fate of lipids Flashcards

1
Q

what is the difference in the composition of fats compared to carbohydrates and proteins.

A

contain much less oxygen than is contained in carbohydrates or proteins. therefore fats are more reduced and yield more energy when oxidized

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2
Q

what are the major lipids in the diet

A

triacyglycerols

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3
Q

describe how lipids are metabolised

A

Key points

  1. Fat is transported out of the intestines as chylomicrons out of the intestinal cells
  2. In times of excess of glucose, triacylglycerols are synthesised in the liver and transported out of the liver as very low density lipoproteins (VLDLs)
  3. The triacylglycerols can be taken out of the chylomicrons and VLDLs and converted to fatty acids and glycerol, once they are in the blood vessels of the adipose tissue
  4. Fatty acids and glycerol is converted into triacylglycerols in the adipose, where they are stored as an energy source.
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4
Q
A
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5
Q

what makes digestion of fats more complex than digestion of carbohydrates or protein

A

theyre not very soluble in water

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6
Q

triacylglycerols of the diet are emulsified where by what

A

intestine by bile salts

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7
Q

what does pancreatic lipase do to triacyglycerols

A

converts them in the lumen of the intestine to fatty acids and 2-monoacyglycerols which interact with bile salts to form micelles to be absorbed into the intestinal epithelial cells to be resynthesized into triacyglycerols

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8
Q

chylomicrons include what other substances and end up where

A

The triacylglycerols are packaged with proteins, phospholipids, cholesterol, and other compounds into the lipoprotein complexes known as chylomicrons, which are secreted into the lymph and ultimately enter the bloodstream.

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9
Q

what types of lipoproteins are produced in the fed state and what are their major functions

A
  • chylomicrons
  • VLDL

provide a blood transport system for triacyglycerols which are insoluble in water

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10
Q

what would happen if triacyglycerols directly eneterd the blood without a lipoprotein

A

they would coalesce impeding blood flow

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11
Q

what is beta oxidation

A

Beta-oxidation is a catabolic process in which fatty acids are broken down to generate acetyl-coA, which can then enter the Krebs cycle.

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12
Q

where do chylomicrons go

A

Chylomicrons are synthesized in intestinal epithelial cells, secreted into the lymph, pass into the blood, and become mature chylomicrons. The chylomicrons are taken to the adipose cells and on capillary walls in adipose tissue and muscle, lipoprotein lipase (LPL) digests the triacylglycerols (TG) of chylomicrons to fatty acids and glycerol.

Fatty acids (FA) are oxidized in muscle or stored in adipose cells as triacylglycerols. The remnants of the chylomicrons are taken up by the liver by receptor-mediated endocytosis. Lysosomal enzymes within the hepatocyte digest the remnants, releasing the products into the cytosol.

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13
Q

what is lipogenesis

A

the metabolic formation of fat:
Fatty acids are synthesized whenever an excess of calories is ingested. The major source of carbon for the synthesis of fatty acids is dietary carbohydrate. An excess of dietary protein also can result in an increase in fatty acid synthesis.

When an excess of dietary carbohydrate is consumed, glucose is converted to acetyl CoA and this can then be used as the building start for fat synthesis. This occurs in the liver.

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14
Q

how are fatty acids produced

A

in the hepatocytes and are combined with a glycerol molecule

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15
Q

how are triacylglycerols exported from hepatocytes

A

The triacylglycerol is packaged with cholesterol, phospholipids, and proteins to form very low density lipoproteins (VLDL). VLDL is secreted into the blood by the liver. VLDLs enable hydrophobic molecules, like lipids, to be transported into the bloodstream.

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16
Q

how are fatty acids stored in adipose tissue in the fed state

A

Step 1: Lipoprotein lipase (LPL) which is attached to capillary endothelial cells, cleaves the triacylglycerols in both VLDL and chylomicrons, forming fatty acids and glycerol. The LPL is activated by the increased levels of insulin.

Step 2: The fatty acids enter the adipose cells and are activated, forming fatty acyl CoA, which reacts with glycerol 3-phosphate (formed from glucose) to form triacylglycerol by the same pathway used in the liver. Because adipose tissue lacks glycerol kinase and cannot use the glycerol produced by LPL, the glycerol travels through the blood to the liver, which uses it for the synthesis of triacylglycerol. The resulting triacylglycerols are stored as large fat droplets in the adipose cells.

Furthermore, insulin stimulates the conversion of glucose to fatty acids in adipose cells, although the liver tends to be the major site of fatty acid synthesis.

17
Q

how are lipods metabolised in the fasting/starved state

A

during fasting, adipose triacylglycerols are mobilized by the process of lipolysis, which releases fatty acids and glycerol into the blood.

