Ignet

Gene Information

Gene symbol: ADH4

Gene name: alcohol dehydrogenase 4 (class II), pi polypeptide

HGNC ID: 252

Synonyms: ADH-2

Related Genes

#	Gene Symbol	Number of hits
1	ADH1B	1 hits
2	ALDH2	1 hits
3	ALDH9A1	1 hits
4	AVP	1 hits
5	INS	1 hits
6	PRKCA	1 hits

Related Sentences

#	PMID	Sentence
1	1192687	Chlorpropamide, carbamazepine and clofibrate have an antidiuretic action in patients with neurohypophyseal diabetes insipidus which is qualitatively similar to that of antidiuretic hormone (ADH). 2.
2	1391802	Diabetes insipidus (DI) is a disorder characterized by polyuria, polydipsia and increased thirst [1] while pituitary DI is a syndrome that is known to result from deficient release of the antidiuretic hormone (ADH) [2,3].
3	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
4	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
5	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
6	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
7	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
8	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
9	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
10	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
11	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
12	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
13	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
14	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
15	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
16	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
17	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
18	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
19	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
20	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
21	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
22	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
23	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
24	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
25	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
26	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
27	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
28	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
29	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
30	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
31	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
32	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
33	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
34	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
35	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
36	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
37	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
38	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
39	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
40	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
41	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
42	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
43	15318096	ALDH2/ADH2 polymorphism associated with vasculopathy and neuropathy in type 2 diabetes.
44	15318096	A mechanism of CPAF has been regarded as the inhibition of aldehyde dehydrogenase 2 (ALDH2) by an N-alkyl-substituted derivative of chlorpropamide, and the expression of these mutations of ALDH2 and alcohol dehydrogenase 2 (ADH2) could determine the alcohol tolerance among the Japanese population.
45	15318096	Therefore, we hypothesized that expression of different ALDH2 and ADH2 polymorphisms may induce differences in vascular complications in diabetes and conducted two studies.
46	15318096	To know the association of ALDH2/AHD2 polymorphism with diabetic vasculopathy and neuropathy, a total of 158 patients with type 2 diabetes were divided into four groups on the basis of ALDH2 "activity" and ADH2 "superactivity."
47	15318096	The frequency of proteinuria and the percentage of proliferative retinopathy among the patients with retinopathy was higher in those with active ALDH2 and superactive ADH2.
48	15318096	We speculated that protein kinase C isoforms up-regulated by 4-hydroxynonenal that was detoxified by ALDH2 and ADH2 may account for the long-term development of diabetic nephropathy and severe retinopathy.
49	15318096	As for neuropathy, the frequency of symptomatic neuropathy was higher in patients with inactive ALDH2 and usual ADH2.
50	15318096	We speculate that increased tissue levels of toxic aldehyde could result from inactive ALDH2 and usual ADH2 expression, which results in the increased level of reactive aldehyde in sensory neuron pathway, thereby causing symptomatic polyneuropathy.
