Ignet

Gene Information

Gene symbol: LIPC

Gene name: lipase, hepatic

HGNC ID: 6619

Synonyms: HL, HTGL

Related Genes

#	Gene Symbol	Number of hits
1	ABCA1	1 hits
2	ADRB3	1 hits
3	AGPAT1	1 hits
4	ANGPTL3	1 hits
5	APOA1	1 hits
6	APOB	1 hits
7	APOC3	1 hits
8	APOE	1 hits
9	ASIP	1 hits
10	CAST	1 hits
11	CES1	1 hits
12	CETP	1 hits
13	CFH	1 hits
14	CLCNKB	1 hits
15	CRP	1 hits
16	CTLA4	1 hits
17	CTNS	1 hits
18	DLG2	1 hits
19	ELOVL2	1 hits
20	GALNT2	1 hits
21	GCKR	1 hits
22	GHR	1 hits
23	GYS1	1 hits
24	HK2	1 hits
25	HMGCR	1 hits
26	HNF1A	1 hits
27	HSD17B2	1 hits
28	IDDM2	1 hits
29	IKBKAP	1 hits
30	INS	1 hits
31	IRS1	1 hits
32	KCNH7	1 hits
33	KCNJ11	1 hits
34	LASS4	1 hits
35	LCAT	1 hits
36	LDLR	1 hits
37	LEPR	1 hits
38	LIPE	1 hits
39	LIPG	1 hits
40	LIPH	1 hits
41	LPAL2	1 hits
42	LPL	1 hits
43	MLXIPL	1 hits
44	MOGAT1	1 hits
45	MTTP	1 hits
46	NCAN	1 hits
47	P2RY2	1 hits
48	PCDH20	1 hits
49	PCSK9	1 hits
50	PDXDC1	1 hits
51	PKLR	1 hits
52	PLA2G7	1 hits
53	PLD2	1 hits
54	PNLIP	1 hits
55	PNLIPRP2	1 hits
56	PON1	1 hits
57	PON2	1 hits
58	PPP1R3A	1 hits
59	PRODH2	1 hits
60	PWCR	1 hits
61	SCARB1	1 hits
62	SLC16A7	1 hits
63	SLC25A20	1 hits
64	SLC2A4	1 hits
65	SLC4A1	1 hits
66	SYT9	1 hits
67	TNF	1 hits
68	TRH	1 hits
69	VLDLR	1 hits
70	VWF	1 hits

Related Sentences

#	PMID	Sentence
1	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
2	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
3	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
4	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
5	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
6	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
7	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
8	759824	The role of insulin in the regulation of LPL has been well documented.
9	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
10	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
11	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
12	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
13	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
14	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
15	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
16	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
17	759824	The role of insulin in the regulation of LPL has been well documented.
18	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
19	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
20	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
21	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
22	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
23	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
24	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
25	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
26	759824	The role of insulin in the regulation of LPL has been well documented.
27	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
28	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
29	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
30	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
31	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
32	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
33	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
34	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
35	759824	The role of insulin in the regulation of LPL has been well documented.
36	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
37	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
38	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
39	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
40	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
41	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
42	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
43	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
44	759824	The role of insulin in the regulation of LPL has been well documented.
45	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
46	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
47	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
48	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
49	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
50	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
51	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
52	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
53	759824	The role of insulin in the regulation of LPL has been well documented.
54	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
55	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
56	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
57	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
58	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
59	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
60	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
61	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
62	759824	The role of insulin in the regulation of LPL has been well documented.
63	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
64	759824	The function of the hepatic triglyceride lipase (H-TGL) is not yet clear.
65	759824	H-TGL was the lipase activity remaining after inhibition of lipoprotein lipase (LPL) by 1.0 M NaCl.
66	759824	The contributions of H-TGL and LPL to the total plasma triacylglycerol hydrolase (TGH) activity depend on the amount of heparin injected and the time of blood withdrawal after heparin injection.
67	759824	H-TGL was maximally released at higher heparin (50 U/250 g body weight) concentrations, compared to LPL which was maximally released at lower heparin (5 U/250 g body weight) concentrations.
