an insulin secretory defect similar to that in type 2 diabetes. Cell. 96:329-339.
-
(1999)
Cell.
, vol.96
, pp. 329-339
-
-
Kulkarni, R.N.1
-
12
-
-
0033636523
-
Loss of insulin signalling in hepatocytes leads to severe insulin resistance and progressive hepatic dysfunction
-
Michael, M.D., et al. 2000. Loss of insulin signalling in hepatocytes leads to severe insulin resistance and progressive hepatic dysfunction. Mol. Cell. 6:87-97.
-
(2000)
Mol. Cell.
, vol.6
, pp. 87-97
-
-
Michael, M.D.1
-
13
-
-
0028032894
-
Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1
-
Tamemoto, H., et al. 1994. Insulin resistance and growth retardation in mice lacking insulin receptor substrate-1. Nature. 372:182-186.
-
(1994)
Nature
, vol.372
, pp. 182-186
-
-
Tamemoto, H.1
-
14
-
-
0028032895
-
Alternative pathway of insulin signaling in mice with targeted disruption of the IRS-1 gene
-
Araki, E., et al. 1994. Alternative pathway of insulin signaling in mice with targeted disruption of the IRS-1 gene. Nature. 372:186-190.
-
(1994)
Nature
, vol.372
, pp. 186-190
-
-
Araki, E.1
-
15
-
-
0030961962
-
Development of non-insulin-dependent diabetes mellitus in the double knockout mice with disruption of insulin receptor substrate-1 and β cell glucokinase genes: Genetic reconstitution of diabetes as a polygenic disease
-
Terauchi, Y., et al. 1997. Development of non-insulin-dependent diabetes mellitus in the double knockout mice with disruption of insulin receptor substrate-1 and β cell glucokinase genes: genetic reconstitution of diabetes as a polygenic disease. J. Clin. Invest. 99:861-866.
-
(1997)
J. Clin. Invest.
, vol.99
, pp. 861-866
-
-
Terauchi, Y.1
-
16
-
-
0028810236
-
4PS/Insulin receptor substrate (IRS)-2 is the alternative substrate of the insulin receptor in IRS-1-deficient mice
-
Patti, M.E., et al. 1995. 4PS/Insulin receptor substrate (IRS)-2 is the alternative substrate of the insulin receptor in IRS-1-deficient mice. J. Biol. Chem. 270:24670-24673.
-
(1995)
J. Biol. Chem.
, vol.270
, pp. 24670-24673
-
-
Patti, M.E.1
-
17
-
-
0028957037
-
Identification of a 190-kDa protein as a novel substrate for the insulin receptor kinase functionally similar to insulin receptor substrate-1
-
Tobe, K., Tamemoto, H., Yamauchi, T., Yazaki, Y., and Kadowaki, T. 1995. Identification of a 190-kDa protein as a novel substrate for the insulin receptor kinase functionally similar to insulin receptor substrate-1. J. Biol. Chem. 270:5698-5701.
-
(1995)
J. Biol. Chem.
, vol.270
, pp. 5698-5701
-
-
Tobe, K.1
Tamemoto, H.2
Yamauchi, T.3
Yazaki, Y.4
Kadowaki, T.5
-
18
-
-
0029148591
-
Role of IRS-2 in insulin and cytokine signalling
-
Sun, X.J., et al. 1995. Role of IRS-2 in insulin and cytokine signalling. Nature. 377:173-177.
-
(1995)
Nature
, vol.377
, pp. 173-177
-
-
Sun, X.J.1
-
19
-
-
0029897280
-
Insulin signalling and insulin actions in the muscle and liver of insulin resistant IRS-1 deficient mice
-
Yamauchi, T., et al. 1996. Insulin signalling and insulin actions in the muscle and liver of insulin resistant IRS-1 deficient mice. Mol. Cell. Biol. 16:3074-3084.
-
(1996)
Mol. Cell. Biol.
, vol.16
, pp. 3074-3084
-
-
Yamauchi, T.1
-
20
-
-
0040973209
-
Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells
-
Brüning, J.C., Winnay, J., Cheatham, B., Kahn, R.C. 1997. Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells. Mol. Cell. Biol. 17:1513-1521.
-
(1997)
Mol. Cell. Biol.
, vol.17
, pp. 1513-1521
-
-
Brüning, J.C.1
Winnay, J.2
Cheatham, B.3
Kahn, R.C.4
-
21
-
-
0030848724
-
Role of insulin receptor substrate-1 and pp60 in the regulation of insulin-induced glucose transport and GLUT4 translocation in primary adipocytes
-
Kaburagi, Y., et al. 1997. Role of insulin receptor substrate-1 and pp60 in the regulation of insulin-induced glucose transport and GLUT4 translocation in primary adipocytes. J. Biol. Chem. 272:25839-25844.
