Vitamins: Water and Fat Soluble

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Vitamins and urine discoloration

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Vitamins are organic molecules that function in a wide variety of capacities within the body. The most prominent function of the vitamins is to serve as cofactors co-enzymes for enzymatic reactions. The distinguishing feature of the vitamins is that they generally cannot be synthesized by mammalian cells and, therefore, must be supplied in the diet. The vitamins are of two distinct types, vitamins and urine discoloration, water soluble and fat soluble.

For more information on the food products that are good sources of the individual vitamins and urine discoloration visit the Supplement Science page. The minerals that are considered of dietary significance are those that are necessary to support biochemical vitamins and urine discoloration by serving both functional and structural roles as well as those serving as electrolytes. The use of the term dietary mineral is considered archaic since the intent of the term "mineral" is to describe ions not actual minerals.

There are both quantity elements required by the body and trace elements. The quantity elements are sodium, magnesium, phosphorous, sulfur, chlorine, potassium and calcium. The essential trace elements are manganese, iron, cobalt, nickel, copper, zinc, selenium, molybdenum, and iodine, vitamins and urine discoloration. Additional trace elements although not considered essential are boron, chromium, fluoride, vitamins and urine discoloration, and silicon.

Thiamine also written thiamin is also known as vitamin B 1. Thiamine is derived from a substituted pyrimidine and a thiazole which are coupled by a methylene bridge. Thiamine is the form of vitamin B 1 that is absorbed from the small intestine. Thiamine uptake from the intestines is a function of the solute carrier transporter family member encoded by the SLC19A2 gene.

Thiamine is rapidly converted to its active form, thiamine pyrophosphate, TPP, by the enzyme thiamine pyrophosphokinase 1, TPK1. The TPK1 gene is located on chromosome 7q34q35 and is composed of 27 exons that generate two alternatively spliced mRNAs encoding isoforms of amino acids isoform a and amino acids isoform b. Expression of the TPK1 gene is highest in the liver and brain. Uptake of thiamine into cells occurs primarily through the activity of the SLC19A3 encoded transporter.

TPP is necessary as a cofactor for three critical dehydrogenases, vitamins and urine discoloration. These three dehydrogenases also require the co-factors derived from the vitamins lipoic acid, vitamins and urine discoloration, pantothenic acid CoAriboflavin, and niacin.

For this reason these three dehydrogenases are often referred to as the T ender thiamine L oving lipoic acid C are CoA F or flavin N ancy niacin enzymes. In addition to these three dehydrogenases, TPP is a required co-factor for the transketolase catalyzed reactions of the pentose phosphate pathway. A deficiency in thiamine intake leads to a severely reduced capacity of cells to generate energy and to carry out reductive biosynthetic reactions as well as to synthesize nucleotides because of its role in each of these enzymes.

The dietary requirement for thiamine is proportional to the caloric intake of the diet and ranges from 1. The richest sources of vitamin B 1 include yeasts and animal liver. Additional sources include whole-grain cereals, rye and whole-wheat flour, navy beans, vitamins and urine discoloration, kidney beans, wheat germ, as well as pork and fish. The earliest symptoms of thiamine deficiency include constipation, appetite suppression, and nausea.

Progressive deficiency will lead to mental depression, peripheral neuropathy vitamins and urine discoloration fatigue. Chronic thiamine deficiency leads to more severe neurological symptoms including ataxia, mental confusion and loss of eye coordination nystagmus. A highly diagnostic physical test of thiamine deficiency is vertical nystagmus. Vertical nystagmus is characterized by spontaneous upbeating or downbeating of the eyeball. There are numerous causes or horizontal nystagmus but vertical is only seen due to the CNS damage associated with thiamine deficiency or with phencyclidine PCP intoxication.

Additional clinical symptoms of prolonged thiamine deficiency are related to cardiovascular and musculature defects. Dietary thiamine deficiency is known as beri beriis most often the result of a diet that is carbohydrate rich and thiamine deficient. An additional thiamine deficiency related syndrome is known as Wernicke syndrome which is most often associated with chronic alcohol consumption. This disease is most commonly found in chronic alcoholics due to the fact that alcohol impairs thiamine uptake from the small intestine as well as the fact that these individuals generally have poor dietetic lifestyles.

Wernicke syndrome is also referred to as dry beri beri. Prolonged dietary deficiency in thiamine leads to wet beri beri. The wet form of the disease is the result the cardiac involvement in the deficiency. At this stage in the deficiency all four chambers of the heart enlarge due to loss of energy generation and fluid retention resulting in what is called dilated cardiomyopathy.

Systole relates to the force associated with cardiac contraction expelling blood to arteries. Blood pumped from the left ventricle enters the aorta and is delivered to the body, whereas blood pumped from the right ventricle is sent to the lungs.

When thiamine deficiency manifests with CNS involvement it is called Korsakoff encephalopathy or Korsakoff psychosis and is also commonly referred to as Wernicke-Korsakoff syndrome WKS.

WKS is characterized by acute encephalopathy progressing to chronic vitamins and urine discoloration of short-term memory. Thiamine supplementation can reverse the symptoms of beri beri and Wernicke syndrome, however, the vitamins and urine discoloration of severe deficiency WKS are irreversible. The confabulation of Korsakoff psychosis is due to destruction vitamins and urine discoloration the mammillary bodies in the brain, vitamins and urine discoloration.

The mammillary bodies are composed of two small round structures at the underside of the brain that are part of the limbic system, specifically they are part of the Papez circuit. This circuit is also called the hippocampal-mammillo-thalamo-cortical pathway. The consequence of destruction of the mammillary bodies is retrograde amnesia. Persons afflicted with an inherited form of Wernicke-Korsakoff syndrome appear to have an inborn error of metabolism that is clinically important only when the diet is inadequate in thiamine.

