Ignet

Gene Information

Gene symbol: APOC3

Gene name: apolipoprotein C-III

HGNC ID: 610

Related Genes

#	Gene Symbol	Number of hits
1	ABCA1	1 hits
2	AKT1	1 hits
3	ALDOB	1 hits
4	APOA4	1 hits
5	APOA5	1 hits
6	APOB	1 hits
7	APOC2	1 hits
8	APOE	1 hits
9	CAV1	1 hits
10	CETP	1 hits
11	CYBA	1 hits
12	FABP1	1 hits
13	FABP2	1 hits
14	FABP4	1 hits
15	FOXO1	1 hits
16	GJA4	1 hits
17	HBB	1 hits
18	HNF1A	1 hits
19	HNF4A	1 hits
20	HSD11B1	1 hits
21	IL1B	1 hits
22	INS	1 hits
23	JUN	1 hits
24	LIPC	1 hits
25	LPAL2	1 hits
26	LPL	1 hits
27	MAPK1	1 hits
28	MTTP	1 hits
29	NFKB1	1 hits
30	NOX5	1 hits
31	NR0B2	1 hits
32	NR1H4	1 hits
33	PCK2	1 hits
34	PIK3CA	1 hits
35	PKLR	1 hits
36	PLA2G7	1 hits
37	PON1	1 hits
38	PON2	1 hits
39	PPARA	1 hits
40	PPP1R3A	1 hits
41	SCARB1	1 hits
42	SLC2A2	1 hits
43	SLC2A4	1 hits
44	SLC37A4	1 hits
45	SREBF1	1 hits
46	SST	1 hits
47	TNF	1 hits
48	VLDLR	1 hits

Related Sentences

#	PMID	Sentence
1	3128878	Plasma apolipoprotein C-III levels in children with type I diabetes.
2	7106445	Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia.
3	7106445	The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations.
4	7106445	Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments.
5	7106445	A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides.
6	7106445	In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal.
7	7106445	Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia.
8	7106445	The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations.
9	7106445	Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments.
10	7106445	A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides.
11	7106445	In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal.
12	7106445	Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia.
13	7106445	The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations.
14	7106445	Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments.
15	7106445	A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides.
16	7106445	In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal.
17	9768372	Acarbose inhibited the postprandial decline of apolipoprotein C-II, and decreased the postprandial serum apolipoprotein C-III level.
18	9932215	Apolipoprotein CIII (ApoCIII) appears to play a key role in triglyceride-rich lipoprotein (TRL) metabolism.
19	9932215	Overexpression of the human ApoCIII gene in transgenic animals results in hypertriglyceridaemia, which can be corrected by overexpression of the ApoE gene.
20	9932215	ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants.
21	9932215	There appears to be an interaction between ApoCIII and ApoE at the surface of the lipoprotein.
22	9932215	Our recent study of ApoCIII levels in TRL and intermediate-density lipoprotein isolated from hyperlipidaemic Type III and IV individuals confirmed the importance of the ApoCIII/ApoE ratio in these lipoproteins.
23	9932215	Apolipoprotein CIII (ApoCIII) appears to play a key role in triglyceride-rich lipoprotein (TRL) metabolism.
24	9932215	Overexpression of the human ApoCIII gene in transgenic animals results in hypertriglyceridaemia, which can be corrected by overexpression of the ApoE gene.
25	9932215	ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants.
26	9932215	There appears to be an interaction between ApoCIII and ApoE at the surface of the lipoprotein.
27	9932215	Our recent study of ApoCIII levels in TRL and intermediate-density lipoprotein isolated from hyperlipidaemic Type III and IV individuals confirmed the importance of the ApoCIII/ApoE ratio in these lipoproteins.
28	9932215	Apolipoprotein CIII (ApoCIII) appears to play a key role in triglyceride-rich lipoprotein (TRL) metabolism.
29	9932215	Overexpression of the human ApoCIII gene in transgenic animals results in hypertriglyceridaemia, which can be corrected by overexpression of the ApoE gene.
30	9932215	ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants.
31	9932215	There appears to be an interaction between ApoCIII and ApoE at the surface of the lipoprotein.
32	9932215	Our recent study of ApoCIII levels in TRL and intermediate-density lipoprotein isolated from hyperlipidaemic Type III and IV individuals confirmed the importance of the ApoCIII/ApoE ratio in these lipoproteins.
33	9932215	Apolipoprotein CIII (ApoCIII) appears to play a key role in triglyceride-rich lipoprotein (TRL) metabolism.
34	9932215	Overexpression of the human ApoCIII gene in transgenic animals results in hypertriglyceridaemia, which can be corrected by overexpression of the ApoE gene.
35	9932215	ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants.
36	9932215	There appears to be an interaction between ApoCIII and ApoE at the surface of the lipoprotein.
37	9932215	Our recent study of ApoCIII levels in TRL and intermediate-density lipoprotein isolated from hyperlipidaemic Type III and IV individuals confirmed the importance of the ApoCIII/ApoE ratio in these lipoproteins.
38	9932215	Apolipoprotein CIII (ApoCIII) appears to play a key role in triglyceride-rich lipoprotein (TRL) metabolism.
39	9932215	Overexpression of the human ApoCIII gene in transgenic animals results in hypertriglyceridaemia, which can be corrected by overexpression of the ApoE gene.
40	9932215	ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants.
41	9932215	There appears to be an interaction between ApoCIII and ApoE at the surface of the lipoprotein.
42	9932215	Our recent study of ApoCIII levels in TRL and intermediate-density lipoprotein isolated from hyperlipidaemic Type III and IV individuals confirmed the importance of the ApoCIII/ApoE ratio in these lipoproteins.
43	10198561	[Gender differences and diabetic status in the relationship of blood apolipoprotein C-III, free fatty acids and triglycerides in subjects at risk for glucose intolerance].
44	10198561	Conversely, apolipoprotein C-III (apoC-III) is an inhibitor of the catabolism of TG-rich lipoproteins.
45	10198561	[Gender differences and diabetic status in the relationship of blood apolipoprotein C-III, free fatty acids and triglycerides in subjects at risk for glucose intolerance].
46	10198561	Conversely, apolipoprotein C-III (apoC-III) is an inhibitor of the catabolism of TG-rich lipoproteins.
47	11123853	PPAR alpha activated by fibric acids form heterodimers with the 9-cis retinoic acid receptor (RXR).
48	11123853	Furthermore, they decrease triglycerides by increasing lipoprotein lipase gene expression and by decreasing apolipoprotein C-III gene expression.
49	11123853	Fibric acids increase high-density lipoprotein (HDL) cholesterol partly by increasing apolipoprotein A-I and apolipoprotein A-II gene expression.
50	11423471	Mutations in the HNF4alpha gene are responsible for type 1 maturity-onset diabetes of the young (MODY1), which is characterized by a defect in insulin secretion.
51	11423471	Recent evidence has implicated AMP-activated protein kinase (AMPK) in the modulation of both insulin secretion by pancreatic beta-cells and the control of glucose-dependent gene expression in both hepatocytes and beta-cells.