68	759824	H-TGL and H-TGL/total TGH were 9.49 +/- 0.99 and 0.551 +/- 0.071, respectively, in rats 3 days after STZ injection, compared to H-TGL (13.46 +/- 0.69) and H-TGL/total TGH (0.739 +/- 0.052) in control nondiabetic rats.
69	759824	When diabetic rats were treated with insulin, total TGH (14.37 +/- 3.01) and H-TGL (6.77 +/- 4.12) rose to 25.16 +/- 1.02 (total TGH) and 16.49 +/- 1.13 (H-TGL), that were comparable to activities in control nondiabetic rats.
70	759824	Separation of H-TGL and LPL was performed using heparin-Sepharose affinity chromatography of postheparin plasma.
71	759824	The role of insulin in the regulation of LPL has been well documented.
72	759824	Our findings suggest that H-TGL also is under hormonal regulation by insulin in rats.
73	3360217	Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%).
74	3360217	Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera.
75	3360217	Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12).
76	3360217	Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion.
77	3360217	Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.
78	3360217	Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%).
79	3360217	Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera.
80	3360217	Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12).
81	3360217	Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion.
82	3360217	Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.
83	3360217	Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%).
84	3360217	Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera.
85	3360217	Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12).
86	3360217	Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion.
87	3360217	Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.
88	3360217	Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%).
89	3360217	Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera.
90	3360217	Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12).
91	3360217	Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion.
92	3360217	Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.
93	3360217	Eluted from heparin-Sepharose in a barbital buffer containing 6 mg/ml heparin, plasma lipolytic activities in 20 subjects were distributed between hepatic triglyceride lipase (HTGL, mean +/- SE 60.6 +/- 4.6%) and extrahepatic lipoprotein lipase (LPL, 39.4 +/- 4.6%).
94	3360217	Confirmation of the identities of HTGL and LPL was provided by inhibitory antisera.
95	3360217	Both preheparin HTGL and LPL activities correlated with the respective activities measured in plasma obtained 15 min after intravenous injection of heparin (rs = + .774 and + .685, respectively; n = 12).
96	3360217	Evidence for the metabolic regulation of preheparin lipases was provided by measurement of significant increases in LPL and HTGL activities after oral glucose ingestion.
97	3360217	Overall, preheparin plasma HTGL and LPL activities may reflect ongoing lipoprotein lipolytic activity in tissue beds, and because these measurements do not require the administration of intravenous heparin, they should prove useful for additional studies of short-term regulation of the lipases.
98	3396267	Postheparin plasma lipoprotein lipase increased markedly during the exercise period while no change occurred in adipose tissue lipoprotein lipase, hepatic lipase or lecithin:cholesterol acyltransferase.
99	3535412	More physically active persons tend to have lower plasma triglycerides and very low density lipoprotein concentrations, and a greater high-density lipoprotein mass due to higher concentrations of the subfraction HDL2 and apoprotein A-I.
100	3535412	These exercise effects are most likely mediated by alterations in the activity of enzymes involved in the synthesis, transport and catabolism of the various lipoproteins including lipoprotein lipase, hepatic lipase and lecithin: cholesterol acyltransferase.
101	3584394	The activity of lipoprotein lipase (LPL), the enzyme responsible for HDL cholesterol production, and the activity of hepatic triglyceride lipase (HTGL), the enzyme that facilitates the catabolism of HDL, were measured in plasma obtained after iv injection of heparin.
102	3584394	Body weight and insulin requirement correlated directly with HTGL activity and inversely with serum HDL cholesterol levels.
103	3584394	The activity of lipoprotein lipase (LPL), the enzyme responsible for HDL cholesterol production, and the activity of hepatic triglyceride lipase (HTGL), the enzyme that facilitates the catabolism of HDL, were measured in plasma obtained after iv injection of heparin.
104	3584394	Body weight and insulin requirement correlated directly with HTGL activity and inversely with serum HDL cholesterol levels.
105	3883096	Circulating triglyceride is cleared by a combination of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL).
106	3883096	Although LPL has been extensively studied in diabetes, the effect of insulinization on H-TGL activity has not been well characterized.
107	3883096	To determine whether H-TGL activity is altered in insulin-deficient diabetes, postheparin plasma was obtained from eight beagle dogs: three normal (nondiabetic) control dogs and five pancreatectomized diabetic dogs were studied acutely in poor diabetic control (underinsulinized), and again in short-term good control (well insulinized).