These individuals were thought to harbor an abnormality in the enzyme, vitamins and urine discoloration, transketolase. Although a variant transketolase enzyme has been proposed to be associated with Wernicke-Korsakoff syndrome, no mutations have been found in the gene spiriva and importantce TKT encoding this enzyme when cloned from patients exhibiting the syndrome. It has been speculated that the protein encoded by a transketolase-related gene transketolase-like 1: Intense interest in the TKTL1 gene, and its encoded protein, was stimulated because it saunas and weight loss shown that the level of TKTL1 expression correlated with poor patient outcomes and metastasis in many solid tumours.

A Wernicke-like encephalopathy is associated with mutations in one of the thiamine transporter genes. As indicated above, cellular uptake of thiamine occurs via the transporter encoded by the SLC19A3 gene. Riboflavin is also known as vitamin B 2. Dietary riboflavin is absorbed from the small intestine through the action of the solute carrier family member transporter encoded by the SLC52A3 gene.

The SLC52A2 gene is highly expressed in the brain and mutations in this gene result in the autosomal recessive progressive neurological disorder known as Brown-Vialetto-Van Laere syndrome 2. RFK introduces a phosphate group onto the terminal hydroxyl of riboflavin. The RFK gene is located on chromosome 9q The FLAD1 gene is located on chromosome 1q Several flavoproteins also contain metal ions and are termed metalloflavoproteins.

Additional important metabolic regulatory enzymes that require flavin as a co-factor include, succinate dehydrogenase TCA cycle and complex II of oxidative phosphorylationglycerolphosphate dehydrogenase involved in the glycerol phosphate shuttle and triglyceride synthesisand xanthine oxidase involved in purine nucleotide catabolism.

The normal vitamin k and blood thinner requirement for riboflavin is 1. Riboflavin is found in dairy products, lean meats, poultry, fish, grains, broccoli, turnip greens, asparagus, vitamins and urine discoloration, spinach, and enriched food products.

Riboflavin deficiencies are rare in the United States due to the presence of adequate amounts of the vitamin in eggs, milk, meat and cereals. Riboflavin deficiency is often seen in chronic alcoholics due to their poor dietetic habits. Symptoms associated with riboflavin deficiency include itching and burning eyes, angular stomatitis and cheilosis cracks and sores in the mouth and lipsbloodshot eyes, glossitis inflammation of the tongue leading vitamins and urine discoloration purplish discolorationseborrhea dandruff, flaking skin on scalp and facetrembling, sluggishness, and photophobia excessive light sensitivity.

Riboflavin decomposes when exposed to visible light. This characteristic can lead to riboflavin deficiencies in newborns treated for hyperbilirubinemia by phototherapy requiring dietary supplementation in these infants.

Niacin nicotinic acid is also known as vitamin B 3. With respect to niacin the designation NAD and NADP refers to the chemical backbone of the active form of the vitamin-derived cofactor. NADH is shown in the box insert where the "R" represents the adenine dinucleotide portion. The nicotinamide is then absorbed and delivered to the blood. Nicotinamide can also be hydrolyzed to nicotinic acid NA in the lumen of the small intestines and then absorbed. Intestinal uptake of nicotinic acid and nicotinamide is the function of the solute carrier family transporter encoded by the SLC22A13 gene.

The SLC22A13 encoded transporter is also involved in high affinity nicotinic acid exchange in the kidneys. Niacin is not a true vitamin in the strictest definition since NAD can be derived from the amino acid tryptophan.

However, the ability to utilize tryptophan for niacin synthesis is inefficient given that approximately 60 mg of tryptophan are required to synthesize 1 mg of NAD.

Also, synthesis of NAD from tryptophan requires vitamins B 1B 2 and B 6 which would be limiting in themselves on a marginal diet. The recommended daily requirement for niacin is 1319 niacin equivalents NE per day for a normal adult. One NE is equivalent to 1 mg of free niacin.

Niacin is found in liver, meat, peanuts and other nuts, vitamins and urine discoloration, and whole grains. In addition, foods that are rich in protein, with exception of tryptophan-poor grains, vitamins and urine discoloration, can satisfy some of the demand for niacin. However, due to the critical vitamin and mineral health benefits for NAD, most cells recycle the cofactor via salvage pathways as opposed to de novo synthesis, vitamins and urine discoloration.

The salvage pathways for NAD synthesis take place in both the nucleus and the mitochondria. Formation of NAD from nicotinamide NAM occurs in a two-step process and from nicotinic acid in a three-step process referred to as the Preiss-Handler pathway. Both reaction pathways require the activated form of ribose, 5-phosphoribosyl 1-pyrophosphate PRPP. PRPP is the same activated ribose required for nucleotide synthesis.

Nicotinamide is converted to nicotinamide mononucleotide NMN in what is a salvage pathway utilizing nicotinamide phosphoribosyltransferase which is encoded by the NAMPT gene, vitamins and urine discoloration.

Interestingly there was an activity that was identified at high levels in white adipose tissue that was purported to have insulin mimetic effects. This purported activity was originally called visfatin. The level of NAMPT activity changes under vitamins and urine discoloration dietary states such as nutrient status, stress, and during exercise.

Of clinical salmon and vitamin d is the fact that NAMPT levels are reduced in obesity decreasing its role in stress responses.

SIRT enzymes are critical in the regulation of gene expression through their ability to deacetylate histone proteinsthereby altering vitamins and urine discoloration structure. The NMNAT3 gene is located on lesson plan on anger 3q23 and is composed of 14 exons that generate seven alternatively spliced mRNAs collectively encode six different protein isoforms.

 

Vitamins and urine discoloration

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