52	11423471	Therefore, the question could be raised as to whether AMPK plays a role in these processes by modulating HNF-4alpha function.
53	11423471	In this study, we show that activation of AMPK by 5-amino-4-imidazolecarboxamide riboside (AICAR) in hepatocytes greatly diminished HNF-4alpha protein levels and consequently downregulates the expression of HNF-4alpha target genes.
54	11423471	Quantitative evaluation of HNF-4alpha target gene expression revealed diminished mRNA levels for HNF-1alpha, GLUT2, L-type pyruvate kinase, aldolase B, apolipoprotein (apo)-B, and apoCIII.
55	11423471	Our data clearly demonstrate that the MODY1/HNF-4alpha transcription factor is a novel target of AMPK in hepatocytes.
56	11423471	Accordingly, it can be suggested that in pancreatic beta-cells, AMPK also acts by decreasing HNF-4alpha protein level, and therefore insulin secretion.
57	11474486	Fibrates bind to the peroxisome proliferator-activated receptor (PPAR)-alpha, and thiazolidinediones are ligands of PPAR-gamma.
58	11474486	To elucidate the target genes regulated by these compounds, we treated Zucker diabetic fatty rats (ZDF) for 15 days with a PPAR-alpha-specific compound, fenofibrate, a PPAR-gamma-specific ligand, rosiglitazone, and a PPAR-alpha/-gamma coagonist, GW2331, and measured the levels of several messenger RNAs (mRNAs) in liver by real-time polymerase chain reaction.
59	11474486	Fenofibrate and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs.
60	11474486	Rosiglitazone modestly increased apolipoprotein C-III mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of glucose transporter 4 and phosphoenolpyruvate carboxykinase in adipose tissue.
61	11474486	We identified a novel target in liver, mitogen-activated phosphokinase phosphatase 1, whose down-regulation by PPAR-alpha agonists may improve insulin sensitivity in that tissue by prolonging insulin responses.
62	11474486	The results of these studies suggest that activation of PPAR-alpha as well as PPAR-gamma in therapy for type 2 diabetes will enhance glucose and triglyceride control by combining actions in hepatic and peripheral tissues.
63	11474486	Fibrates bind to the peroxisome proliferator-activated receptor (PPAR)-alpha, and thiazolidinediones are ligands of PPAR-gamma.
64	11474486	To elucidate the target genes regulated by these compounds, we treated Zucker diabetic fatty rats (ZDF) for 15 days with a PPAR-alpha-specific compound, fenofibrate, a PPAR-gamma-specific ligand, rosiglitazone, and a PPAR-alpha/-gamma coagonist, GW2331, and measured the levels of several messenger RNAs (mRNAs) in liver by real-time polymerase chain reaction.
65	11474486	Fenofibrate and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs.
66	11474486	Rosiglitazone modestly increased apolipoprotein C-III mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of glucose transporter 4 and phosphoenolpyruvate carboxykinase in adipose tissue.
67	11474486	We identified a novel target in liver, mitogen-activated phosphokinase phosphatase 1, whose down-regulation by PPAR-alpha agonists may improve insulin sensitivity in that tissue by prolonging insulin responses.
68	11474486	The results of these studies suggest that activation of PPAR-alpha as well as PPAR-gamma in therapy for type 2 diabetes will enhance glucose and triglyceride control by combining actions in hepatic and peripheral tissues.
69	11512679	We found differences between the two subpopulations in the allele frequencies of several candidate genes, including APOE, LIPC, APOC3, PON1, PON2, and PPP1R3.
70	11900401	They enhance lipoprotein lipase, apoAI and apoAII transcription and reduce that of apoCIII.
71	12048138	Three polymorphisms in the peroxisome proliferator activated receptor alpha (PPARalpha) gene were investigated (L162V, G>A in intron 2 and G>C in intron 7), two in the apolipoprotein CIII (APOC3) gene (-482C>T and -455T>C) and one in the beta-fibrinogen (FIBB) gene (-455G>A).
72	12118856	Apolipoprotein C-III and E polymorphisms and cardiovascular syndrome, hyperlipidemia, and insulin resistance in renal transplantation.
73	12118856	In the general population, the S2 allelic variant of the apoprotein (apo) C-III gene has been associated with hypertriglyceridemia and an insulin resistant state, whereas the E4 allele of the apo E has been associated with hypercholesterolemia and atherosclerosis.
74	12606523	The metabolic syndrome is characterized by insulin resistance and abnormal apolipoprotein AI (apoAI) and apolipoprotein B-100 (apoB) metabolism that may collectively accelerate atherosclerosis.
75	12606523	Both agents significantly lowered plasma triglycerides and apoCIII concentrations, but only atorvastatin significantly lowered (P < 0.001) plasma cholesteryl ester transfer protein activity.
76	12679979	The findings in the diabetic patients corresponded to those in non-diabetic patients with renal failure, but diabetic patients have higher apolipoprotein C-III and apolipoprotein E concentrations.
77	12818412	High apoCIII concentration in apoB lipoproteins is a prominent component of atherogenic dyslipidemia, and explains the risk of coronary heart disease (CHD) associated with high triglyceride (TG).
78	12818412	Using immunoaffinity chromatography and ultracentrifugation, we prepared large and small VLDL, IDL and LDL with or without apoCIII or apoE.
79	12818412	High apoCIII concentration in apoB lipoproteins is a prominent component of atherogenic dyslipidemia, and explains the risk of coronary heart disease (CHD) associated with high triglyceride (TG).
80	12818412	Using immunoaffinity chromatography and ultracentrifugation, we prepared large and small VLDL, IDL and LDL with or without apoCIII or apoE.
81	14709372	Multivariate logistic regression analysis with adjustment for age, body mass index, and the prevalence of smoking, hypertension, diabetes mellitus, and hyperuricemia revealed that three polymorphisms [994G --> T (Val279Phe) in the platelet-activating factor acetylhydrolase gene, 242C --> T (His72Tyr) in the NADH/NADPH oxidase p22 phox gene, and 1100C --> T in the apolipoprotein C-III gene] were significantly associated with CAD in men with hypercholesterolemia.
82	14978155	As renal function fails, many patients become progressively malnourished, as evidenced by reduced levels of albumin, prealbumin, and transferrin.
83	14978155	Malnourished patients have increased levels of C reactive protein (CRP), interleukin-6 (IL-6), and concomitant cardiovascular disease when they reach end stage.
84	14978155	Apolipoprotein C III (apo C III), a competitive inhibitor of lipoprotein lipase is increased in CKD.
85	15047603	FXR expression was decreased in livers of streptozotocin-induced diabetic rats and normalized upon insulin supplementation.
86	15047603	In primary rat hepatocytes, D-glucose increased FXR mRNA in a dose- and time-dependent manner, whereas insulin counteracted this effect.
87	15047603	Finally, expression of the FXR target genes, SHP and apolipoprotein C-III, were additively regulated by D-glucose and FXR ligands.
88	15047603	Dysregulation of FXR expression may contribute to alterations in lipid and bile acid metabolism in patients with diabetes or insulin resistance.