108	3883096	Thus, insulin-deficient diabetes in dogs increases H-TGL, and short-term improvement of glycemic control with insulin partially corrects this increase.
109	3883096	Circulating triglyceride is cleared by a combination of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL).
110	3883096	Although LPL has been extensively studied in diabetes, the effect of insulinization on H-TGL activity has not been well characterized.
111	3883096	To determine whether H-TGL activity is altered in insulin-deficient diabetes, postheparin plasma was obtained from eight beagle dogs: three normal (nondiabetic) control dogs and five pancreatectomized diabetic dogs were studied acutely in poor diabetic control (underinsulinized), and again in short-term good control (well insulinized).
112	3883096	Thus, insulin-deficient diabetes in dogs increases H-TGL, and short-term improvement of glycemic control with insulin partially corrects this increase.
113	3883096	Circulating triglyceride is cleared by a combination of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL).
114	3883096	Although LPL has been extensively studied in diabetes, the effect of insulinization on H-TGL activity has not been well characterized.
115	3883096	To determine whether H-TGL activity is altered in insulin-deficient diabetes, postheparin plasma was obtained from eight beagle dogs: three normal (nondiabetic) control dogs and five pancreatectomized diabetic dogs were studied acutely in poor diabetic control (underinsulinized), and again in short-term good control (well insulinized).
116	3883096	Thus, insulin-deficient diabetes in dogs increases H-TGL, and short-term improvement of glycemic control with insulin partially corrects this increase.
117	3883096	Circulating triglyceride is cleared by a combination of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL).
118	3883096	Although LPL has been extensively studied in diabetes, the effect of insulinization on H-TGL activity has not been well characterized.
119	3883096	To determine whether H-TGL activity is altered in insulin-deficient diabetes, postheparin plasma was obtained from eight beagle dogs: three normal (nondiabetic) control dogs and five pancreatectomized diabetic dogs were studied acutely in poor diabetic control (underinsulinized), and again in short-term good control (well insulinized).
120	3883096	Thus, insulin-deficient diabetes in dogs increases H-TGL, and short-term improvement of glycemic control with insulin partially corrects this increase.
121	3889539	The activities of both hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were measured in plasma after intravenous administration of heparin.
122	3889539	Insulin-deficient diabetic rats had normal H-TGL activity.
123	3889539	From these experiments, it is concluded that H-TGL is not an insulin-dependent enzyme.
124	3889539	As far as LPL is concerned, this enzyme was increased in both insulin-treated rats and rats with VMH lesions.
125	3889539	This was consistent with the established fact that insulin has a stimulatory effect on adipose tissue LPL.
126	3889539	The LPL activity in postheparin plasma was not decreased in insulin-deficient rats.
127	3889539	The activities of both hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were measured in plasma after intravenous administration of heparin.
128	3889539	Insulin-deficient diabetic rats had normal H-TGL activity.
129	3889539	From these experiments, it is concluded that H-TGL is not an insulin-dependent enzyme.
130	3889539	As far as LPL is concerned, this enzyme was increased in both insulin-treated rats and rats with VMH lesions.
131	3889539	This was consistent with the established fact that insulin has a stimulatory effect on adipose tissue LPL.
132	3889539	The LPL activity in postheparin plasma was not decreased in insulin-deficient rats.
133	3889539	The activities of both hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were measured in plasma after intravenous administration of heparin.
134	3889539	Insulin-deficient diabetic rats had normal H-TGL activity.
135	3889539	From these experiments, it is concluded that H-TGL is not an insulin-dependent enzyme.
136	3889539	As far as LPL is concerned, this enzyme was increased in both insulin-treated rats and rats with VMH lesions.
137	3889539	This was consistent with the established fact that insulin has a stimulatory effect on adipose tissue LPL.
138	3889539	The LPL activity in postheparin plasma was not decreased in insulin-deficient rats.
139	6384714	Fasting in normal rats produced a fall in hepatic triglyceride lipase (H-TGL) activity as well as lipoprotein lipase (LPL) activities of adipose tissue and psoas minor muscle.
