Đề 13 – Bài tập, đề thi trắc nghiệm online Hóa sinh lipid

Chylomicrons are the largest and least dense lipoproteins, specifically designed to transport dietary (exogenous) triacylglycerols and other lipids from the intestines to the rest of the body. VLDL transports endogenously synthesized triacylglycerols from the liver. LDL and HDL are involved in cholesterol transport.

Adipocytes are specialized cells designed for the storage of energy in the form of triacylglycerols (triglycerides). They contain large lipid droplets primarily composed of triacylglycerols. While adipocytes also contain other lipids like phospholipids and cholesterol as components of their membranes, the bulk of lipid storage in adipocytes is in the form of triacylglycerols.

Cholesterol serves as a precursor for steroid hormones and bile acids, and is a crucial component of cell membranes, affecting their fluidity. However, cholesterol is not a primary energy storage molecule; triacylglycerols fulfill that role. Cholesterol is transported in lipoproteins, not directly stored in adipose tissue for energy.

Glycolipids are primarily located in the outer leaflet of the plasma membrane in eukaryotic cells. The carbohydrate portion extends into the extracellular space, where they play roles in cell-cell recognition, cell adhesion, and as receptors for toxins and pathogens. They are asymmetrically distributed and not typically found in inner membranes of organelles.

Lipids are defined by their hydrophobic or amphipathic nature, meaning they are poorly soluble or have both hydrophobic and hydrophilic regions, respectively, in water. While they are composed of C, H, and O, and some contain phosphate, hydrophobicity is the unifying characteristic. Not all are polymers or contain phosphate groups (e.g., steroids).

Saturated fatty acids are `saturated` with hydrogen atoms and contain only carbon-carbon single bonds in their hydrocarbon chain. Unsaturated fatty acids contain one or more carbon-carbon double bonds. Benzene rings are not characteristic of fatty acids, and while essential fatty acids exist, saturation refers to bond type, not dietary necessity.

Acetyl-CoA carboxylase (ACC) catalyzes the carboxylation of acetyl-CoA to malonyl-CoA, which is the first committed and rate-limiting step in fatty acid synthesis. Fatty acid synthase is a multi-enzyme complex that carries out the subsequent steps of fatty acid chain elongation. Carnitine acyltransferase I is involved in fatty acid transport into mitochondria for beta-oxidation. HMG-CoA reductase is the rate-limiting enzyme in cholesterol synthesis.

Beta-oxidation of fatty acids, the process of breaking down fatty acids to generate acetyl-CoA for energy production, primarily occurs in the mitochondrial matrix in eukaryotic cells. This compartmentalization allows for efficient energy generation and prevents interference with other cellular processes in the cytoplasm.

In lipid absorption, micelles are small, spherical aggregates formed in the intestinal lumen from bile acids, fatty acids, 2-monoacylglycerol, and cholesterol. These micelles are crucial for transporting poorly soluble lipid digestion products to the surface of intestinal epithelial cells, facilitating their absorption. They are not large fat globules, vesicles for intracellular transport, or lipoproteins for blood transport.

A high carbohydrate diet, especially when caloric intake exceeds energy expenditure, typically leads to increased lipogenesis in the liver. Excess glucose is converted to acetyl-CoA, which is then used for fatty acid synthesis. Insulin, which is elevated in response to high glucose, promotes lipogenesis. Prolonged fasting, insulin deficiency, and increased glucagon levels (associated with low glucose) generally suppress lipogenesis and promote fatty acid oxidation and gluconeogenesis instead.

Triacylglycerols are formed by the esterification of three fatty acids to a glycerol molecule. This structure allows for efficient energy storage because of the high energy content of fatty acids and the neutral, hydrophobic nature of the molecule, enabling dense packing.

Phospholipids, specifically glycerophospholipids, are built upon a glycerol backbone to which two fatty acids and a phosphate group are attached. The phosphate group is often further esterified to a polar head group, contributing to the amphipathic nature of phospholipids. Sphingosine is the backbone for sphingolipids, not glycerophospholipids. Cholesterol is a steroid lipid, not a phospholipid.