89	15059615	Multivariate logistic regression analysis with adjustment for age, body mass index, and the prevalence of smoking, hypertension, hypercholesterolemia, and hyperuricemia revealed that the following polymorphisms were significantly (P < 0.005) associated with CAD: the 1019C -->T of the connexin 37 gene for men with type 2 diabetes; the 2445G -->A in the fatty acid-binding protein 2 gene for women with this condition; the -863C-->A in the tumor necrosis factor-alpha gene, the -219G-->T in the apolipoprotein E gene, the 1019C-->T in the connexin 37 gene for men without type 2 diabetes; and the -482C-->T in the apolipoprotein C-III gene for women without this condition.
90	15161788	Atorvastatin decreases apolipoprotein C-III in apolipoprotein B-containing lipoprotein and HDL in type 2 diabetes: a potential mechanism to lower plasma triglycerides.
91	15210953	We now demonstrate that apolipoprotein CIII (apoCIII) is increased in serum from T1D patients and that this serum factor both induces increased cytoplasmic free intracellular Ca(2+) concentration ([Ca(2+)](i)) and beta cell death.
92	15364160	Association of serum apolipoprotein C III levels and apolipoprotein C III gene Sst I polymorphism with carotid intima-media thickness in Chinese type 2 diabetic patients.
93	15364160	Apolipoprotein C III (apo C III) plays a central role in regulating plasma metabolism of triglyceride-rich lipoprotein (TRL).
94	15364160	Association of serum apolipoprotein C III levels and apolipoprotein C III gene Sst I polymorphism with carotid intima-media thickness in Chinese type 2 diabetic patients.
95	15364160	Apolipoprotein C III (apo C III) plays a central role in regulating plasma metabolism of triglyceride-rich lipoprotein (TRL).
96	15375785	Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses.
97	15375785	Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear.
98	15375785	Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c).
99	15375785	Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses.
100	15375785	Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses.
101	15375785	Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear.
102	15375785	Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c).
103	15375785	Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses.
104	15375785	Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses.
105	15375785	Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear.
106	15375785	Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c).
107	15375785	Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses.
108	15375785	Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses.
109	15375785	Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear.
110	15375785	Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c).
111	15375785	Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses.
112	15585206	This study was aimed to examine cholesteryl ester transfer protein (CETP), apolipoprotein AI and CIII gene polymorphisms, and to verify whether these genetic determinants are associated with the prevalence of myocardial infarction (MI) or type 2 diabetes.
113	15585206	The TaqIB restriction fragment length polymorphism (RFLP) in intron I of the CETP gene, the MspI in the third intron of the APOAI gene, and also SstI in the 3' untranslated region of the APOCIII gene were determined using standard methods.
114	15585206	Therefore, among these genetic polymorphisms, TaqIB of CETP and MspI of apolipoprotein AI appeared to help significantly to identify diabetic individuals.
115	15598690	Polymorphisms in the fatty acid-binding protein 2 and apolipoprotein C-III genes are associated with the metabolic syndrome and dyslipidemia in a South Indian population.
116	15598690	The Ala54Thr polymorphism in the fatty acid-binding protein 2 (FABP2) gene as well as the T-455C and C-482T polymorphisms in the apolipoprotein C-III (APOC3) gene promoter have been associated with features of the MS in specific populations.
117	15598690	Allelic frequencies in 70 controls and 110 patients with diabetes from the Chennai Urban Population Study were 52.9% for FABP2 Thr54, 73.0% for APOC3 -482T, and 80.2% for APOC3 -455C.
118	15598690	Polymorphisms in the fatty acid-binding protein 2 and apolipoprotein C-III genes are associated with the metabolic syndrome and dyslipidemia in a South Indian population.
119	15598690	The Ala54Thr polymorphism in the fatty acid-binding protein 2 (FABP2) gene as well as the T-455C and C-482T polymorphisms in the apolipoprotein C-III (APOC3) gene promoter have been associated with features of the MS in specific populations.
120	15598690	Allelic frequencies in 70 controls and 110 patients with diabetes from the Chennai Urban Population Study were 52.9% for FABP2 Thr54, 73.0% for APOC3 -482T, and 80.2% for APOC3 -455C.
121	15598690	Polymorphisms in the fatty acid-binding protein 2 and apolipoprotein C-III genes are associated with the metabolic syndrome and dyslipidemia in a South Indian population.
122	15598690	The Ala54Thr polymorphism in the fatty acid-binding protein 2 (FABP2) gene as well as the T-455C and C-482T polymorphisms in the apolipoprotein C-III (APOC3) gene promoter have been associated with features of the MS in specific populations.
123	15598690	Allelic frequencies in 70 controls and 110 patients with diabetes from the Chennai Urban Population Study were 52.9% for FABP2 Thr54, 73.0% for APOC3 -482T, and 80.2% for APOC3 -455C.
124	15642486	Apolipoprotein C-III protein concentrations and gene polymorphisms in Type 1 diabetes: associations with microvascular disease complications in the DCCT/EDIC cohort.
125	15715433	Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population.
126	15715433	Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG).
127	15715433	The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population.
128	15715433	The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals.
129	15715433	Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population.
130	15715433	Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG).
131	15715433	The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population.
132	15715433	The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals.
133	15715433	Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population.
134	15715433	Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG).
135	15715433	The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population.
136	15715433	The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals.
137	15734841	Apolipoprotein C3 deficiency results in diet-induced obesity and aggravated insulin resistance in mice.
138	15734841	Our aim was to study whether the absence of apolipoprotein (apo) C3, a strong inhibitor of lipoprotein lipase (LPL), accelerates the development of obesity and consequently insulin resistance.
139	15734841	LPL-independent uptake of albumin-bound fatty acids did not differ.
140	15734841	Absence of apoC3, the natural LPL inhibitor, enhances fatty acid uptake from plasma triglycerides in adipose tissue, which leads to higher susceptibility to diet-induced obesity followed by more severe development of insulin resistance.
141	15734841	Therefore, apoC3 is a potential target for treatment of obesity and insulin resistance.
142	15734841	Apolipoprotein C3 deficiency results in diet-induced obesity and aggravated insulin resistance in mice.
143	15734841	Our aim was to study whether the absence of apolipoprotein (apo) C3, a strong inhibitor of lipoprotein lipase (LPL), accelerates the development of obesity and consequently insulin resistance.
144	15734841	LPL-independent uptake of albumin-bound fatty acids did not differ.
145	15734841	Absence of apoC3, the natural LPL inhibitor, enhances fatty acid uptake from plasma triglycerides in adipose tissue, which leads to higher susceptibility to diet-induced obesity followed by more severe development of insulin resistance.
146	15734841	Therefore, apoC3 is a potential target for treatment of obesity and insulin resistance.
147	15735069	Polyunsaturated fatty acids interact with the PPARA-L162V polymorphism to affect plasma triglyceride and apolipoprotein C-III concentrations in the Framingham Heart Study.
148	15735069	We found significant gene-nutrient interactions between the L162V polymorphism and total PUFA intake, which modulated plasma triglycerides (TG; P < 0.05) and apolipoprotein C-III (apoC-III; P < 0.05) concentrations.
