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Gene Information

Gene symbol: PDAP1

Gene name: PDGFA associated protein 1

HGNC ID: 14634

Synonyms: PAP1, PAP, HASPP28

Related Genes

# Gene Symbol Number of hits
1 C20orf181 1 hits
2 F2 1 hits
3 INS 1 hits
4 KCNA3 1 hits
5 LPIN1 1 hits
6 LPIN2 1 hits
7 LPIN3 1 hits
8 LYST 1 hits
9 PLAT 1 hits
10 REG3A 1 hits
11 RP9 1 hits
12 SERPINE1 1 hits
13 SERPINF2 1 hits
14 SHPK 1 hits

Related Sentences

# PMID Sentence
1 9184412 In the selected study population of 81 men and 19 women with fibrinogen concentration either > or = 3.5 g/l (n = 70) or < or = 2.5 g/l (n = 30) hyperfibrinogenemia was found to be significantly associated with increased concentrations of plasmin-alpha 2-antiplasmin complex [PAP [median (25.-75. percentile)], 534 (361-680) micrograms/l vs. 289 (243-440) micrograms/l; p < 0.001] and tissue plasminogen activator (t-PA) antigen [9 (6-11) micrograms/l vs 8 (5-9) micrograms/l; p < 0.05] while this association was lost in the subgroup of patients with angiographically normal coronary arteries (n = 26).
2 9184412 In addition to these findings fibrinogen was significantly correlated with PAP (r = 0.40, p < 0.001; n = 224) and t-PA antigen (r = 0.2, p < 0.01; n = 224) after adjustment for age, diabetes mellitus, lipid parameters and leucocyte counts.
3 9184412 In the selected study population of 81 men and 19 women with fibrinogen concentration either > or = 3.5 g/l (n = 70) or < or = 2.5 g/l (n = 30) hyperfibrinogenemia was found to be significantly associated with increased concentrations of plasmin-alpha 2-antiplasmin complex [PAP [median (25.-75. percentile)], 534 (361-680) micrograms/l vs. 289 (243-440) micrograms/l; p < 0.001] and tissue plasminogen activator (t-PA) antigen [9 (6-11) micrograms/l vs 8 (5-9) micrograms/l; p < 0.05] while this association was lost in the subgroup of patients with angiographically normal coronary arteries (n = 26).
4 9184412 In addition to these findings fibrinogen was significantly correlated with PAP (r = 0.40, p < 0.001; n = 224) and t-PA antigen (r = 0.2, p < 0.01; n = 224) after adjustment for age, diabetes mellitus, lipid parameters and leucocyte counts.
5 10073949 In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37).
6 10073949 PAP was negatively related to factors associated with the insulin resistance syndrome (IRS) (eg, fasting insulin, r=-0.26; body mass index, r=-0.26), possibly reflecting an association with plasminogen activator inhibitor-1 (r=-0.29).
7 10073949 Although our study did not have sufficient power to detect a significant interaction, PAP and AAI appeared to be more weakly associated in subjects with more manifestations of the IRS: PAP appeared more strongly associated with AAI in the subgroup with 0 or 1 metabolic disorders (P</=0.001; slope estimate, -0.14) compared with the subgroup with 2 or more metabolic disorders (P=0.10; slope estimate, -0.08) and in those with non-insulin-dependent diabetes mellitus (P=0.46; slope estimate, -0.04).
8 10073949 Although PAP reflects reactive fibrinolysis and is associated with subclinical atherosclerosis, this relationship may be weaker in populations with characteristics of the IRS, possibly reflecting the inhibitory effects of plasminogen activator inhibitor-1 on PAP.
9 10073949 In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37).
10 10073949 PAP was negatively related to factors associated with the insulin resistance syndrome (IRS) (eg, fasting insulin, r=-0.26; body mass index, r=-0.26), possibly reflecting an association with plasminogen activator inhibitor-1 (r=-0.29).
11 10073949 Although our study did not have sufficient power to detect a significant interaction, PAP and AAI appeared to be more weakly associated in subjects with more manifestations of the IRS: PAP appeared more strongly associated with AAI in the subgroup with 0 or 1 metabolic disorders (P</=0.001; slope estimate, -0.14) compared with the subgroup with 2 or more metabolic disorders (P=0.10; slope estimate, -0.08) and in those with non-insulin-dependent diabetes mellitus (P=0.46; slope estimate, -0.04).
12 10073949 Although PAP reflects reactive fibrinolysis and is associated with subclinical atherosclerosis, this relationship may be weaker in populations with characteristics of the IRS, possibly reflecting the inhibitory effects of plasminogen activator inhibitor-1 on PAP.
13 10073949 In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37).
14 10073949 PAP was negatively related to factors associated with the insulin resistance syndrome (IRS) (eg, fasting insulin, r=-0.26; body mass index, r=-0.26), possibly reflecting an association with plasminogen activator inhibitor-1 (r=-0.29).
15 10073949 Although our study did not have sufficient power to detect a significant interaction, PAP and AAI appeared to be more weakly associated in subjects with more manifestations of the IRS: PAP appeared more strongly associated with AAI in the subgroup with 0 or 1 metabolic disorders (P</=0.001; slope estimate, -0.14) compared with the subgroup with 2 or more metabolic disorders (P=0.10; slope estimate, -0.08) and in those with non-insulin-dependent diabetes mellitus (P=0.46; slope estimate, -0.04).
16 10073949 Although PAP reflects reactive fibrinolysis and is associated with subclinical atherosclerosis, this relationship may be weaker in populations with characteristics of the IRS, possibly reflecting the inhibitory effects of plasminogen activator inhibitor-1 on PAP.
17 10073949 In CHS, PAP levels increased with age (r=0. 30), procoagulant factors (eg, factor VIIc, r=0.15), thrombin activity (prothrombin fragment F1+2, r=0.29), and inflammation-sensitive proteins (eg, fibrinogen, r=0.44; factor VIIIc, r=0.37).
