Lipids and Lipoproteins

These flashcards cover key vocabulary terms and their definitions related to the lecture on lipids and lipoproteins, providing essential information for exam preparation.

Fatty Acids (FA)

Organic compounds that are the building blocks of lipids, characterized by long hydrocarbon chains.

Saturated Fatty Acids (SFA)

Fatty acids with no double bonds between carbon atoms.

Monounsaturated Fatty Acids (MUFA)

Fatty acids that contain one double bond in their structure.

Polyunsaturated Fatty Acids (PUFA)

Fatty acids that have two or more double bonds present in their hydrocarbon chain.

Cis Configuration

A type of unsaturated fatty acid configuration where hydrogen atoms are on the same side of the double bond.

Trans Configuration

A type of unsaturated fatty acid configuration where hydrogen atoms are on opposite sides of the double bond.

Essential Fatty Acids

Fatty acids that are necessary for human health but cannot be synthesized by the body.

Linoleic Acid (18:2 n-6)

An essential fatty acid that is a precursor to various long-chain fatty acids.

Triacylglycerols (Triglycerides)

A type of fat stored in the body, composed of glycerol and three fatty acids.

Phospholipids

Lipids that contain a phosphate group, important for forming cell membranes.

Sterols

A type of lipid characterized by a four-ring core structure, such as cholesterol.

Lipoproteins

Complexes of lipids and proteins that transport fats through the bloodstream.

Chylomicrons

Lipoproteins that transport dietary lipids from the intestines to other locations in the body.

Apolipoproteins

Protein components of lipoproteins that help stabilize them and direct them to their targets.

Atherosclerosis

A condition characterized by the buildup of lipids in the artery wall, which can lead to cardiovascular disease.

Eicosanoids

Signaling molecules derived from fatty acids that play important roles in inflammation and other physiological functions.

Ketogenesis

The process by which the liver converts excess fatty acids into ketone bodies during fasting.

Beta-Oxidation

The metabolic process that breaks down fatty acids into acetyl CoA for energy production.

Name the two main essential fatty acids and specify their omega classification and common food sources.

Linoleic Acid and Alpha-Linolenic Acid

How does the chain length of short / medium fatty acids affect their absorption?

Absorbed directly into the portal vein.

List food sources high in:

1. Monounsaturated Fatty Acids (MUFA)

2. Omega-3 Fatty Acids

3. Omega-6 Fatty Acids

1. Monounsaturated Fatty Acids (MUFA):

   • Olive oil, avocados, almonds, peanuts, cashews, sesame seeds.

2. Omega-3 Fatty Acids:

   • Fatty fish (salmon, mackerel, sardines), flaxseeds, chia seeds, walnuts, canola oil, soybean oil.

3. Omega-6 Fatty Acids:

   • Soybean oil, corn oil, sunflower oil, safflower oil, nuts, seeds.

Briefly describe the stages of lipid digestion, absorption, and transport.

1. Digestion:

   • Begins in mouth (lingual lipase) and stomach (gastric lipase) for short/medium chains.

   • Primarily occurs in small intestine: bile emulsifies fats, pancreatic lipase breaks down triacylglycerols into monoglycerides and free fatty acids.

2. Absorption:

   • In intestinal cells, monoglycerides and fatty acids are re-esterified into triacylglycerols.

   • Packaged with cholesterol, phospholipids, and apolipoproteins into chylomicrons.

3. Transport:

   • Chylomicrons transport dietary lipids from intestines via lymphatic system to bloodstream, delivering triacylglycerols to tissues.

   • Liver processes chylomicron remnants and synthesizes other lipoproteins (VLDL, LDL, HDL) for further lipid transport.

Body fat is stored as what primary compound in adipose tissue?

Body fat is primarily stored as triacylglycerols (triglycerides).

What is the key difference between phospholipids and glycolipids?

1. Phospholipids: Contain a phosphate group in their hydrophilic head; crucial components of cell membranes.

2. Glycolipids: Contain a carbohydrate group (sugar) in their hydrophilic head, but lack a phosphate group; involved in cell recognition and adhesion.

Name key compounds formed from cholesterol.

1. Steroid Hormones (e.g., cortisol, estrogen, testosterone)
2. Vitamin D
3. Bile Acids/Salts

Explain the source and role of bile, and discuss enterohepatic recirculation.

1. Source & Role of Bile:
   • Produced by the liver, stored in the gallbladder.
   • Role: Emulsifies dietary fats in the small intestine, increasing surface area for enzymatic digestion and aiding absorption of fats and fat-soluble vitamins.
2. Enterohepatic Recirculation:
   • About 95\% of bile salts are reabsorbed in the ileum and returned to the liver via the portal vein.
   • The liver then resecretes them, efficiently recycling bile and conserving cholesterol stores.

Describe lipid metabolism during the fed state (postprandial) and fasting state.