149	15735069	Polyunsaturated fatty acids interact with the PPARA-L162V polymorphism to affect plasma triglyceride and apolipoprotein C-III concentrations in the Framingham Heart Study.
150	15735069	We found significant gene-nutrient interactions between the L162V polymorphism and total PUFA intake, which modulated plasma triglycerides (TG; P < 0.05) and apolipoprotein C-III (apoC-III; P < 0.05) concentrations.
151	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.
152	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).
153	15949705	Variation in the insulin gene (INS) variable number tandem repeat (VNTR) has been found to predispose to type 1 and type 2 diabetes.
154	15949705	We tested for gene:gene interaction between the INS VNTR and both the LIPC-514C>T and APOC3-482T>C.
155	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.
156	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.
157	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).
158	15949705	Variation in the insulin gene (INS) variable number tandem repeat (VNTR) has been found to predispose to type 1 and type 2 diabetes.
159	15949705	We tested for gene:gene interaction between the INS VNTR and both the LIPC-514C>T and APOC3-482T>C.
160	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.
161	15995172	The sdLDLs of both types of patients were enriched in apolipoprotein C-III (apoC-III) and were depleted of apoC-I, apoA-I, and apoE compared with matched healthy controls with the A phenotype.
162	16192625	Genetic variation in the APOC3 and APOA5 genes has been associated with plasma triglyceride concentrations and may affect the risk of myocardial infarction (MI).
163	16192625	To assess whether APOC3/A5 haplotypes are associated with risk of MI, we examined three single-nucleotide polymorphisms (SNPs) in APOC3 (3238C>G, -455T>C, and -482C>T) and six SNPs in the APOA5 gene (-1131T>C, c.-3A>G, c.56C>G, IVS3+476G>A, c.553G>T, and c.1259T>C) in incident cases (n = 1,703) of a first nonfatal MI matched for gender, age, and area of residence with population-based controls (n = 1,703).
164	16192625	Although the APOC3 3238G, APOA5 -1131C, APOA5 c.-3G, and APOA5 c.1259C alleles were associated with higher triglyceride plasma concentrations, these effects could not explain the associations with MI in this population.
165	16192625	In summary, this study supports the hypothesis that haplotypes in the APOC3 gene but not in the APOA5 gene increase susceptibility to MI.
166	16192625	Genetic variation in the APOC3 and APOA5 genes has been associated with plasma triglyceride concentrations and may affect the risk of myocardial infarction (MI).
167	16192625	To assess whether APOC3/A5 haplotypes are associated with risk of MI, we examined three single-nucleotide polymorphisms (SNPs) in APOC3 (3238C>G, -455T>C, and -482C>T) and six SNPs in the APOA5 gene (-1131T>C, c.-3A>G, c.56C>G, IVS3+476G>A, c.553G>T, and c.1259T>C) in incident cases (n = 1,703) of a first nonfatal MI matched for gender, age, and area of residence with population-based controls (n = 1,703).
168	16192625	Although the APOC3 3238G, APOA5 -1131C, APOA5 c.-3G, and APOA5 c.1259C alleles were associated with higher triglyceride plasma concentrations, these effects could not explain the associations with MI in this population.
169	16192625	In summary, this study supports the hypothesis that haplotypes in the APOC3 gene but not in the APOA5 gene increase susceptibility to MI.
170	16192625	Genetic variation in the APOC3 and APOA5 genes has been associated with plasma triglyceride concentrations and may affect the risk of myocardial infarction (MI).
171	16192625	To assess whether APOC3/A5 haplotypes are associated with risk of MI, we examined three single-nucleotide polymorphisms (SNPs) in APOC3 (3238C>G, -455T>C, and -482C>T) and six SNPs in the APOA5 gene (-1131T>C, c.-3A>G, c.56C>G, IVS3+476G>A, c.553G>T, and c.1259T>C) in incident cases (n = 1,703) of a first nonfatal MI matched for gender, age, and area of residence with population-based controls (n = 1,703).
172	16192625	Although the APOC3 3238G, APOA5 -1131C, APOA5 c.-3G, and APOA5 c.1259C alleles were associated with higher triglyceride plasma concentrations, these effects could not explain the associations with MI in this population.
173	16192625	In summary, this study supports the hypothesis that haplotypes in the APOC3 gene but not in the APOA5 gene increase susceptibility to MI.
174	16192625	Genetic variation in the APOC3 and APOA5 genes has been associated with plasma triglyceride concentrations and may affect the risk of myocardial infarction (MI).
175	16192625	To assess whether APOC3/A5 haplotypes are associated with risk of MI, we examined three single-nucleotide polymorphisms (SNPs) in APOC3 (3238C>G, -455T>C, and -482C>T) and six SNPs in the APOA5 gene (-1131T>C, c.-3A>G, c.56C>G, IVS3+476G>A, c.553G>T, and c.1259T>C) in incident cases (n = 1,703) of a first nonfatal MI matched for gender, age, and area of residence with population-based controls (n = 1,703).
176	16192625	Although the APOC3 3238G, APOA5 -1131C, APOA5 c.-3G, and APOA5 c.1259C alleles were associated with higher triglyceride plasma concentrations, these effects could not explain the associations with MI in this population.
177	16192625	In summary, this study supports the hypothesis that haplotypes in the APOC3 gene but not in the APOA5 gene increase susceptibility to MI.
178	16223942	Mechanisms of mutual functional interactions between HNF-4alpha and HNF-1alpha revealed by mutations that cause maturity onset diabetes of the young.
179	16223942	HNF-4alpha and HNF-1alpha cooperatively activate genes with binding sites for both factors, whereas suppressive interactions occur at regulatory sequences with a binding site for only one factor.
180	16223942	The liver fatty acid binding protein gene (Fabp1) has binding sites for both factors, and chromatin precipitation assays were utilized to demonstrate that HNF-4alpha increased HNF-1alpha Fabp1 promoter occupancy during cooperative transcriptional activation.
181	16223942	The HNF4 P2 promoter contains a HNF-1 but not HNF-4 binding site, and HNF-4alpha suppressed HNF-1alpha HNF4 P2 activation and decreased promoter HNF-1alpha occupancy.
182	16223942	The apolipoprotein C III (APOC3) promoter contains a HNF-4 but not HNF-1 binding site, and HNF-1alpha suppressed HNF-4alpha APOC3 activation and decreased HNF-4alpha promoter occupancy.
183	16223942	Maturity onset diabetes of the young (MODY) as well as defects in hepatic lipid metabolism result from mutations in either HNF-4alpha or HNF-1alpha.
184	16223942	We found that MODY missense mutant R127W HNF-4alpha retained wild-type individual Fabp1 activation and bound to HNF-1alpha better than wild-type HNF-4alpha, yet did not cooperate with HNF-1alpha or increase HNF-1alpha Fabp1 promoter occupancy.
185	16223942	The HNF-1alpha R131Q MODY mutant also retained wild-type Fabp1 activation and bound to HNF-4alpha as well as the wild type but was defective in both suppressing HNF-4alpha APOC3 activation and decreasing HNF-4alpha promoter occupancy.