140	6440312	Using a selective immunochemical method, the activities of postheparin plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) were measured in 7 children with newly diagnosed IDDM, 39 on a conventional subcutaneous insulin regimen (CSC), and 11 children receiving continuous subcutaneous infusion of insulin (CSII).
141	6440312	LPL activity was decreased in untreated patients, and insulin treatment resulted in an increase in the LPL activity with a concomitant normalization of serum triglyceride and HDL-cholesterol levels.
142	7084127	The enzymatic activities of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were 14.2 and 1.50 mumoles/ml/hour, respectively.
143	7084127	H-TGL activity was normal, while LPL activity was extremely low compared to those of normal subjects.
144	7084127	However, the serum level of triglyceride was decreased and both H-TGL and LPL activities were increased to 19.3 and 2.7 mumoles/ml/hour, respectively.
145	7084127	The enzymatic activities of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were 14.2 and 1.50 mumoles/ml/hour, respectively.
146	7084127	H-TGL activity was normal, while LPL activity was extremely low compared to those of normal subjects.
147	7084127	However, the serum level of triglyceride was decreased and both H-TGL and LPL activities were increased to 19.3 and 2.7 mumoles/ml/hour, respectively.
148	7084127	The enzymatic activities of hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) were 14.2 and 1.50 mumoles/ml/hour, respectively.
149	7084127	H-TGL activity was normal, while LPL activity was extremely low compared to those of normal subjects.
150	7084127	However, the serum level of triglyceride was decreased and both H-TGL and LPL activities were increased to 19.3 and 2.7 mumoles/ml/hour, respectively.
151	7113604	It is suggested that 1) growth hormone may play some role on the pathogenesis of hyperlipidaemia associated with acromegaly, and 2) growth hormone has an inhibitory effect on H-TGL and LPL, and so hyperlipoproteinaemia in some cases of acromegaly might be caused by low H-TGL or LPL activity resulting from high growth hormone levels.
152	7589821	Loci included the insulin-responsive (GLUT4) glucose transporter, hexokinase 2, glucagon, growth hormone, insulin receptor substrate 1 (IRS1), phosphoenolpyruvate carboxykinase, hepatic and muscle forms of pyruvate kinase, hepatic phosphofructokinase, the apolipoprotein B and the apolipoprotein A2 cluster, lipoprotein lipase, hepatic triglyceride lipase, the very-low-density-lipoprotein receptor, and the Pima insulin resistance locus on chromosome 4.
153	9032097	Effects of multiple daily insulin injections and intraperitoneal insulin therapy on cholesteryl ester transfer and lipoprotein lipase activities in NIDDM.
154	9032097	Although directional changes in lipoprotein lipase (LpL) and hepatic triglyceride lipase (HTGL) similar to those found in IDDM after MDI and IP were observed, they were not statistically significant.
155	9225215	Both hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL) activities in the postheparin plasma were lower in the diabetic rats than in the controls, and the reduction of HTGL activity was greater than that of LPL activity in the diabetic rats.
156	9225215	The HTGL-catalyzed fatty acid (FA) releases from the diabetic VLDL and IDL were lower than those from the normal rat VLDL and IDL, while the LPL-catalyzed FA release in the diabetic rats was not different from those in the controls.
157	9225215	The decreases in LPL and HTGL activities and the markedly impaired susceptibility of IDL to HTGL coincide well with the postheparin changes in plasma lipoproteins in diabetic rats, an increase in IDL and a decrease in LDL.
158	9225215	Both hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL) activities in the postheparin plasma were lower in the diabetic rats than in the controls, and the reduction of HTGL activity was greater than that of LPL activity in the diabetic rats.
159	9225215	The HTGL-catalyzed fatty acid (FA) releases from the diabetic VLDL and IDL were lower than those from the normal rat VLDL and IDL, while the LPL-catalyzed FA release in the diabetic rats was not different from those in the controls.
160	9225215	The decreases in LPL and HTGL activities and the markedly impaired susceptibility of IDL to HTGL coincide well with the postheparin changes in plasma lipoproteins in diabetic rats, an increase in IDL and a decrease in LDL.
161	9225215	Both hepatic triglyceride lipase (HTGL) and lipoprotein lipase (LPL) activities in the postheparin plasma were lower in the diabetic rats than in the controls, and the reduction of HTGL activity was greater than that of LPL activity in the diabetic rats.