-
(1997)
J. Biol. Chem.
, vol.272
, pp. 25839-25844
-
-
Kaburagi, Y.1
-
22
-
-
0030995946
-
The 60-kDa phosphotyrosine protein in insulin-treated adipocytes is a new member of the insulin receptor substrate family
-
Lavan, B.E., Lane, W.S., and Lienhard, G.E. 1997. The 60-kDa phosphotyrosine protein in insulin-treated adipocytes is a new member of the insulin receptor substrate family. J. Biol. Chem. 272:11439-11443.
-
(1997)
J. Biol. Chem.
, vol.272
, pp. 11439-11443
-
-
Lavan, B.E.1
Lane, W.S.2
Lienhard, G.E.3
-
23
-
-
0032523085
-
Hypertension, hypertriglyceridemia, and impaired endothelium-dependent vascular relaxation in mice lacking insulin receptor substrate-1
-
Abe, H., et al. 1998. Hypertension, hypertriglyceridemia, and impaired endothelium-dependent vascular relaxation in mice lacking insulin receptor substrate-1. J. Clin. Invest. 101:1784-1788.
-
(1998)
J. Clin. Invest.
, vol.101
, pp. 1784-1788
-
-
Abe, H.1
-
24
-
-
0032567937
-
Disruption of IRS-2 causes type 2 diabetes in mice
-
Withers, D.J., et al. 1998. Disruption of IRS-2 causes type 2 diabetes in mice. Nature. 391:900-904.
-
(1998)
Nature
, vol.391
, pp. 900-904
-
-
Withers, D.J.1
-
25
-
-
0033755408
-
Disruption of insulin receptor substrate-2 causes type 2 diabetes due to liver insulin resistance and lack of compensatory β-cell hyperplasia
-
In press
-
Kubota, N., et al. 2000. Disruption of insulin receptor substrate-2 causes type 2 diabetes due to liver insulin resistance and lack of compensatory β-cell hyperplasia. Diabetes. In press.
-
(2000)
Diabetes
-
-
Kubota, N.1
-
26
-
-
0032841435
-
Irs-2 coordinates Igf-1 receptor-mediated beta-cell development and peripheral insulin signalling
-
Withers, D.J., et al. 1999. Irs-2 coordinates Igf-1 receptor-mediated beta-cell development and peripheral insulin signalling. Nat. Genet. 23:32-40.
-
(1999)
Nat. Genet.
, vol.23
, pp. 32-40
-
-
Withers, D.J.1
-
27
-
-
0033581023
-
Insulin receptor substrate 3 is not essential for growth or glucose homeostasis
-
Liu, S.C., Wang, Q., Lienhard, G.E., and Keller, S.R. 1999. Insulin receptor substrate 3 is not essential for growth or glucose homeostasis. J. Biol. Chem. 274:18093-18099.
-
(1999)
J. Biol. Chem.
, vol.274
, pp. 18093-18099
-
-
Liu, S.C.1
Wang, Q.2
Lienhard, G.E.3
Keller, S.R.4
-
28
-
-
0032909703
-
Increased insulin sensitivity and hypoglycaemia in mice lacking the p85α subunit of phosphoinositide 3-kinase
-
Terauchi, Y., et al. 1999. Increased insulin sensitivity and hypoglycaemia in mice lacking the p85α subunit of phosphoinositide 3-kinase. Nat. Genet. 21:230-235.
-
(1999)
Nat. Genet.
, vol.21
, pp. 230-235
-
-
Terauchi, Y.1
-
29
-
-
0030271565
-
Structural organization and alternative splicing of the murine phosphoinositide 3-kinase p85α gene
-
Fruman, D.A., Cantley, L.C., and Carpenter, C.L. 1996. Structural organization and alternative splicing of the murine phosphoinositide 3-kinase p85α gene. Genomics. 37:113-121.
-
(1996)
Genomics
, vol.37
, pp. 113-121
-
-
Fruman, D.A.1
Cantley, L.C.2
Carpenter, C.L.3
-
30
-
-
0029148426
-
Cardiac and adipose tissue abnormalities but not diabetes in mice deficient in GLUT4
-
Katz, E.B., Stenbit, A.E., Hatton, K., DePinho, R., and Charron, M.J. 1995. Cardiac and adipose tissue abnormalities but not diabetes in mice deficient in GLUT4. Nature. 377:151-155.