186	16223942	Mechanisms of mutual functional interactions between HNF-4alpha and HNF-1alpha revealed by mutations that cause maturity onset diabetes of the young.
187	16223942	HNF-4alpha and HNF-1alpha cooperatively activate genes with binding sites for both factors, whereas suppressive interactions occur at regulatory sequences with a binding site for only one factor.
188	16223942	The liver fatty acid binding protein gene (Fabp1) has binding sites for both factors, and chromatin precipitation assays were utilized to demonstrate that HNF-4alpha increased HNF-1alpha Fabp1 promoter occupancy during cooperative transcriptional activation.
189	16223942	The HNF4 P2 promoter contains a HNF-1 but not HNF-4 binding site, and HNF-4alpha suppressed HNF-1alpha HNF4 P2 activation and decreased promoter HNF-1alpha occupancy.
190	16223942	The apolipoprotein C III (APOC3) promoter contains a HNF-4 but not HNF-1 binding site, and HNF-1alpha suppressed HNF-4alpha APOC3 activation and decreased HNF-4alpha promoter occupancy.
191	16223942	Maturity onset diabetes of the young (MODY) as well as defects in hepatic lipid metabolism result from mutations in either HNF-4alpha or HNF-1alpha.
192	16223942	We found that MODY missense mutant R127W HNF-4alpha retained wild-type individual Fabp1 activation and bound to HNF-1alpha better than wild-type HNF-4alpha, yet did not cooperate with HNF-1alpha or increase HNF-1alpha Fabp1 promoter occupancy.
193	16223942	The HNF-1alpha R131Q MODY mutant also retained wild-type Fabp1 activation and bound to HNF-4alpha as well as the wild type but was defective in both suppressing HNF-4alpha APOC3 activation and decreasing HNF-4alpha promoter occupancy.
194	16298371	Increased apolipoprotein C-III levels associated with insulin resistance contribute to dyslipidemia in normoglycemic and diabetic subjects from a triethnic population.
195	16298371	Despite the major role of insulin in regulating apolipoprotein C-III (apo C-III) production, little is known about the relationship between apo C-III and insulin resistance.
196	16298371	Increased apolipoprotein C-III levels associated with insulin resistance contribute to dyslipidemia in normoglycemic and diabetic subjects from a triethnic population.
197	16298371	Despite the major role of insulin in regulating apolipoprotein C-III (apo C-III) production, little is known about the relationship between apo C-III and insulin resistance.
198	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.
199	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).
200	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).
201	16343038	In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance.
202	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.
203	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.
204	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).
205	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).
206	16343038	In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance.
207	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.
208	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.
209	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).
210	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).
211	16343038	In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance.
212	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.
213	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.
214	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).
215	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).
216	16343038	In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance.
217	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.
218	16505251	Genetic variation within the apolipoprotein CIII (apoCIII) gene alters apoCIII levels, which are increased in type 1 diabetes and induce beta-cell apoptosis.
219	16781717	The apolipoprotein gene cluster (APOA1/C3/A4/A5) was recently associated with triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C) in non-diabetic population.
220	16781717	In addition, APOC3 promoter polymorphism -455T/C showed significant associations with fasting TG levels (P=0.006), whereas APOA4 +347T/A showed significant associations with lower levels of HDL-C (P=0.017).
221	16813599	Association of lipoprotein lipase S447X, apolipoprotein E exon 4, and apoC3 -455T>C polymorphisms on the susceptibility to diabetic nephropathy.
222	16813599	The LPL S447X and apolipoprotein E (APOE) exon 4 polymorphisms affect TG levels, and the APOC3 -455T>C polymorphism affects LPL activity.
223	16813599	LPL 447X-containing genotypes (447X+) were significantly decreased in DN patients [18.6 vs 25.6%, odds ratio (OR) = 0.66, p = 0.02], as were APOE epsilon3/epsilon3 genotypes (64.8 vs 73.1%, OR = 0.68, p = 0.01).
224	16813599	In addition, combinations of genotypes [APOE epsilon3/epsilon3 and LPL 447X+ (OR = 0.56), APOC3 CC and LPL 447X+ (OR = 0.31), APOE epsilon3/epsilon3 and APOC3 CC (OR = 0.61] were protective for DN compared with the most common combination of the respective polymorphisms.
225	16813599	Association of lipoprotein lipase S447X, apolipoprotein E exon 4, and apoC3 -455T>C polymorphisms on the susceptibility to diabetic nephropathy.
226	16813599	The LPL S447X and apolipoprotein E (APOE) exon 4 polymorphisms affect TG levels, and the APOC3 -455T>C polymorphism affects LPL activity.
227	16813599	LPL 447X-containing genotypes (447X+) were significantly decreased in DN patients [18.6 vs 25.6%, odds ratio (OR) = 0.66, p = 0.02], as were APOE epsilon3/epsilon3 genotypes (64.8 vs 73.1%, OR = 0.68, p = 0.01).
228	16813599	In addition, combinations of genotypes [APOE epsilon3/epsilon3 and LPL 447X+ (OR = 0.56), APOC3 CC and LPL 447X+ (OR = 0.31), APOE epsilon3/epsilon3 and APOC3 CC (OR = 0.61] were protective for DN compared with the most common combination of the respective polymorphisms.
229	16813599	Association of lipoprotein lipase S447X, apolipoprotein E exon 4, and apoC3 -455T>C polymorphisms on the susceptibility to diabetic nephropathy.
230	16813599	The LPL S447X and apolipoprotein E (APOE) exon 4 polymorphisms affect TG levels, and the APOC3 -455T>C polymorphism affects LPL activity.
231	16813599	LPL 447X-containing genotypes (447X+) were significantly decreased in DN patients [18.6 vs 25.6%, odds ratio (OR) = 0.66, p = 0.02], as were APOE epsilon3/epsilon3 genotypes (64.8 vs 73.1%, OR = 0.68, p = 0.01).
232	16813599	In addition, combinations of genotypes [APOE epsilon3/epsilon3 and LPL 447X+ (OR = 0.56), APOC3 CC and LPL 447X+ (OR = 0.31), APOE epsilon3/epsilon3 and APOC3 CC (OR = 0.61] were protective for DN compared with the most common combination of the respective polymorphisms.
233	16901410	The mechanism for these effects is still being clarified, but may involve enhancement of triglyceride clearance (in the case of pioglitazone), alteration of apolipoprotein C-III levels, reduction of hepatic lipase, and increase in ATP binding cassette A1 (ABCA1) activity.
234	17102149	Apolipoprotein C-III is excluded from the most abundant LDL (i.e., that of intermediate density: 1.034 < d < 1.050 g/ml) but associated with both small and large LDL(-).
235	17197160	The effect of APOA5 and APOC3 variants on lipid parameters in European Whites, Indian Asians and Afro-Caribbeans with type 2 diabetes.
236	17197160	Common variants in APOA5 and APOC3 have been associated with differences in plasma triglyceride (TG) levels in healthy individuals.
