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PathWhiz ID Pathway Meta Data

PW091256

Pw091256 View Pathway
metabolic

Visceral Fat Deposits and the Metabolic Syndrome

Homo sapiens
Although abdominal obesity or visceral obesity is considered to be one of the components of metabolic syndrome and to have an important role in a cluster of cardiovascular risks, there is no consensus about the definition and diagnostic criteria for this syndrome, probably because there is considerable disagreement about the location and definition of abdominal obesity or visceral obesity. The importance of diagnosing metabolic syndrome, in which visceral fat accumulation plays an essential role in the development of multiple risk factors, should be emphasized because lifestyle modification for the reduction of visceral fat may be very effective for the reduction of risks of this type, namely metabolic syndrome in the narrow sense.

PW132533

Pw132533 View Pathway
metabolic

Vismodegib Drug Metabolism

Homo sapiens
Vismodegib is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Vismodegib passes through the liver and is then excreted from the body mainly through the kidney.

PW145850

Pw145850 View Pathway
drug action

Vismodegib Drug Metabolism Action Pathway

Homo sapiens

PW121979

Pw121979 View Pathway
disease

Vitamin A Deficiency

Rattus norvegicus
Vitamin A deficiency can be caused by many causes. A defect in the BCMO1 gene which codes for beta,beta-carotene 15,15’-monooxygenase is one of them. Beta,beta-carotene 15,15’-monooxygenase catalyzes the chemical reaction where the two substrates are beta-carotene and O2, whereas its product is retinal. A defect in this enzyme results in decrease of levels of retinal and vitamin A in serum; Signs and symptoms include night blindness, poor adaptation to darkness, dry skin and hair.

PW121754

Pw121754 View Pathway
disease

Vitamin A Deficiency

Mus musculus
Vitamin A deficiency can be caused by many causes. A defect in the BCMO1 gene which codes for beta,beta-carotene 15,15’-monooxygenase is one of them. Beta,beta-carotene 15,15’-monooxygenase catalyzes the chemical reaction where the two substrates are beta-carotene and O2, whereas its product is retinal. A defect in this enzyme results in decrease of levels of retinal and vitamin A in serum; Signs and symptoms include night blindness, poor adaptation to darkness, dry skin and hair.

PW000210

Pw000210 View Pathway
disease

Vitamin A Deficiency

Homo sapiens
Vitamin A deficiency can be caused by many causes. A defect in the BCMO1 gene which codes for beta,beta-carotene 15,15’-monooxygenase is one of them. Beta,beta-carotene 15,15’-monooxygenase catalyzes the chemical reaction where the two substrates are beta-carotene and O2, whereas its product is retinal. A defect in this enzyme results in decrease of levels of retinal and vitamin A in serum; Signs and symptoms include night blindness, poor adaptation to darkness, dry skin and hair.

PW127355

Pw127355 View Pathway
disease

Vitamin A Deficiency

Homo sapiens
Vitamin A deficiency can be caused by many causes. A defect in the BCMO1 gene which codes for beta,beta-carotene 15,15’-monooxygenase is one of them. Beta,beta-carotene 15,15’-monooxygenase catalyzes the chemical reaction where the two substrates are beta-carotene and O2, whereas its product is retinal. A defect in this enzyme results in decrease of levels of retinal and vitamin A in serum; Signs and symptoms include night blindness, poor adaptation to darkness, dry skin and hair.

PW144298

Pw144298 View Pathway
drug action

Vitamin A Drug Metabolism Action Pathway

Homo sapiens

PW000892

Pw000892 View Pathway
metabolic

Vitamin B1/Thiamine

Escherichia coli (strain K12)

PW002486

Pw002486 View Pathway
metabolic

Vitamin B1/Thiamine Metabolism

Saccharomyces cerevisiae
The biosynthesis of thiamine begins with pyrithiamine reacting with thiaminase 2 resulting in the release of 4-Amino-5-hydroxymethyl-2-methylpyrimidine. The latter compound reacts with a hydroxymethylpyrimidine/phosphomethylpyrimidine kinase resulting in the release of 4-amino-2-methyl-5-phosphomethylpyrimidine. The latter compound reacts with a hydroxymethylpyrimidine/phosphomethylpyrimidine kinase resulting in the release of 2-Methyl-4-amino-5-hydroxymethylpyrimidine diphosphate. The latter compound reacts with 4-methyl-5-(2-phosphonooxyethyl)thiazole, a product of oxythiamine metabolism, through a Thiamine biosynthetic bifunctional enzyme resultin in the release of a Thiamine monophosphate. The latter compound is phosphatased through a acid phosphatase complex resulting in the release of thiamine. The latter compound is phosphorylated through a thiamin pyrophosphokinase resulting in the release of thiamine pyrophosphate.