-
(1995)
Nature
, vol.377
, pp. 151-155
-
-
Katz, E.B.1
Stenbit, A.E.2
Hatton, K.3
DePinho, R.4
Charron, M.J.5
-
31
-
-
0030756249
-
Muscle-specific transgenic complementation of GLUT4-deficient mice. Effects on glucose but not lipid metabolism
-
Tsao, T.S., et al. 1997. Muscle-specific transgenic complementation of GLUT4-deficient mice. Effects on glucose but not lipid metabolism. J. Clin. Invest. 100:671-677.
-
(1997)
J. Clin. Invest.
, vol.100
, pp. 671-677
-
-
Tsao, T.S.1
-
32
-
-
0030839435
-
GLUT4 heterozygous knockout mice develop muscle insulin resistance and diabetes
-
Stenbit, A.E., et al. 1997. GLUT4 heterozygous knockout mice develop muscle insulin resistance and diabetes. Nat. Med. 3:1096-1101.
-
(1997)
Nat. Med.
, vol.3
, pp. 1096-1101
-
-
Stenbit, A.E.1
-
33
-
-
0030967868
-
Peripheral but not hepatic insulin resistance in mice with one disrupted allele of the glucose transporter type 4 (GLUT4) gene
-
Rossetti, L., et al. 1997. Peripheral but not hepatic insulin resistance in mice with one disrupted allele of the glucose transporter type 4 (GLUT4) gene. J. Clin. Invest. 100:1831-1839.
-
(1997)
J. Clin. Invest.
, vol.100
, pp. 1831-1839
-
-
Rossetti, L.1
-
34
-
-
0033042121
-
Prevention of insulin resistance and diabetes in mice heterozygous for GLUT4 ablation by transgenic complementation of GLUT4 in skeletal muscle
-
Tsao, T.S., et al. 1999. Prevention of insulin resistance and diabetes in mice heterozygous for GLUT4 ablation by transgenic complementation of GLUT4 in skeletal muscle. Diabetes. 48:775-782.
-
(1999)
Diabetes
, vol.48
, pp. 775-782
-
-
Tsao, T.S.1
-
35
-
-
0033834248
-
Targeted disruption of the glucose transporter 4 selectively in muscle causes insulin resistance and glucose intolerance
-
In press
-
Zisman, A., et al. 2000. Targeted disruption of the glucose transporter 4 selectively in muscle causes insulin resistance and glucose intolerance. Nat. Med. In press.
-
(2000)
Nat. Med.
-
-
Zisman, A.1
-
36
-
-
0032588487
-
PPARγ, the ultimate thrifty gene
-
Auwerx, J. 1999. PPARγ, the ultimate thrifty gene. Diabetologia. 42:1033-1049.
-
(1999)
Diabetologia
, vol.42
, pp. 1033-1049
-
-
Auwerx, J.1
-
37
-
-
0032520921
-
Troglitazone increases the number of small adipocytes without the change of white adipose tissue mass in obese Zucker rats
-
Okuno, A., et al. 1998. Troglitazone increases the number of small adipocytes without the change of white adipose tissue mass in obese Zucker rats. J. Clin. Invest. 101:1354-1361.
-
(1998)
J. Clin. Invest.
, vol.101
, pp. 1354-1361
-
-
Okuno, A.1
-
38
-
-
0033212964
-
PPARγ mediates high-fat diet-induced adipocyte hypertrophy and insulin resistance
-
Kubota, N., et al. 1999. PPARγ mediates high-fat diet-induced adipocyte hypertrophy and insulin resistance. Mol. Cell. 4:597-609.
-
(1999)
Mol. Cell.
, vol.4
, pp. 597-609
-
-
Kubota, N.1
-
39
-
-
0033213637
-
PPAR gamma is required for placental, cardiac, and adipose tissue development
-
Barak, Y., et al. 1999. PPAR gamma is required for placental, cardiac, and adipose tissue development. Mol. Cell. 4:585-595.
-
(1999)
Mol. Cell.
, vol.4
, pp. 585-595
-
-
Barak, Y.1
-
40
-
-
0033213631
-
PPAR gamma is required for the differentiation of adipose tissue in vivo
-
Rosen, E.D., et al. 1999. PPAR gamma is required for the differentiation of adipose tissue in vivo. Mol. Cell. 4:611-617.
-
(1999)
Mol. Cell.