162	9225215	The HTGL-catalyzed fatty acid (FA) releases from the diabetic VLDL and IDL were lower than those from the normal rat VLDL and IDL, while the LPL-catalyzed FA release in the diabetic rats was not different from those in the controls.
163	9225215	The decreases in LPL and HTGL activities and the markedly impaired susceptibility of IDL to HTGL coincide well with the postheparin changes in plasma lipoproteins in diabetic rats, an increase in IDL and a decrease in LDL.
164	9326333	Using both parametric and nonparametric methods, we found no evidence of linkage of obesity to any of nine candidate genes/regions, including the Prader-Willi chromosomal region (PWS), the human homologue of the mouse agouti gene (ASP), and the genes for leptin (OB), the leptin receptor (OBR/DB), the beta3-adrenergic receptor (ADRB3), lipoprotein lipase (LPL), hepatic lipase (LIPC), glycogen synthase (GYS), and tumor necrosis factor alpha (TNFA).
165	9720257	Combined lipase deficiency (cld/cld) in mice affects differently post-translational processing of lipoprotein lipase, hepatic lipase and pancreatic lipase.
166	9720257	Lipoprotein lipase (LPL) and hepatic lipase (HL), which act on plasma lipoproteins, belong to the same gene family as pancreatic lipase.
167	9720257	Cld/cld mice have very low LPL and HL activities (< 5% of normal), yet normal pancreatic lipase activity.
168	9720257	Our findings indicate that LPL, HL and pancreatic lipase, although closely related, are processed differently.
169	9878681	While a few genes have been identified whose mutant alleles have large effects on this trait (e.g., LDLR, familial defective apoB-100), variability in cholesterol levels among individuals in most families is influenced by allelic variation in many genes (polymorphisms) as well as environmental exposures.
170	9878681	High density lipoprotein cholesterol levels are genetically influenced and are related to apoA1 and hepatic lipase (LIPC) gene functions.
171	9878681	Mutations in the apoA1 gene are rare and there are data which suggest a role of allelic variation at or linked LIPC gene in high density lipoprotein cholesterol levels.
172	9878681	While a few genes have been identified whose mutant alleles have large effects on this trait (e.g., LDLR, familial defective apoB-100), variability in cholesterol levels among individuals in most families is influenced by allelic variation in many genes (polymorphisms) as well as environmental exposures.
173	9878681	High density lipoprotein cholesterol levels are genetically influenced and are related to apoA1 and hepatic lipase (LIPC) gene functions.
174	9878681	Mutations in the apoA1 gene are rare and there are data which suggest a role of allelic variation at or linked LIPC gene in high density lipoprotein cholesterol levels.
175	11279518	Tcf1-/- liver has decreased expression of the basolateral membrane bile acid transporters Slc10a1, Slc21a3 and Slc21a5, leading to impaired portal bile acid uptake and elevated plasma bile acid concentrations.
176	11279518	In intestine and kidneys, Tcf1-/- mice lack expression of the ileal bile acid transporter (Slc10a2), resulting in increased fecal and urinary bile acid excretion.
177	11279518	The Tcf1 protein (also known as HNF-1alpha) also regulates transcription of the gene (Nr1h4) encoding the farnesoid X receptor-1 (Fxr-1), thereby leading to reduced expression of small heterodimer partner-1 (Shp-1) and repression of Cyp7a1, the rate-limiting enzyme in the classic bile acid biosynthesis pathway.
178	11279518	This is most likely due to reduced activity of the HDL-catabolic enzyme hepatic lipase (Lipc) and increased expression of HDL-cholesterol esterifying enzyme lecithin:cholesterol acyl transferase (Lcat).
179	11279518	Our studies demonstrate that Tcf1, in addition to being an important regulator of insulin secretion, is an essential transcriptional regulator of bile acid and HDL-cholesterol metabolism.
180	11512679	We found differences between the two subpopulations in the allele frequencies of several candidate genes, including APOE, LIPC, APOC3, PON1, PON2, and PPP1R3.
181	11916946	This study examined the relation between the LIPC-480C>T and CAC in type 1 diabetes.