1. Fed State:
   • Excess energy from carbohydrates/proteins is converted into fatty acids and triacylglycerols in liver and adipose tissue (lipogenesis).
   • Triacylglycerols are transported in VLDL from the liver or stored in adipose tissue.
   • Glucose is the primary fuel source; fatty acid oxidation is suppressed.
2. Fasting State:
   • Stored triacylglycerols from adipose tissue are mobilized, broken into fatty acids and glycerol.
   • Fatty acids become a primary fuel source via beta-oxidation.
   • Prolonged fasting leads to the liver converting excess acetyl CoA from fatty acid oxidation into ketone bodies (ketogenesis) for alternative fuel.

Outline the process of atherosclerosis development.

1. Endothelial Damage: Initiated by risk factors (e.g., high blood pressure, LDL cholesterol, smoking).

2. Lipid Infiltration: LDL particles (especially oxidized LDL) penetrate and accumulate in the damaged arterial wall.

3. Immune Response: Macrophages infiltrate, engulf LDL, forming foam cells (fatty streaks).

4. Plaque Formation: Smooth muscle cells migrate, proliferate, and produce fibrous tissue. This combines with foam cells, calcium, and debris to form hard plaques that narrow arteries and can rupture, leading to thrombosis.

How do different types of fatty acids relate to cardiovascular disease (CVD) risk?

1. Saturated Fatty Acids (SFA): High intake associated with increased LDL cholesterol, raising CVD risk.

2. Trans Configuration (Trans Fatty Acids): Significantly raise LDL cholesterol and lower HDL cholesterol; considered most detrimental for CVD.

3. Monounsaturated Fatty Acids (MUFA): Generally beneficial; can lower LDL cholesterol and maintain/raise HDL, reducing CVD risk.

4. Polyunsaturated Fatty Acids (PUFA): Also help lower LDL cholesterol.

   • Omega-3 PUFAs: Anti-inflammatory, anti-arrhythmic, triglyceride-lowering effects; protective against CVD.

   • Omega-6 PUFAs: Reduce LDL cholesterol.

What is HMG-CoA reductase and what is its function?

HMG-CoA reductase (3-hydroxy-3-methylglutaryl-CoA reductase) is the rate-limiting enzyme in the mevalonate pathway, which is responsible for cholesterol synthesis. Its function is to catalyze the reduction of HMG-CoA to mevalonate, a key step in cholesterol production. It is the target of statin drugs.

Does an elevation of insulin level favor the synthesis of triacylglycerols or their breakdown?

An elevation of insulin level favors the synthesis of triacylglycerols (lipogenesis) and inhibits their breakdown (lipolysis). Insulin, an anabolic hormone, promotes glucose uptake, enhances fatty acid synthesis, and suppresses fat breakdown.

Explain fatty acid synthesis and beta-oxidation of fatty acids.

1. Fatty Acid Synthesis (Lipogenesis):

   • Occurs in the cytoplasm (primarily liver, adipose cells) when energy is abundant.

   • Acetyl CoA (from glucose metabolism) is the building block.

   • 2-carbon units are added to form long-chain fatty acids (e.g., palmitate), which then combine with glycerol to form triacylglycerols for storage.

2. Beta-Oxidation:

   • Metabolic process in the mitochondria that breaks down fatty acids into acetyl CoA for energy.

   • Fatty acyl-CoA molecules are systematically broken down in cycles, removing 2 carbons at a time, producing 1 acetyl CoA, 1 FADH_2, and 1 NADH per cycle.

Under what conditions does the usual concentration of ketone bodies in the bloodstream increase?

The concentration of ketone bodies increases under conditions where the body relies heavily on fat for energy due to carbohydrate scarcity or impaired glucose use:

1. Prolonged Fasting or Starvation

2. Low-Carbohydrate (Ketogenic) Diets

3. Uncontrolled Type 1 Diabetes Mellitus

Why would a diet rich in simple carbohydrates increase triacylglycerol synthesis in the body?

A diet rich in simple carbohydrates increases triacylglycerol synthesis due to:

1. Excess Glucose Intake: Glucose intake exceeds immediate energy needs and glycogen storage capacity.

2. Lipogenesis: Excess glucose is converted to acetyl CoA via glycolysis, then shunted into fatty acid synthesis (lipogenesis) in the liver.

3. Insulin Release: High blood glucose from simple carbs triggers significant insulin release. Insulin promotes fat storage by stimulating glucose uptake, enhancing fatty acid synthesis, and inhibiting fat breakdown.

4. VLDL Synthesis: Newly synthesized triacylglycerols are packaged into VLDL and secreted by the liver for transport and storage in adipose tissue.

What roles do apolipoproteins have in lipid metabolism?

Apolipoproteins (protein components of lipoproteins) play crucial roles in lipid metabolism:

1. Structural Integrity: Stabilize lipoprotein structure, making them soluble in blood.

2. Enzyme Cofactors: Activate enzymes involved in lipid metabolism (e.g., Apo C-II activates lipoprotein lipase).

3. Receptor Ligands: Direct lipoproteins to target tissues by binding to cell surface receptors (e.g., Apo B-100, Apo E).

4. Regulation: Regulate synthesis, secretion, processing, and clearance of lipoproteins, controlling lipid distribution.

how does chain length for long chain fatty acids effect absorption?

Packaged into chylomicrons for transport via the lymphatic system before entering the bloodstream.