How are ketones formed quizlet nutrition?

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cells like RBCs that lack mitochondria, rely only on this to produce ATP because without the mitochondria, you can't use the electron transport chain and oxidative phosphorylation pathways

Therefore, when RBCs convert glucose to pyruvate, NADH + H+ builds up in the cell. Eventually, NAD+ concentration falls too low to permit glycolysis to continue. The anaerobic pathway makes lactate to regenerate NAD+

the lactate produced is then released into the blood, picked up mostly by the liver, and then used to synthesize pyruvate, glucose, or some other intermediate

when anaerobic glycolysis frees NAD+, it returns it to the glycolysis pathway to pick up more hydrogen ions and electrons

In anaerobic environments, some microorganisms like yeast produce ethanol, instead of lactate from glucose. Other microorganisms produce various forms of short chain fatty acids. All of these anaerobic metabolisms are fermentation.

Ketosis is a condition that can occur through the metabolic process of developing ketone bodies, which is influenced by a diet with inadequate carbohydrates and hormonal imbalances (such as deficient insulin production). When someone consumes a diet with inadequate carbs, oxaloacetate can become deficient, and the citric acid cycle can consequently decrease its activity. Lipolysis, a process within fat metabolism, will continue though, so acetyl-CoA production from fatty acids will proceed, causing an acetyl-CoA build up, as an effect of oxaloacetate not being readily available to permit acetyl-CoA to enter into the citric acid cycle. Since acetyl-CoA is prevented from entering the citric acid cycle, these molecules can join together and form ketone bodies (result from the incomplete breakdown of fats, contain 3-4 carbons, contain a ketone chemical group). Most ketone bodies revert to being converted back into acetyl-CoA in other body cells, and they then can enter the citric acid cycle, where they can become fuel.

One unique and interesting symptom of ketosis is that the patient may have a fruity scented breath because acetone, a ketone body, can exit the body during exhalation.

Unmanaged type 1 diabetes can also cause a proneness to a type of ketosis called diabetic ketoacidosis because normal fat and carbohydrate metabolism is being prevented, as an effect of deficient insulin. Consequently, cells can't readily use glucose, although lipolysis continues, causing excessive ketone body production. When the blood's quantity of ketone bodies exceeds optimal limits, they can spill into the urine, pulling sodium and potassium (electrolytes) with them. Eventually, severe ion imbalances occur, and the body becomes more acidic because ⅔ of ketone bodies have acid groups. This form of ketosis can even lead to coma or death if untreated, and these patients require immediate treatment with insulin, electrolytes, and fluid.

When someone is fasting, ketosis can also arise because the quantity of blood glucose falls, along with insulin. The decreased insulin then causes fatty acids to flood into the bloodstream, causing ketone bodies to form in the liver. This type of malnutrition triggers a survival mechanism, and the heart, muscles, and portions of the kidney can utilize ketone bodies for energy. After a few days with ketosis from hunger, the brain also reverts to metabolizing ketone bodies for energy. As more body cells rely on ketone bodies for energy, the necessity for glucose declines, which decreases the liver and kidneys needs for glucose from amino acids and the glycerol released from lipolysis, which "spares" a lot of the body protein from being broken down for fuel. The maintenance of body protein mass is also an essential survival mechanism, and death becomes more likely when ½ of the body's protein mass has been depleted (around 50-70 days of starvation).

present only in liver cells and certain kidney cells

pathway that produces glucose from certain amino acids

The starting material is oxaloacetate, which is derived primarily from the carbon skeletons of some amino acids like alanine. Pyruvate can also be converted to oxaloacetate, as well as other glucogenic precursors, like lactate and glycerol

begins in the mitochondria with the production of oxaloacetate. The 4 carbon oxaloacetate eventually returns to the cytosol, where it loses 1 CO2, forming the 3 carbon compound called phosphoenolpyruvate, which then reverses the path back through glycolysis to form glucose. It takes 2 of these 3 carbon compounds to produce the 6 carbon glucose. The whole process requires ATP, as well as the coenzyme forms of the B vitamins biotin, riboflavin, niacin, and B-6

The liver responds to hormones and makes use of vitamins. Liver stores nutrients, too.

ATP, enzymes, hormones, vitamins, and minerals also regulate

the hepatic metabolic function is conversion (the liver hosts many nutrient interconversions, and most nutrients must first pass through the liver after absorption)

some hepatic conversions are between forms of simple sugars, fat synthesis, ketone body production, amino acid metabolism, urea production, alcohol metabolism,

in 1/10,000 births to 1/15,000 births; more common in Irish people

Dx by simple blood test within a few days of life because all states require PKU testing

most cases occur because the phenylalanine hydroxylase enzyme doesn't function efficiently in the liver. Normally, this enzyme doesn't function efficiently in the liver. Normally, this enzyme would convert phenylalanine into tyrosine. If this doesn't take place, phenylalanine will build up in the blood and tyrosine will become deficient. If not corrected within 30 days after birth, the phenylalanine build up leads to the production of toxic phenylalanine by-products, like phenylpyruvic acid, which can lead to severe irreversible intellectual disability.

After Dx, patient is put on restricted diet (phenylalanine is essential, but these patients require controlled amounts to prevent toxic build up). Your child will need a special formula, and there are even these sorts of formulas for adults. When you introduce solid foods, fruits and vegetables (generally low in phenylalanine), and grains (moderate phenylalanine) will be allowed, but dairy products, eggs, meats, and nuts (high phenylalanine) won't be allowed. Avoid all foods that contain the ingredient "aspartame" because it contains phenylalanine.

Discontinuing the special diet early can lead to decreased intelligence, increased behavior problems like aggressiveness or hyperactivity, decreased attention span,

a woman with this condition must follow the proper diet at least 6 months before becoming pregnant because otherwise the fetus (even though he/she may not have PKU), will be exposed to a high blood phenylalanine level and the related toxic products from the mother. Birth defects or death can even occur. All pregnancies of PKU patients need close supervision.

Congenital conditions where someone lacks a specific enzyme needed to perform normal metabolic functions. As an effect, the metabolic pathway that needs that enzyme won't function normally. This causes alternative metabolic products to be formed, which can be toxic to the body.

These occur when someone inherits a defective gene coding for a specific enzyme from both parents. Both parents have to be carriers of the defected gene.

When someone has a defective gene, they'll produce a defective protein based on the instructions given.

Symptoms usually appear after birth, when an otherwise physically well child loses appetite, vomits, is dehydrated, weak, or experiences developmental delays after birth

These usually involve one to a few enzymes, which usually participate in catabolic pathways.

No cure, but these conditions can be controlled (how depends on the type)

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