182	12762846	We used a novel combination of expression data from a TCF1 knockout mouse (TCF1 codes for the transcription factor HNF1a), and human and mouse genome sequences, to search 2kb upstream of 28 genes downregulated in TCF1 null mice compared to wild type mice.
183	12762846	This identified 8 genes as candidates for being directly regulated by HNF1a: LIPC, CRP, F13B, PRODH2, HSD17B2, SCL7A9, SLC16A7, PAH.
184	12762846	For comparison we also examined 25 genes up-regulated in TCF1 null mice; only one gene was selected and there was little evidence for conservation of this putative binding site between human and mouse.
185	15156410	Association of the -514C-->T polymorphism in the hepatic lipase gene (LIPC) promoter with elevated fasting insulin concentrations, but not insulin resistance, in non-diabetic Germans.
186	15949705	Interaction between insulin (VNTR) and hepatic lipase (LIPC-514C>T) variants on the response to an oral glucose tolerance test in the EARSII group of young healthy men.
187	15949705	We have shown that variations in APOC3-482T>C and hepatic lipase (LIPC)-514C>T), individually (APOC3 alone) and interactively, modulate insulin and glucose levels after an OGTT in young healthy men participating in the European Atherosclerosis Research Study II (EARSII).
188	15949705	Variation in the insulin gene (INS) variable number tandem repeat (VNTR) has been found to predispose to type 1 and type 2 diabetes.
189	15949705	We tested for gene:gene interaction between the INS VNTR and both the LIPC-514C>T and APOC3-482T>C.
190	15949705	While there was a significant interaction between INS VNTR and LIPC-514C>T on AUC glucose (P=0.013) and on AUC insulin (P=0.015), there was no interaction with APOC3-482T>C.
191	15949705	Interaction between insulin (VNTR) and hepatic lipase (LIPC-514C>T) variants on the response to an oral glucose tolerance test in the EARSII group of young healthy men.
192	15949705	We have shown that variations in APOC3-482T>C and hepatic lipase (LIPC)-514C>T), individually (APOC3 alone) and interactively, modulate insulin and glucose levels after an OGTT in young healthy men participating in the European Atherosclerosis Research Study II (EARSII).
193	15949705	Variation in the insulin gene (INS) variable number tandem repeat (VNTR) has been found to predispose to type 1 and type 2 diabetes.
194	15949705	We tested for gene:gene interaction between the INS VNTR and both the LIPC-514C>T and APOC3-482T>C.
195	15949705	While there was a significant interaction between INS VNTR and LIPC-514C>T on AUC glucose (P=0.013) and on AUC insulin (P=0.015), there was no interaction with APOC3-482T>C.
196	15949705	Interaction between insulin (VNTR) and hepatic lipase (LIPC-514C>T) variants on the response to an oral glucose tolerance test in the EARSII group of young healthy men.
197	15949705	We have shown that variations in APOC3-482T>C and hepatic lipase (LIPC)-514C>T), individually (APOC3 alone) and interactively, modulate insulin and glucose levels after an OGTT in young healthy men participating in the European Atherosclerosis Research Study II (EARSII).
198	15949705	Variation in the insulin gene (INS) variable number tandem repeat (VNTR) has been found to predispose to type 1 and type 2 diabetes.
199	15949705	We tested for gene:gene interaction between the INS VNTR and both the LIPC-514C>T and APOC3-482T>C.
200	15949705	While there was a significant interaction between INS VNTR and LIPC-514C>T on AUC glucose (P=0.013) and on AUC insulin (P=0.015), there was no interaction with APOC3-482T>C.
201	15949705	Interaction between insulin (VNTR) and hepatic lipase (LIPC-514C>T) variants on the response to an oral glucose tolerance test in the EARSII group of young healthy men.
202	15949705	We have shown that variations in APOC3-482T>C and hepatic lipase (LIPC)-514C>T), individually (APOC3 alone) and interactively, modulate insulin and glucose levels after an OGTT in young healthy men participating in the European Atherosclerosis Research Study II (EARSII).
203	15949705	Variation in the insulin gene (INS) variable number tandem repeat (VNTR) has been found to predispose to type 1 and type 2 diabetes.
204	15949705	We tested for gene:gene interaction between the INS VNTR and both the LIPC-514C>T and APOC3-482T>C.