237	17197160	While the variable size effects of the two APOA5 SNPs on TG levels may result from ethnically different gene-gene or gene-environment interactions, APOA5 and APOC3 variants did not affect parameters of T2D.
238	17197160	The effect of APOA5 and APOC3 variants on lipid parameters in European Whites, Indian Asians and Afro-Caribbeans with type 2 diabetes.
239	17197160	Common variants in APOA5 and APOC3 have been associated with differences in plasma triglyceride (TG) levels in healthy individuals.
240	17197160	While the variable size effects of the two APOA5 SNPs on TG levels may result from ethnically different gene-gene or gene-environment interactions, APOA5 and APOC3 variants did not affect parameters of T2D.
241	17197160	The effect of APOA5 and APOC3 variants on lipid parameters in European Whites, Indian Asians and Afro-Caribbeans with type 2 diabetes.
242	17197160	Common variants in APOA5 and APOC3 have been associated with differences in plasma triglyceride (TG) levels in healthy individuals.
243	17197160	While the variable size effects of the two APOA5 SNPs on TG levels may result from ethnically different gene-gene or gene-environment interactions, APOA5 and APOC3 variants did not affect parameters of T2D.
244	17726453	Allelic variation in ApoC3, ApoA5 and LPL genes and first and second generation antipsychotic effects on serum lipids in patients with schizophrenia.
245	17726453	We have investigated in an exploratory study whether polymorphisms in the apolipoprotein C-III (ApoC3), apolipoprotein A-V gene (ApoA5) and lipoprotein lipase genes influence differential lipid response to treatment with three second generation antipsychotics-olanzapine, clozapine and risperidone-or treatment with a first generation antipsychotic.
246	17726453	Allelic variation in ApoC3, ApoA5 and LPL genes and first and second generation antipsychotic effects on serum lipids in patients with schizophrenia.
247	17726453	We have investigated in an exploratory study whether polymorphisms in the apolipoprotein C-III (ApoC3), apolipoprotein A-V gene (ApoA5) and lipoprotein lipase genes influence differential lipid response to treatment with three second generation antipsychotics-olanzapine, clozapine and risperidone-or treatment with a first generation antipsychotic.
248	18188530	A large population (n=552) of cardiovascular patients, without diabetes and/or lipid-lowering therapy, with or without metabolic syndrome (MetSyn), was genotyped for epsilon2/epsilon3/epsilon4 polymorphism and their ApoCIII/ApoE ratio was evaluated.
249	18188530	The ApoCIII/ ApoE ratio showed an opposite trend, gradually increasing from E2/E2 to E4/E4 subjects.
250	18188530	ApoE epsilon2/epsilon3/epsilon4 gene polymorphism is a determinant of the relative proportion of apolipoprotein C-III to E.
251	18188530	Carriers of the unfavourable E4 allele present the highest ApoCIII/ApoE ratio and are twofold more frequent among individuals affected by MetSyn.
252	18188530	A large population (n=552) of cardiovascular patients, without diabetes and/or lipid-lowering therapy, with or without metabolic syndrome (MetSyn), was genotyped for epsilon2/epsilon3/epsilon4 polymorphism and their ApoCIII/ApoE ratio was evaluated.
253	18188530	The ApoCIII/ ApoE ratio showed an opposite trend, gradually increasing from E2/E2 to E4/E4 subjects.
254	18188530	ApoE epsilon2/epsilon3/epsilon4 gene polymorphism is a determinant of the relative proportion of apolipoprotein C-III to E.
255	18188530	Carriers of the unfavourable E4 allele present the highest ApoCIII/ApoE ratio and are twofold more frequent among individuals affected by MetSyn.
256	18188530	A large population (n=552) of cardiovascular patients, without diabetes and/or lipid-lowering therapy, with or without metabolic syndrome (MetSyn), was genotyped for epsilon2/epsilon3/epsilon4 polymorphism and their ApoCIII/ApoE ratio was evaluated.
257	18188530	The ApoCIII/ ApoE ratio showed an opposite trend, gradually increasing from E2/E2 to E4/E4 subjects.
258	18188530	ApoE epsilon2/epsilon3/epsilon4 gene polymorphism is a determinant of the relative proportion of apolipoprotein C-III to E.
259	18188530	Carriers of the unfavourable E4 allele present the highest ApoCIII/ApoE ratio and are twofold more frequent among individuals affected by MetSyn.
260	18188530	A large population (n=552) of cardiovascular patients, without diabetes and/or lipid-lowering therapy, with or without metabolic syndrome (MetSyn), was genotyped for epsilon2/epsilon3/epsilon4 polymorphism and their ApoCIII/ApoE ratio was evaluated.
261	18188530	The ApoCIII/ ApoE ratio showed an opposite trend, gradually increasing from E2/E2 to E4/E4 subjects.
262	18188530	ApoE epsilon2/epsilon3/epsilon4 gene polymorphism is a determinant of the relative proportion of apolipoprotein C-III to E.
263	18188530	Carriers of the unfavourable E4 allele present the highest ApoCIII/ApoE ratio and are twofold more frequent among individuals affected by MetSyn.
264	18201179	An ABC of apolipoprotein C-III: a clinically useful new cardiovascular risk factor?
265	18421072	The aim of this study was to evaluate the impact of adipocyte fatty acid binding protein 4 (FABP4) on the lipid profile in type 2 diabetic subjects.
266	18421072	Plasma levels of FABP4 and adiponectin and an extensive lipid profile were analyzed in 169 type 2 diabetic subjects and 105 controls.
267	18421072	In type 2 diabetic subjects, FABP4 was positively correlated with plasma triglycerides (P = 0.007), apolipoprotein C-III (apoC-III) (P = 0.009), and all the components of triglyceride-rich lipoproteins, including VLDL triglycerides (P = 0.002), VLDL-cholesterol (P = 0.001), and VLDL apoB (P = 0.001).
268	18421072	These correlations are not significantly affected by age, gender, body mass index, adiponectin, insulin, or any pharmacological treatment.
269	18421072	The associations are even stronger when the FABP4/adiponectin ratio is considered.
270	18421072	High FABP4 and low adiponectin levels are independent predictors of atherogenic dyslipidemia.
271	18421072	In conclusion, FABP4 plasma concentrations hold strong potential for development as a clinical biomarker for atherogenic dyslipidemia, independent of obesity and insulin resistance, in type 2 diabetic subjects.
272	18509206	Dose-dependent effect of rosuvastatin on VLDL-apolipoprotein C-III kinetics in the metabolic syndrome.
273	19168150	As a general rule, high fat diet-induced adipogenesis is aggravated by stimulated LPL activity (e.g. by adipose tissue-specific overexpression of LPL or deficiency for apoCIII), and attenuated by inhibited LPL activity (e.g. by adipose-specific deficiency for LPL, overexpression of apoCI or angptl4, or by deficiency for apoE or the VLDL receptor).
274	19262004	Interestingly, apoCIII-rich HDL did not reduce the adhesion of monocytes to vascular ECs, whereas HDL without apoCIII decreased their adhesion, suggesting that apoCIII in HDL counteracts the anti-inflammatory property of HDL.