18 10073949 PAP was negatively related to factors associated with the insulin resistance syndrome (IRS) (eg, fasting insulin, r=-0.26; body mass index, r=-0.26), possibly reflecting an association with plasminogen activator inhibitor-1 (r=-0.29).
19 10073949 Although our study did not have sufficient power to detect a significant interaction, PAP and AAI appeared to be more weakly associated in subjects with more manifestations of the IRS: PAP appeared more strongly associated with AAI in the subgroup with 0 or 1 metabolic disorders (P</=0.001; slope estimate, -0.14) compared with the subgroup with 2 or more metabolic disorders (P=0.10; slope estimate, -0.08) and in those with non-insulin-dependent diabetes mellitus (P=0.46; slope estimate, -0.04).
20 10073949 Although PAP reflects reactive fibrinolysis and is associated with subclinical atherosclerosis, this relationship may be weaker in populations with characteristics of the IRS, possibly reflecting the inhibitory effects of plasminogen activator inhibitor-1 on PAP.
21 16142016 Both treatments significantly declined plasma glucose, total-cholesterol, LDL-cholesterol, triglycerides, PAI-1, PAP levels and increased HDL-cholesterol.
22 16142016 Lowering in plasma PAI-1 and PAP levels was significantly greater in repaglinide group.
23 16142016 Furthermore, repaglinide administration resulted in a significant decrease in fasting plasma free fatty acids, fibrinogen, thrombin-antithrombin complex and reaction product of malondialdehyde with thiobarbituric acid (TBARS) levels, in absence of significant difference in fasting plasma insulin levels.
24 16142016 At time 120' of meal test, repaglinide vs glimepiride administration was associated with a significant decline in plasma triglycerides, free fatty acids, fibrinogen, Plasminogen Activator Inhibitor-1, plasmin-alpha(2)-antiplasmin complex, thrombin-antithrombin complex, TBARS levels and increase in plasma HDL-cholesterol levels.
25 16142016 Both treatments significantly declined plasma glucose, total-cholesterol, LDL-cholesterol, triglycerides, PAI-1, PAP levels and increased HDL-cholesterol.
26 16142016 Lowering in plasma PAI-1 and PAP levels was significantly greater in repaglinide group.
27 16142016 Furthermore, repaglinide administration resulted in a significant decrease in fasting plasma free fatty acids, fibrinogen, thrombin-antithrombin complex and reaction product of malondialdehyde with thiobarbituric acid (TBARS) levels, in absence of significant difference in fasting plasma insulin levels.
28 16142016 At time 120' of meal test, repaglinide vs glimepiride administration was associated with a significant decline in plasma triglycerides, free fatty acids, fibrinogen, Plasminogen Activator Inhibitor-1, plasmin-alpha(2)-antiplasmin complex, thrombin-antithrombin complex, TBARS levels and increase in plasma HDL-cholesterol levels.
29 17088564 Here we demonstrate that disease-associated autoreactive T cells from patients with type-1 diabetes mellitus or rheumatoid arthritis (RA) are mainly CD4+ CCR7- CD45RA- effector memory T cells (T(EM) cells) with elevated Kv1.3 potassium channel expression.
30 17088564 In T(EM) cells, Kv1.3 traffics to the immunological synapse during antigen presentation where it colocalizes with Kvbeta2, SAP97, ZIP, p56(lck), and CD4.
31 17088564 Although Kv1.3 inhibitors [ShK(L5)-amide (SL5) and PAP1] do not prevent immunological synapse formation, they suppress Ca2+-signaling, cytokine production, and proliferation of autoantigen-specific T(EM) cells at pharmacologically relevant concentrations while sparing other classes of T cells.
32 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
33 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
34 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
35 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
36 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
37 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
38 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
39 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
40 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
41 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
42 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
43 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
44 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
45 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
46 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
47 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
48 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
49 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
50 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
51 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
52 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
53 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
54 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
55 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
56 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
57 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
58 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
59 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
60 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
61 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
62 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
63 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
64 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
65 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
66 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
67 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
68 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
69 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
70 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