205	15949705	While there was a significant interaction between INS VNTR and LIPC-514C>T on AUC glucose (P=0.013) and on AUC insulin (P=0.015), there was no interaction with APOC3-482T>C.
206	15983229	We investigated the associations between the hepatic lipase gene (LIPC) -514C>T polymorphism and lipases, lipoproteins, and insulin sensitivity (Si) responses to exercise training.
207	15983229	Black CC homozygotes had lower baseline lipoprotein lipase activity, HDL cholesterol, HDL3, and apolipoprotein (apo)A-1 concentrations.
208	15983229	White CC homozygotes had lower baseline HDL cholesterol, apoA-1, LDL cholesterol, and apoB levels that remained low post-exercise training.
209	16343038	To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes.
210	16343038	The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02).
211	16343038	Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02).
212	16343038	In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance.
213	16343038	The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome.
214	16534522	The hormone-sensitive lipase C-60G promoter polymorphism is associated with increased waist circumference in normal-weight subjects.
215	17061453	Fish proteins effect compared with casein was determined on triacylglycerols (TG) metabolism and activities of hepatic triacylglycerol lipase (HTGL) and tissue lipoprotein lipases (LPL), in SHR and diabetic SHR.
216	17137217	Analyses of covariance adjusting for age, body mass index, hyperlipidemia, diabetes, smoking, drinking, and antihypertensive medication revealed that 17 polymorphisms in 16 genes (APOB, CAST, CLCNKB, CTNS, GHR, GYS1, HF1, IKBKAP, KCNJ11, LIPC, LPL, P2RY2, PON2, SLC4A1, TRH, VWF) were significantly associated with blood pressure variations.
217	17137217	Multivariate logistic regression analysis with adjustment for the same factors revealed that 11 polymorphisms in 11 genes (CAST, CTLA4, F5, GC, GHR, LIPC, PLA2G7, SLC4A1, SLCI8A1, TRH, VWF) showed significant associations with hypertension.
218	17137217	Five polymorphisms in five genes, CAST(calpastatin), LIPC (hepatic lipase), SLC4A1 (band 3 anion transporter), TRH (thyrotropin-releasing hormone), and VWF (von Willebrand factor), were significantly associated with both blood pressure variation and hypertension.
219	17137217	Analyses of covariance adjusting for age, body mass index, hyperlipidemia, diabetes, smoking, drinking, and antihypertensive medication revealed that 17 polymorphisms in 16 genes (APOB, CAST, CLCNKB, CTNS, GHR, GYS1, HF1, IKBKAP, KCNJ11, LIPC, LPL, P2RY2, PON2, SLC4A1, TRH, VWF) were significantly associated with blood pressure variations.
220	17137217	Multivariate logistic regression analysis with adjustment for the same factors revealed that 11 polymorphisms in 11 genes (CAST, CTLA4, F5, GC, GHR, LIPC, PLA2G7, SLC4A1, SLCI8A1, TRH, VWF) showed significant associations with hypertension.
221	17137217	Five polymorphisms in five genes, CAST(calpastatin), LIPC (hepatic lipase), SLC4A1 (band 3 anion transporter), TRH (thyrotropin-releasing hormone), and VWF (von Willebrand factor), were significantly associated with both blood pressure variation and hypertension.
222	17137217	Analyses of covariance adjusting for age, body mass index, hyperlipidemia, diabetes, smoking, drinking, and antihypertensive medication revealed that 17 polymorphisms in 16 genes (APOB, CAST, CLCNKB, CTNS, GHR, GYS1, HF1, IKBKAP, KCNJ11, LIPC, LPL, P2RY2, PON2, SLC4A1, TRH, VWF) were significantly associated with blood pressure variations.
223	17137217	Multivariate logistic regression analysis with adjustment for the same factors revealed that 11 polymorphisms in 11 genes (CAST, CTLA4, F5, GC, GHR, LIPC, PLA2G7, SLC4A1, SLCI8A1, TRH, VWF) showed significant associations with hypertension.
224	17137217	Five polymorphisms in five genes, CAST(calpastatin), LIPC (hepatic lipase), SLC4A1 (band 3 anion transporter), TRH (thyrotropin-releasing hormone), and VWF (von Willebrand factor), were significantly associated with both blood pressure variation and hypertension.