275	19262004	ApoCIII alone as well as VLDL CIII+also activated vascular ECs through the activation of NF-kappaB, and induced the recruitment of monocytes to vascular ECs.
276	19262004	Moreover, apoCIII induced insulin resistance in vascular ECs and caused endothelial dysfunction.
277	19262004	Interestingly, apoCIII-rich HDL did not reduce the adhesion of monocytes to vascular ECs, whereas HDL without apoCIII decreased their adhesion, suggesting that apoCIII in HDL counteracts the anti-inflammatory property of HDL.
278	19262004	ApoCIII alone as well as VLDL CIII+also activated vascular ECs through the activation of NF-kappaB, and induced the recruitment of monocytes to vascular ECs.
279	19262004	Moreover, apoCIII induced insulin resistance in vascular ECs and caused endothelial dysfunction.
280	19262004	Interestingly, apoCIII-rich HDL did not reduce the adhesion of monocytes to vascular ECs, whereas HDL without apoCIII decreased their adhesion, suggesting that apoCIII in HDL counteracts the anti-inflammatory property of HDL.
281	19262004	ApoCIII alone as well as VLDL CIII+also activated vascular ECs through the activation of NF-kappaB, and induced the recruitment of monocytes to vascular ECs.
282	19262004	Moreover, apoCIII induced insulin resistance in vascular ECs and caused endothelial dysfunction.
283	19292868	Novel genes in cell cycle control and lipid metabolism with dynamically regulated binding sites for sterol regulatory element-binding protein 1 and RNA polymerase II in HepG2 cells detected by chromatin immunoprecipitation with microarray detection.
284	19292868	Sterol regulatory element-binding proteins 1 and 2 (SREBP-1 and SREBP-2) are important regulators of genes involved in cholesterol and fatty acid metabolism, but have also been implicated in the regulation of the cell cycle and have been associated with the pathogenesis of type 2 diabetes, atherosclerosis and obesity, among others.
285	19292868	Our data identified novel binding sites for SREBP-1 in genes directly or indirectly involved in cholesterol metabolism, e.g. apolipoprotein C-III (APOC3).
286	19292868	The most interesting biological findings were the binding sites for SREBP-1 in genes for host cell factor C1 (HCFC1), involved in cell cycle regulation, and for filamin A (FLNA).
287	19292868	Furthermore, we found evidence of sterol-regulated binding of SREBP-1 and RNA polymerase II to HCFC1 and FLNA.
288	20655898	Recent evidence suggests that the forkhead transcription factor Foxo1 plays an important role in the regulation of glucose and triglyceride metabolism at the gene transcription level for glucose-6 phosphatase (G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and apolipoprotein C-III (apoC-III).
289	21185820	APOC3 -482C>T polymorphism, circulating apolipoprotein C-III and smoking: interrelation and roles in predicting type-2 diabetes and coronary disease.
290	21199528	Polymorphisms within apolipoprotein C3 (APOC3) gene have been linked to NAFLD in lean Indian men.
291	21443465	Preclinical studies show that FoxO1 plays a pivotal role in controlling insulin-dependent regulation of microsomal triglyceride transfer protein (MTP) and apolipoprotein C-III (ApoC-III), two key components that catalyze the rate-limiting steps in the production and clearance of triglyceride-rich lipoproteins.
292	21499891	Association of lipoprotein lipase and apolipoprotein C-III genes polymorphism with acute myocardial infarction in diabetic patients.
293	21499891	Lipoprotein lipase (LPL) and Apolipoprotein C-III (APOC-III) play an important role in lipid metabolism.
294	21499891	The aim of this study was to explore the possible associations of the gene polymorphisms (LPL HindIII, LPL Ser(447)-Ter and APOC3 SstI), diabetes mellitus, and plasma lipids with myocardial infarction.
295	21499891	Association of lipoprotein lipase and apolipoprotein C-III genes polymorphism with acute myocardial infarction in diabetic patients.
296	21499891	Lipoprotein lipase (LPL) and Apolipoprotein C-III (APOC-III) play an important role in lipid metabolism.
297	21499891	The aim of this study was to explore the possible associations of the gene polymorphisms (LPL HindIII, LPL Ser(447)-Ter and APOC3 SstI), diabetes mellitus, and plasma lipids with myocardial infarction.
298	21499891	Association of lipoprotein lipase and apolipoprotein C-III genes polymorphism with acute myocardial infarction in diabetic patients.
299	21499891	Lipoprotein lipase (LPL) and Apolipoprotein C-III (APOC-III) play an important role in lipid metabolism.
300	21499891	The aim of this study was to explore the possible associations of the gene polymorphisms (LPL HindIII, LPL Ser(447)-Ter and APOC3 SstI), diabetes mellitus, and plasma lipids with myocardial infarction.
301	21670290	Serum levels of apolipoprotein CIII (apoCIII) are increased in type 1 diabetic patients, and when β cells are exposed to these diabetic sera, apoptosis occurs, an effect abolished by an antibody against apoCIII.
302	21670290	The endogenous levels of apoCIII were reduced by treating prediabetic animals with an antisense against this apolipoprotein, resulting in a significantly delayed onset of diabetes.
303	21670290	ApoCIII thus serves as a diabetogenic factor, and intervention with this apolipoprotein in the prediabetic state can arrest disease progression.
304	21670290	Serum levels of apolipoprotein CIII (apoCIII) are increased in type 1 diabetic patients, and when β cells are exposed to these diabetic sera, apoptosis occurs, an effect abolished by an antibody against apoCIII.
305	21670290	The endogenous levels of apoCIII were reduced by treating prediabetic animals with an antisense against this apolipoprotein, resulting in a significantly delayed onset of diabetes.
306	21670290	ApoCIII thus serves as a diabetogenic factor, and intervention with this apolipoprotein in the prediabetic state can arrest disease progression.
307	21670290	Serum levels of apolipoprotein CIII (apoCIII) are increased in type 1 diabetic patients, and when β cells are exposed to these diabetic sera, apoptosis occurs, an effect abolished by an antibody against apoCIII.
308	21670290	The endogenous levels of apoCIII were reduced by treating prediabetic animals with an antisense against this apolipoprotein, resulting in a significantly delayed onset of diabetes.
309	21670290	ApoCIII thus serves as a diabetogenic factor, and intervention with this apolipoprotein in the prediabetic state can arrest disease progression.
310	21693679	Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway.
311	21693679	Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism.
312	21693679	In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function.
313	21693679	ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation.
314	21693679	Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt.
315	21693679	Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis.
316	21693679	We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt.
317	21693679	Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway.
318	21693679	Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism.
319	21693679	In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function.
320	21693679	ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation.
321	21693679	Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt.
322	21693679	Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis.
323	21693679	We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt.
324	21693679	Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway.
325	21693679	Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism.
326	21693679	In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function.
327	21693679	ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation.
328	21693679	Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt.
329	21693679	Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis.
330	21693679	We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt.
331	21693679	Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway.
332	21693679	Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism.
333	21693679	In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function.
334	21693679	ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation.
335	21693679	Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt.
336	21693679	Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis.
337	21693679	We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt.
338	21693679	Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway.
339	21693679	Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism.
