NUTR*4510 - Unit 5: Alcohol and Nutrition

The primary enzyme responsible for ethanol metabolism in the liver, converting ethanol to acetaldehyde. This enzyme is most active at low to moderate alcohol consumption.

A cytochrome P450 enzyme that plays a significant role in ethanol metabolism, particularly at high or chronic alcohol consumption. It converts ethanol to acetaldehyde.

A highly reactive molecule that can damage DNA, proteins, and lipids, leading to cellular damage. It is a byproduct of the ethanol metabolism process, particularly via CYP2E1.

A vital antioxidant that helps protect cells from damage caused by reactive oxygen species . It is essential in counteracting the negative effects of ROS generated during alcohol metabolism.

An enzyme that converts acetaldehyde to acetate, the final product of ethanol metabolism.

The primary enzyme responsible for ethanol metabolism within the brain.

Single nucleotide polymorphisms (SNPs) are variations in the DNA sequence, and their presence in genes involved in ethanol metabolism can impact individual responses to alcohol, influencing the rate and efficiency of metabolism.

The extent to which ethanol is metabolized by ADH or CYP2E1 is influenced by factors like the amount of alcohol consumed, its frequency, and the individual's genetic makeup (SNPs).

Alcohol is rapidly absorbed into the bloodstream due to its small size and ability to dissolve in both fats and water. The majority of alcohol is absorbed in the small intestine, with a smaller portion absorbed in the stomach.

Ethanol, the parent compound of alcohol, is the active agent that affects the central nervous system. Ethanol is not broken down into another substance before it exerts its effects.

Alcohol affects the brain by altering the function of synapses. It works by interrupting communication between nerve cells.

Alcohol metabolism in the liver involves two primary enzymes: alcohol dehydrogenase and acetaldehyde dehydrogenase. About 80% of alcohol is metabolized by alcohol dehydrogenase, while the remaining 20% is metabolized by CYP2E1.

Alcohol dehydrogenase is an enzyme found in the liver that converts alcohol into acetaldehyde. Acetaldehyde is a harmful product that can damage DNA, proteins, and lipids, leading to tissue damage like cirrhosis.

Acetaldehyde dehydrogenase is an enzyme found in the mitochondria of liver cells. It metabolizes acetaldehyde, a toxic compound, into acetic acid. This is a crucial step in detoxifying alcohol.

Acetic acid, the final metabolic product of alcohol, can be used as a source of energy by the body. It enters the TCA cycle and is converted to Acetyl-CoA, which is used for various metabolic processes.

Chronic alcohol consumption can lead to several health problems due to the cumulative effects of acetaldehyde and reactive oxygen species. Long-term exposure causes inflammation and scarring in tissues, particularly the liver.

Alcohol use disorders can result in pancreatitis, impacting the pancreas' ability to release enzymes needed for lipid and protein digestion. This affects the absorption of fat-soluble vitamins, particularly vitamin D, leading to decreased calcium levels and potential bone health issues.

Alcohol consumption can lead to impaired lipid digestion, causing steatorrhea (fat in the stool) due to the reduced absorption of fat-soluble vitamins, especially vitamin D.

Alcohol can negatively impact protein digestion and absorption, leading to diarrhea. This can cause deficiencies in nutrients essential for crucial metabolic processes, potentially impacting overall health.

Impaired lipid digestion in alcoholic drinkers can lead to decreased absorption of fat-soluble vitamins, like vitamin D. This can contribute to poor calcium status and increase the risk of osteoporosis due to inadequate bone mineralization.

Alcohol consumption can impair the liver's function, which affects bile composition. This, in turn, further disrupts lipid digestion and the movement of lipophilic vitamins throughout the body. This compounded effect significantly impacts overall nutrient absorption and can contribute to multiple health issues.

Ethanol affects the small intestine's ability to move food properly. It disrupts the enteric nervous system, causing it to misinterpret food signals and reducing digestive wave activity. This leads to faster food movement and diarrhea.

Ethanol's disruption of small intestine motility prevents mixing of food with digestive enzymes and reduces nutrient absorption. This can lead to malabsorption and nutrient deficiencies over time.

Ethanol can cause the tips of the small intestine's villi to shed, reducing their surface area available for nutrient absorption. This, along with other effects, can lead to nutrient deficiencies and potential bleeding.

Ethanol can lead to a reduction in pancreatic enzyme secretion, which is necessary for efficient digestion of lipids and proteins. This can lead to maldigestion and nutrient deficiencies.

Ethanol can increase the activity of retinyl esterase, an enzyme involved in vitamin A metabolism. The long-term effects of this increased activity are not fully understood.

Excessive alcohol consumption leads to a decrease in the absorption capacity of the small intestine due to the damage to villi. It is a gradual process and may occur even with moderate alcohol consumption.

Long-term heavy drinking results in significant damage to the villi of the small intestine. This leads to malabsorption of nutrients and makes the body more susceptible to infections because the weakened lining can't protect against harmful bacteria.

The damaged small intestine lining causes bleeding into the abdominal cavity. This triggers the body to evacuate the blood, causing an increase in the frequency of bowel movements and diarrhea.

Retinyl palmitate is the primary storage form of vitamin A in the body, primarily found in the liver.

Retinol is the biologically active form of vitamin A, involved in various functions like vision, cell growth, and immune function.

Night blindness is a hallmark deficiency symptom, indicating a lack of functional rhodopsin.

Dietary vitamin A is converted to retinyl palmitate, packaged within chylomicrons, and transported to the liver.

Retinyl palmitate is stored in liver stellate cells until needed, when it's converted back to retinol by retinyl esterase.

Retinol, bound to RBP and PA, circulates in the blood to maintain homeostatic levels and distribute vitamin A to different tissues.

Blood retinol levels reflect whole-body vitamin A status, but they remain stable until liver stores are drastically depleted.

The liver plays a critical role in maintaining vitamin A homeostasis, storing and releasing it based on the body's needs.

The conversion of retinol to retinoic acid by alcohol dehydrogenase (ADH) can lead to vitamin A deficiency by depleting liver stores.

Acute alcohol use stimulates the conversion of retinyl palmitate to retinol, leading to a temporary rise in blood retinol levels.

Chronic alcohol use leads to sustained increase in retinyl esterase activity, which depletes retinyl palmitate stores in stellate cells. This can lead to vitamin A deficiency if not addressed.

Retinyl esterase is an enzyme responsible for converting retinyl palmitate, a stored form of Vitamin A, to retinol, the active form of the vitamin.

Retinol is converted to retinoic acid by alcohol dehydrogenase, which plays a role in gene expression and cell differentiation. The short half-life of retinoic acid requires continuous retinol conversion.

CYP2E1, an enzyme induced by chronic alcohol use, converts retinol to 4-hydroxy-retinol, a form that is then excreted. This can lead to vitamin A deficiency by removing retinol from the body.

Retinol is bound to retinol-binding protein (RBP), which, in turn, binds to prealbumin (PA). This complex enables retinol transport in the bloodstream, maintaining a stable blood concentration.

Alcohol can interfere with vitamin A metabolism and absorption, leading to lower blood retinol levels and vitamin A deficiency, which can have a range of adverse effects on health.