51	15679538	Several potential risk factors have been proposed for AUD in addition to alcohol consumption, including alcohol dehydrogenase2 (ADH2), acetaldehyde dehydrogenase2 (ALDH2), marital status, educational, occupational or past medical history (e.g. diabetes mellitus, hypertension, lung, digestive tract, or chronic liver disease) or smoking habits.
52	15679538	A case-control study was performed on 153 male Japanese AUD patients and age-, gender-, or other confounder-matched controls to investigate the relation multivariately between ADH2, ALDH2 or alcohol drinking and AUD.
53	15679538	Genomic DNA were extracted from nail clippings by the guanidium method, and genotyping of ADH2 and ALDH2 were performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods.
54	15679538	Several potential risk factors have been proposed for AUD in addition to alcohol consumption, including alcohol dehydrogenase2 (ADH2), acetaldehyde dehydrogenase2 (ALDH2), marital status, educational, occupational or past medical history (e.g. diabetes mellitus, hypertension, lung, digestive tract, or chronic liver disease) or smoking habits.
55	15679538	A case-control study was performed on 153 male Japanese AUD patients and age-, gender-, or other confounder-matched controls to investigate the relation multivariately between ADH2, ALDH2 or alcohol drinking and AUD.
56	15679538	Genomic DNA were extracted from nail clippings by the guanidium method, and genotyping of ADH2 and ALDH2 were performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods.
57	15679538	Several potential risk factors have been proposed for AUD in addition to alcohol consumption, including alcohol dehydrogenase2 (ADH2), acetaldehyde dehydrogenase2 (ALDH2), marital status, educational, occupational or past medical history (e.g. diabetes mellitus, hypertension, lung, digestive tract, or chronic liver disease) or smoking habits.
58	15679538	A case-control study was performed on 153 male Japanese AUD patients and age-, gender-, or other confounder-matched controls to investigate the relation multivariately between ADH2, ALDH2 or alcohol drinking and AUD.
59	15679538	Genomic DNA were extracted from nail clippings by the guanidium method, and genotyping of ADH2 and ALDH2 were performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods.
60	16307179	Association of alcohol dehydrogenase 2*1 allele with liver damage and insulin concentration in the Japanese.
61	16307179	The alleles of ADH2 (ADH21 and ADH22) encode more active and less active forms for ethanol metabolism, respectively.
62	16307179	We examined whether liver damage and the insulin-glucose axis vary according to ADH2 genotype in the Japanese.
63	16307179	Clinical evaluations including alcohol consumption, percentage of alcohol drinkers, plasma glucose, HbA1c, insulin, AST, ALT, gamma-GTP, and prevalence of diabetes were compared among the ADH2 genotypes.
64	16307179	While amounts of alcohol consumed and glucose levels were nearly the same between ADH1/2 and ADH22/2, insulin concentrations were lower in ADH22/1 than in ADH22/2 (P < 0.05 in men).
65	16307179	This finding suggests that the ADH2*1 allele is associated with a lower insulin concentration when alcohol intake is light or moderate.
66	16307179	It also suggests that the genetic effect of ADH2*1 plays an important role in alcohol drinking behavior and in the occurrence of liver injury, but the effect is so mild that it does not influence the glucose-insulin axis or prevalence of diabetes.
67	16307179	Association of alcohol dehydrogenase 2*1 allele with liver damage and insulin concentration in the Japanese.
68	16307179	The alleles of ADH2 (ADH21 and ADH22) encode more active and less active forms for ethanol metabolism, respectively.
69	16307179	We examined whether liver damage and the insulin-glucose axis vary according to ADH2 genotype in the Japanese.
70	16307179	Clinical evaluations including alcohol consumption, percentage of alcohol drinkers, plasma glucose, HbA1c, insulin, AST, ALT, gamma-GTP, and prevalence of diabetes were compared among the ADH2 genotypes.
71	16307179	While amounts of alcohol consumed and glucose levels were nearly the same between ADH1/2 and ADH22/2, insulin concentrations were lower in ADH22/1 than in ADH22/2 (P < 0.05 in men).
72	16307179	This finding suggests that the ADH2*1 allele is associated with a lower insulin concentration when alcohol intake is light or moderate.
73	16307179	It also suggests that the genetic effect of ADH2*1 plays an important role in alcohol drinking behavior and in the occurrence of liver injury, but the effect is so mild that it does not influence the glucose-insulin axis or prevalence of diabetes.