Use of fatty acids as a fuel increases with the length of the fast; they are the major fuel oxidized during overnight fasting. As fasting progresses, the liver produces glucose not only by glycogenolysis (the release of glucose from glycogen), but also by a second process called gluconeogenesis (the synthesis of glucose from noncarbohydrate compounds). The major sources of carbon for gluconeogenesis are lactate, glycerol, and amino acids.

When an animal has fasted for 3 or more days, they are in the starved state. The body attempts to spare protein, which will increase the amount of fat mobilised; however amino acids will remain the substrate for gluconeogenesis.

This occurs under the influence of increased glucagon concentrations and decreased insulin concentrations, due to the decreased levels of circulating blood glucose levels.

18
Q

discuss the process of lipolysis

A

Lipolysis: the breakdown of fats and other lipids by hydrolysis to release fatty acids.

During fasting, the decrease of insulin and the increase of glucagon stimulates lipolysis. A hormone-sensitive lipase cleaves a fatty acid from a triacylglycerol. Subsequently, other lipases complete the process of lipolysis, and fatty acids and glycerol are released into the blood.

The fatty acids, which travel in the blood complexed with albumin, enter cells of muscle and other tissues, where they are oxidized to CO2 and water to produce energy. During prolonged fasting, acetyl CoA produced by beta-oxidation of fatty acids in the liver is converted to ketone bodies, which are released into the blood. The glycerol derived from lipolysis in adipose cells is used by the liver during fasting as a source of carbon for gluconeogenesis.

19
Q

summarize the stages of fatty acid oxidation

A

Stage 1: Beta oxidation Pathway

This consists of the oxidative conversion of two carbon units to acetyl-CoA with the generation of NADH and FADH at the same time.

Stage 2: Oxidation of acetyl-CoA

This involves the oxidation of acetyl-CoA into carbon dioxide by the Krebs cycle (TCA), with the generation of NADH and FADH2 at the same time through oxidative phosphorylation (electron chain transport).

Stage 3: ATP generation

ATP is generated from NADH and FADH via the respiratory electron chain.

This process occurs in the liver and adipose tissue.

20
Q

discuss lipid metabolism during a prolonged fasting period

A

During prolonged fasting, adipose tissue continues to break down its triacylglycerol stores, providing fatty acids and glycerol to the blood. These fatty acids serve as the major source of fuel for the body. The glycerol is converted to glucose, whereas the fatty acids are oxidized to CO2 and H2O by tissues such as muscle. In the liver, fatty acids are converted to ketone bodies that are oxidized by many tissues, including the brain.

A number of factors determine how long an animal can fast and still survive. The amount of adipose tissue is one factor, because adipose tissue supplies the body with its major source of fuel. However, body protein levels can also determine the length of time we can fast. Glucose is still used during prolonged fasting (starvation), but in greatly reduced amounts. Although the animal degrades protein to supply amino acids for gluconeogenesis at a slower rate during starvation than during the first days of a fast, they are still losing protein that serves vital functions for our tissues. Protein can become so depleted that the heart, kidney, and other vital tissues stop functioning, or they can develop an infection and not have adequate reserves to mount an immune response. In addition to fuel problems, they are also deprived of the vitamin and mineral precursors of coenzymes and other compounds necessary for tissue function. Because of either a lack of ATP or a decreased intake of electrolytes, the electrolyte composition of the blood or cells could become incompatible with life. Ultimately, they die of starvation.

21
Q

an increased level of glucagon leads to what

A

Lipolysis occurs, which results in fatty acids and glycerol being released into the blood from adipose tissue.

22
Q

what happens to fatty acids entering the liver in times of fasting

A

fatty acids are partially oxidised into ketone bodies

23
Q

Which of the following statements is correct about the digestion of the fat which will be occurring in a dog who has just eaten a high fat meal

A

The fat is emulsified by bile from the gall bladder and digested by lipases in the small intestine to fatty acids and 2-monoacylglycerols.

24
Q

Once the fat has been digested to fatty acids and 2-monoacylglycerols, small fatty acids are taken to the liver via the hepatic portal vein. What happens to the fatty acids once they arrive in the liver?

A

The fatty acids can be converted to ketone bodies via beta oxidation or into triacylglycerols.

25
Q

How are the larger fatty acids transported from the intestines into the lymph

A

Intestinal cells oxidise fatty acids into triacylglycerols and package triacylglycerols together with proteins and phospholipids in chylomicrons for exocytosis.

26
Q

What happens to the chlyomicrons and VLDLs in the peripheral circulation when they reach the adipose tissue

A

The capillary endothelial cells release a lipoprotein lipase to digest the chylomicrons and VLDLs to glucose for absorption into the adipose tissue.