225	17705891	The postprandial lipid response has been shown to be modified by polymorphisms within the genes for apo A-I, A-IV, A-V, E, B, C-I and C-III, lipoprotein lipase, hepatic lipase, fatty acid binding and transport proteins, microsomal triglyceride transfer protein and scavenger receptor class B type I.
226	18193043	Overall, we identify strongly associated variants in eleven loci previously implicated in lipid metabolism (ABCA1, the APOA5-APOA4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in several newly identified loci (near MVK-MMAB and GALNT2, with variants primarily associated with high-density lipoprotein (HDL) cholesterol; near SORT1, with variants primarily associated with low-density lipoprotein (LDL) cholesterol; near TRIB1, MLXIPL and ANGPTL3, with variants primarily associated with triglycerides; and a locus encompassing several genes near NCAN, with variants strongly associated with both triglycerides and LDL cholesterol).
227	18436977	The effects of dietary n-3 polyunsaturated fatty acids on lipoprotein concentrations and on lipoprotein lipase (LPL), hepatic triglyceride lipase (HTGL) and lecithin cholesterol acyltransferase (LCAT) activities were studied in streptozotocin-induced diabetic rats during pregnancy and in their macrosomic offspring from birth to adulthood.
228	18436977	HTGL activity was high while LPL and LCAT activities were low in these rats.
229	18436977	It also restores LPL, HTGL and LCAT activities to normal range.
230	18436977	The effects of dietary n-3 polyunsaturated fatty acids on lipoprotein concentrations and on lipoprotein lipase (LPL), hepatic triglyceride lipase (HTGL) and lecithin cholesterol acyltransferase (LCAT) activities were studied in streptozotocin-induced diabetic rats during pregnancy and in their macrosomic offspring from birth to adulthood.
231	18436977	HTGL activity was high while LPL and LCAT activities were low in these rats.
232	18436977	It also restores LPL, HTGL and LCAT activities to normal range.
233	18436977	The effects of dietary n-3 polyunsaturated fatty acids on lipoprotein concentrations and on lipoprotein lipase (LPL), hepatic triglyceride lipase (HTGL) and lecithin cholesterol acyltransferase (LCAT) activities were studied in streptozotocin-induced diabetic rats during pregnancy and in their macrosomic offspring from birth to adulthood.
234	18436977	HTGL activity was high while LPL and LCAT activities were low in these rats.
235	18436977	It also restores LPL, HTGL and LCAT activities to normal range.
236	20450981	After sacrifice, using the quantitative real-time PCR, we assayed the transcription levels of the HMG-CoA reductase (Hmgcr) for cholesterol biosynthesis, monoacylglycerol O-acyltransferase 1 (Mogat1) as TG synthetase, hepatic triglyceride lipase (Lipc) and lipoprotein lipase (Lpl) as triglycerides (TG) reductase in the liver.
237	20450981	Hmgcr and Mogat1 RNA expression levels were reduced in the livers and those of Tkt were increased in the kidney of BPS treated rats compared with those in untreated rats.
238	22359512	After a correction for multiple comparisons (P-value<2.2×10(-9)), we observed four novel loci significantly associated with phospholipids (PAQR9, AGPAT1, PKD2L1, PDXDC1) and two with sphingolipids (PLD2 and APOE) explaining up to 3.1% of the variance.
239	22359512	Further analysis of the top findings with respect to within class molar proportions uncovered three additional loci for phospholipids (PNLIPRP2, PCDH20, and ABDH3) suggesting their involvement in either fatty acid elongation/saturation processes or fatty acid specific turnover mechanisms.
240	22359512	Among those, 14 loci (KCNH7, AGPAT1, PNLIPRP2, SYT9, FADS1-2-3, DLG2, APOA1, ELOVL2, CDK17, LIPC, PDXDC1, PLD2, LASS4, and APOE) mapped into the glycerophospholipid and 12 loci (ILKAP, ITGA9, AGPAT1, FADS1-2-3, APOA1, PCDH20, LIPC, PDXDC1, SGPP1, APOE, LASS4, and PLD2) to the sphingolipid pathways.