74	16307179	Association of alcohol dehydrogenase 2*1 allele with liver damage and insulin concentration in the Japanese.
75	16307179	The alleles of ADH2 (ADH21 and ADH22) encode more active and less active forms for ethanol metabolism, respectively.
76	16307179	We examined whether liver damage and the insulin-glucose axis vary according to ADH2 genotype in the Japanese.
77	16307179	Clinical evaluations including alcohol consumption, percentage of alcohol drinkers, plasma glucose, HbA1c, insulin, AST, ALT, gamma-GTP, and prevalence of diabetes were compared among the ADH2 genotypes.
78	16307179	While amounts of alcohol consumed and glucose levels were nearly the same between ADH1/2 and ADH22/2, insulin concentrations were lower in ADH22/1 than in ADH22/2 (P < 0.05 in men).
79	16307179	This finding suggests that the ADH2*1 allele is associated with a lower insulin concentration when alcohol intake is light or moderate.
80	16307179	It also suggests that the genetic effect of ADH2*1 plays an important role in alcohol drinking behavior and in the occurrence of liver injury, but the effect is so mild that it does not influence the glucose-insulin axis or prevalence of diabetes.
81	16307179	Association of alcohol dehydrogenase 2*1 allele with liver damage and insulin concentration in the Japanese.
82	16307179	The alleles of ADH2 (ADH21 and ADH22) encode more active and less active forms for ethanol metabolism, respectively.
83	16307179	We examined whether liver damage and the insulin-glucose axis vary according to ADH2 genotype in the Japanese.
84	16307179	Clinical evaluations including alcohol consumption, percentage of alcohol drinkers, plasma glucose, HbA1c, insulin, AST, ALT, gamma-GTP, and prevalence of diabetes were compared among the ADH2 genotypes.
85	16307179	While amounts of alcohol consumed and glucose levels were nearly the same between ADH1/2 and ADH22/2, insulin concentrations were lower in ADH22/1 than in ADH22/2 (P < 0.05 in men).
86	16307179	This finding suggests that the ADH2*1 allele is associated with a lower insulin concentration when alcohol intake is light or moderate.
87	16307179	It also suggests that the genetic effect of ADH2*1 plays an important role in alcohol drinking behavior and in the occurrence of liver injury, but the effect is so mild that it does not influence the glucose-insulin axis or prevalence of diabetes.
88	16307179	Association of alcohol dehydrogenase 2*1 allele with liver damage and insulin concentration in the Japanese.
89	16307179	The alleles of ADH2 (ADH21 and ADH22) encode more active and less active forms for ethanol metabolism, respectively.
90	16307179	We examined whether liver damage and the insulin-glucose axis vary according to ADH2 genotype in the Japanese.
91	16307179	Clinical evaluations including alcohol consumption, percentage of alcohol drinkers, plasma glucose, HbA1c, insulin, AST, ALT, gamma-GTP, and prevalence of diabetes were compared among the ADH2 genotypes.
92	16307179	While amounts of alcohol consumed and glucose levels were nearly the same between ADH1/2 and ADH22/2, insulin concentrations were lower in ADH22/1 than in ADH22/2 (P < 0.05 in men).
93	16307179	This finding suggests that the ADH2*1 allele is associated with a lower insulin concentration when alcohol intake is light or moderate.
94	16307179	It also suggests that the genetic effect of ADH2*1 plays an important role in alcohol drinking behavior and in the occurrence of liver injury, but the effect is so mild that it does not influence the glucose-insulin axis or prevalence of diabetes.
95	16307179	Association of alcohol dehydrogenase 2*1 allele with liver damage and insulin concentration in the Japanese.
96	16307179	The alleles of ADH2 (ADH21 and ADH22) encode more active and less active forms for ethanol metabolism, respectively.
97	16307179	We examined whether liver damage and the insulin-glucose axis vary according to ADH2 genotype in the Japanese.
98	16307179	Clinical evaluations including alcohol consumption, percentage of alcohol drinkers, plasma glucose, HbA1c, insulin, AST, ALT, gamma-GTP, and prevalence of diabetes were compared among the ADH2 genotypes.
99	16307179	While amounts of alcohol consumed and glucose levels were nearly the same between ADH1/2 and ADH22/2, insulin concentrations were lower in ADH22/1 than in ADH22/2 (P < 0.05 in men).
100	16307179	This finding suggests that the ADH2*1 allele is associated with a lower insulin concentration when alcohol intake is light or moderate.
101	16307179	It also suggests that the genetic effect of ADH2*1 plays an important role in alcohol drinking behavior and in the occurrence of liver injury, but the effect is so mild that it does not influence the glucose-insulin axis or prevalence of diabetes.