340	21693679	In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function.
341	21693679	ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation.
342	21693679	Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt.
343	21693679	Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis.
344	21693679	We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt.
345	21693679	Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway.
346	21693679	Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism.
347	21693679	In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function.
348	21693679	ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation.
349	21693679	Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt.
350	21693679	Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis.
351	21693679	We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt.
352	22460246	In the present study, we aim to investigate the effect of -1131T > C, -3A > G, c.56 C > G, and c.553 G > T SNPs in the apolipoprotein A5 (APOA5) gene and 1100C > T and 3238C > G in the apolipoprotein C3 (APOC3) on plasma lipid and lipoprotein levels and risk of coronary artery disease (CAD) in Indians.
353	22460246	Significant associations between minor alleles and higher TG levels were seen for -1131T > C (P < 0.001), -3A > G (P < 0.001), c.56C > G (P = 0.026), and c.553G > T (P = 0.003) SNPs in the APOA5 gene and 1100C > T (P = 0.001) and 3238C > G (P = 0.009) in the APOC3 gene.
354	22460246	The APOA5 and APOC3 locus is a strong determinant of plasma TG levels in Indians.
355	22460246	In the present study, we aim to investigate the effect of -1131T > C, -3A > G, c.56 C > G, and c.553 G > T SNPs in the apolipoprotein A5 (APOA5) gene and 1100C > T and 3238C > G in the apolipoprotein C3 (APOC3) on plasma lipid and lipoprotein levels and risk of coronary artery disease (CAD) in Indians.
356	22460246	Significant associations between minor alleles and higher TG levels were seen for -1131T > C (P < 0.001), -3A > G (P < 0.001), c.56C > G (P = 0.026), and c.553G > T (P = 0.003) SNPs in the APOA5 gene and 1100C > T (P = 0.001) and 3238C > G (P = 0.009) in the APOC3 gene.
357	22460246	The APOA5 and APOC3 locus is a strong determinant of plasma TG levels in Indians.
358	22460246	In the present study, we aim to investigate the effect of -1131T > C, -3A > G, c.56 C > G, and c.553 G > T SNPs in the apolipoprotein A5 (APOA5) gene and 1100C > T and 3238C > G in the apolipoprotein C3 (APOC3) on plasma lipid and lipoprotein levels and risk of coronary artery disease (CAD) in Indians.
359	22460246	Significant associations between minor alleles and higher TG levels were seen for -1131T > C (P < 0.001), -3A > G (P < 0.001), c.56C > G (P = 0.026), and c.553G > T (P = 0.003) SNPs in the APOA5 gene and 1100C > T (P = 0.001) and 3238C > G (P = 0.009) in the APOC3 gene.
360	22460246	The APOA5 and APOC3 locus is a strong determinant of plasma TG levels in Indians.
361	22903714	Apolipoprotein C3 (ApoC3) is synthesized in liver so that levels or isoform distributions may constitute indicators of liver pathogenesis.
362	22911512	In this study, we test the hypothesis that NADPH oxidase 2 (NOX2)-derived ROS may play a key role in dysfunction and apoptosis of pancreatic β-cell induced by VLDL.
363	22911512	Our results show that the ApoCIII transgenic mice displayed increased serum TG levels, enhanced generation of ROS and impaired insulin content in pancreatic β-cells.
364	22911512	In vitro, the treatment of pancreatic NIT-1 cells with 1 mg/ml VLDL for 12 h stimulated NOX2-derived ROS generation, decreased expression and secretion of insulin.
365	22911512	Furthermore, we found that VLDL induced dysfunction and apoptosis of pancreatic β-cells through JNK and p53 pathways, which were rescued by siRNA-mediated NOX2 reduction.
366	22911512	In conclusion, our data demonstrate a critical role of NOX2-derived ROS in dysfunction and apoptosis through JNK and p53 pathways in pancreatic β-cells induced by VLDL.
367	23368640	Apolipoprotein C3 (ApoC3) is one of the many plasma glycoproteins extensively studied for association with disease states.
368	23377670	Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease.
369	23377670	We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors.
370	23377670	The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group.
371	23377670	We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other.
372	23377670	The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD.
373	23377670	Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease.
374	23377670	We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors.
375	23377670	The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group.
376	23377670	We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other.
377	23377670	The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD.
378	23377670	Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease.
379	23377670	We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors.
380	23377670	The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group.
381	23377670	We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other.
382	23377670	The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD.
383	23377670	Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease.
384	23377670	We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors.
385	23377670	The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group.
386	23377670	We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other.
387	23377670	The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD.
388	23542898	Antisense oligonucleotide inhibition of apolipoprotein C-III reduces plasma triglycerides in rodents, nonhuman primates, and humans.
389	23949443	Apolipoprotein CIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
390	23949443	Apolipoprotein CIII (ApoCIII) not only serves as an inhibitor of triglyceride hydrolysis but also participates in diabetes-related pathological events such as hyperactivation of voltage-gated Ca(2+) (CaV) channels in the pancreatic β cell.
391	23949443	We now demonstrate that ApoCIII increased CaV1 channel open probability and density.
392	23949443	Moreover, knockdown of β1 integrin or scavenger receptor class B type I (SR-BI) prevented ApoCIII from hyperactivating β cell CaV channels.
393	23949443	These data reveal that ApoCIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
394	23949443	Apolipoprotein CIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
395	23949443	Apolipoprotein CIII (ApoCIII) not only serves as an inhibitor of triglyceride hydrolysis but also participates in diabetes-related pathological events such as hyperactivation of voltage-gated Ca(2+) (CaV) channels in the pancreatic β cell.
396	23949443	We now demonstrate that ApoCIII increased CaV1 channel open probability and density.
397	23949443	Moreover, knockdown of β1 integrin or scavenger receptor class B type I (SR-BI) prevented ApoCIII from hyperactivating β cell CaV channels.
398	23949443	These data reveal that ApoCIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
399	23949443	Apolipoprotein CIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
400	23949443	Apolipoprotein CIII (ApoCIII) not only serves as an inhibitor of triglyceride hydrolysis but also participates in diabetes-related pathological events such as hyperactivation of voltage-gated Ca(2+) (CaV) channels in the pancreatic β cell.
401	23949443	We now demonstrate that ApoCIII increased CaV1 channel open probability and density.
402	23949443	Moreover, knockdown of β1 integrin or scavenger receptor class B type I (SR-BI) prevented ApoCIII from hyperactivating β cell CaV channels.
403	23949443	These data reveal that ApoCIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
404	23949443	Apolipoprotein CIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.
405	23949443	Apolipoprotein CIII (ApoCIII) not only serves as an inhibitor of triglyceride hydrolysis but also participates in diabetes-related pathological events such as hyperactivation of voltage-gated Ca(2+) (CaV) channels in the pancreatic β cell.
406	23949443	We now demonstrate that ApoCIII increased CaV1 channel open probability and density.
407	23949443	Moreover, knockdown of β1 integrin or scavenger receptor class B type I (SR-BI) prevented ApoCIII from hyperactivating β cell CaV channels.
408	23949443	These data reveal that ApoCIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src.