71 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
72 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
73 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
74 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
75 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
76 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
77 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
78 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
79 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
80 18245816 Glucocorticoids and cyclic AMP selectively increase hepatic lipin-1 expression, and insulin acts antagonistically.
81 18245816 Glucocorticoids (GCs) increase hepatic phosphatidate phosphatase (PAP1) activity.
82 18245816 PAP1 catalyzes the conversion of phosphatidate to diacylglycerol, a key substrate for TAG and phospholipid biosynthesis.
83 18245816 PAP1 enzymes in liver include lipin-1A and -1B (alternatively spliced isoforms) and two distinct gene products, lipin-2 and lipin-3.
84 18245816 We determined the mechanisms by which the composite PAP1 activity is regulated using rat and mouse hepatocytes.
85 18245816 Levels of lipin-1A and -1B mRNA were increased by dexamethasone (dex; a synthetic GC), and this resulted in increased lipin-1 synthesis, protein levels, and PAP1 activity.
86 18245816 Lipin-2 and lipin-3 mRNA were not increased by dex/cAMP, indicating that increased PAP1 activity is attributable specifically to enhanced lipin-1 expression.
87 18245816 Selective lipin-1 expression explains the GC and cAMP effects on increased hepatic PAP1 activity, which occurs in hepatic steatosis during starvation, diabetes, stress, and ethanol consumption.
88 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
89 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
90 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
91 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
92 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
93 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
94 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
95 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.
96 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
97 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
98 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
99 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
100 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
101 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
102 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
103 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.
104 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
105 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
106 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
107 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
108 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
109 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
110 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
111 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.
112 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
113 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
114 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
115 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
116 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
117 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
118 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
119 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.
120 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
121 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
122 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
123 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
124 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
125 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
126 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
127 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.
128 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
129 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
130 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
131 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
132 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
133 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
134 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
135 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.
136 19799857 Here, we studied cardiac PAP(1) activity and lipin expression ex vivo in 8-month-old Zucker diabetic fatty (ZDF) rats and humans with type 2 diabetes mellitus undergoing open heart surgery for coronary bypass grafting.
137 19799857 Compared to non-diabetic littermates (ZDF-fa/+), left ventricular PAP(1) activity was 29% lower in diabetic ZDF-fa/fa rats.
138 19799857 Left ventricular PAP(1) activities were 2.1-fold (ZDF-fa/fa) and 3.6-fold (ZDF-fa/+) higher than the respective atrial activities, indicating marked differences in cardiac distribution of PAP(1).
139 19799857 PAP(1) activity was highly related with cardiac lipin-1 and lipin-3 mRNA expression in ZDF rats (r=0.99 and 0.96).
140 19799857 Consistent with the findings in experimental animals, human atrial tissue displayed PAP(1) activity that was 33% lower in those having diabetes than in non-diabetic controls.
141 19799857 Accordingly, atrial lipin-1 and lipin-3 mRNA expression in diabetic patients was 50% and 59% lower as in non-diabetic patients, respectively.
142 19799857 Insulin therapy increased both PAP(1) activity and lipin mRNA expression in diabetic patients.
143 19799857 We conclude that suppression of cardiac PAP(1) activity/lipin expression may contribute to metabolic dysfunction of the diabetic heart.