, vol.4
, pp. 611-617
-
-
Rosen, E.D.1
-
41
-
-
0033973843
-
Improved insulin-sensitivity in mice heterozygous for PPAR gamma deficiency
-
Miles, P.D., Barak, Y., He, W., Evans, R.M., and Olefsky, J.M. 2000. Improved insulin-sensitivity in mice heterozygous for PPAR gamma deficiency. J. Clin. Invest. 105:287-292.
-
(2000)
J. Clin. Invest.
, vol.105
, pp. 287-292
-
-
Miles, P.D.1
Barak, Y.2
He, W.3
Evans, R.M.4
Olefsky, J.M.5
-
42
-
-
0031595923
-
A Pro 12 Ala substitution in PPARgamma2 associated with decreased receptor activity, low body mass index and improved insulin sensitivity
-
Deeb, S.S., et al. 1998. A Pro 12 Ala substitution in PPARgamma2 associated with decreased receptor activity, low body mass index and improved insulin sensitivity. Nat. Genet. 20:284-287.
-
(1998)
Nat. Genet.
, vol.20
, pp. 284-287
-
-
Deeb, S.S.1
-
43
-
-
0034728762
-
A Pro12Ala polymorphism in PPARg2 may confer resistance to type II diabetes
-
Hara, K., et al. 2000. A Pro12Ala polymorphism in PPARg2 may confer resistance to type II diabetes. Biochem. Biophys. Res. Commun. 271:212-216.
-
(2000)
Biochem. Biophys. Res. Commun.
, vol.271
, pp. 212-216
-
-
Hara, K.1
-
44
-
-
0026793446
-
Role of glucose and insulin resistance in the development of type 2 diabetes mellitus: Results of a 25-year follow-up study
-
Martin, B.C., et al. 1992. Role of glucose and insulin resistance in the development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet. 340:925-929.
-
(1992)
Lancet
, vol.340
, pp. 925-929
-
-
Martin, B.C.1
-
45
-
-
0025100926
-
Islet function and insulin sensitivity in the non-diabetic offspring of conjugal type 2 diabetic patients
-
Johnston, C., Ward, W.K., Beard, J.C., McKnight, B., and Porte, D., Jr. 1990. Islet function and insulin sensitivity in the non-diabetic offspring of conjugal type 2 diabetic patients. Diabet. Med. 7:119-125.
-
(1990)
Diabet. Med.
, vol.7
, pp. 119-125
-
-
Johnston, C.1
Ward, W.K.2
Beard, J.C.3
McKnight, B.4
Porte D., Jr.5
-
46
-
-
0028848244
-
Decreased insulin secretion and increased insulin resistance are independently related to the 7-year risk of NIDDM in Mexican-Americans
-
Haffner, S.M., Miettinen, H., Gaskill, S.P., and Stern, M.P. 1995. Decreased insulin secretion and increased insulin resistance are independently related to the 7-year risk of NIDDM in Mexican-Americans. Diabetes. 44:1386-1391.
-
(1995)
Diabetes
, vol.44
, pp. 1386-1391
-
-
Haffner, S.M.1
Miettinen, H.2
Gaskill, S.P.3
Stern, M.P.4
-
47
-
-
0033842027
-
Interactions between insulin resistance and insulin secretion in the development of glucose intolerance
-
Cavaghan, M.K., Ehrmann, D.A., and Polonsky, K.S. 2000. Interactions between insulin resistance and insulin secretion in the development of glucose intolerance. J. Clin. Invest. 106:329-333.
-
(2000)
J. Clin. Invest.
, vol.106
, pp. 329-333
-
-
Cavaghan, M.K.1
Ehrmann, D.A.2
Polonsky, K.S.3
-
48
-
-
0029417331
-
Pancreatic β-cell-specific targeted disruption of glucokinase gene. Diabetes mellitus due to defective insulin secretion to glucose
-
Terauchi, Y., et al. 1995. Pancreatic β-cell-specific targeted disruption of glucokinase gene. Diabetes mellitus due to defective insulin secretion to glucose. J. Biol. Chem. 270:30253-30256.
-
(1995)
J. Biol. Chem.
, vol.270
, pp. 30253-30256
-
-
Terauchi, Y.1
-
49
-
-
0032928542
-
Loci on chromosome 2 (NIDDM1) and 15 interact to increase susceptability to diabetes in Mexican Americans
-
Cox, N.J., et al. 1999. Loci on chromosome 2 (NIDDM1) and 15 interact to increase susceptability to diabetes in Mexican Americans. Nat. Genet. 21:213-215.
-
(1999)
Nat. Genet.
, vol.21
, pp. 213-215
-
-
Cox, N.J.1
|