PPARs are transcription factors, meaning they bind to DNA and regulate gene expression. They play a central role in regulating the expression of genes involved in various aspects of lipid metabolism, including fatty acid oxidation, lipid uptake, adipogenesis, and inflammation. They do not directly catalyze reactions, transport lipids, or degrade lipids in lysosomes.

High-density lipoproteins (HDL) are often referred to as `good cholesterol` because they are involved in reverse cholesterol transport. HDL particles pick up excess cholesterol from peripheral tissues and transport it back to the liver for excretion or conversion to bile acids. LDL is often termed `bad cholesterol` as it delivers cholesterol to peripheral tissues, and high levels are associated with atherosclerosis.

Bile acids, synthesized from cholesterol in the liver, act as detergents to emulsify dietary lipids in the small intestine. This emulsification breaks down large fat globules into smaller droplets, significantly increasing the surface area available for pancreatic lipases to hydrolyze triacylglycerols. Bile acids do not hydrolyze triacylglycerols themselves nor directly transport fatty acids across cells or synthesize triacylglycerols.

Sphingolipids are characterized by their sphingosine backbone, an 18-carbon amino alcohol. Glycerol is the backbone of glycerolipids and glycerophospholipids. Cholesterol is a steroid lipid. Isoprene is the precursor for isoprenoids, including steroids, but not the direct backbone of sphingolipids.

For a saturated fatty acid with `n` carbons, (n/2) - 1 rounds of beta-oxidation are required for complete oxidation. For a 16-carbon fatty acid (like palmitic acid), it requires (16/2) - 1 = 8 - 1 = 7 rounds of beta-oxidation. Each round removes two carbons in the form of acetyl-CoA.

Cholesterol esterase (also known as cholesterol ester hydrolase) is the enzyme that specifically hydrolyzes cholesterol esters, breaking them down into free cholesterol and fatty acids in the small intestine. Pancreatic lipase acts on triacylglycerols. Phospholipase A2 hydrolyzes phospholipids. Lipoprotein lipase acts on triacylglycerols in lipoproteins in the bloodstream, not in digestion within the intestine.

Linoleic acid (an omega-6 fatty acid) and alpha-linolenic acid (an omega-3 fatty acid) are essential fatty acids for humans. We lack the enzymes to introduce double bonds at certain positions in fatty acid chains, specifically beyond carbon 9 from the carboxyl end. Palmitic, oleic, and stearic acids can be synthesized by the human body.

Ketogenesis is significantly increased during prolonged fasting or in uncontrolled diabetes mellitus. In these conditions, glucose availability is low or glucose cannot be properly utilized (in diabetes), forcing the body to rely on fatty acid oxidation for energy. This leads to excess acetyl-CoA production, which is then diverted to ketogenesis in the liver.

Arachidonic acid, a 20-carbon polyunsaturated fatty acid, is the primary precursor for most eicosanoids, including prostaglandins, thromboxanes, leukotrienes, and lipoxins. These signaling molecules play crucial roles in inflammation, pain, fever, blood clotting, and other physiological processes. Palmitic, stearic, and oleic acids are common fatty acids but not the primary precursors for eicosanoids.

Apolipoprotein B (apoB) is essential for the assembly and secretion of both very-low-density lipoproteins (VLDL) from the liver and chylomicrons from the intestines. In abetalipoproteinemia, the inability to produce apoB leads to a severe deficiency in VLDL and chylomicron formation, resulting in malabsorption of dietary fats and fat-soluble vitamins and very low levels of LDL cholesterol (as LDL is derived from VLDL).

Glycerol-3-phosphate dehydrogenase reduces dihydroxyacetone phosphate (DHAP), an intermediate of glycolysis, to glycerol-3-phosphate. Glycerol-3-phosphate is a precursor for both triacylglycerol synthesis and glycerophospholipid synthesis, as well as in glyceroneogenesis (the synthesis of glycerol-3-phosphate from non-carbohydrate precursors). Glycerol is phosphorylated by glycerol kinase to form glycerol-3-phosphate, but GPDH uses DHAP as a substrate.

Lipids serve roles in energy storage, membrane structure, and signaling. However, the catalysis of biochemical reactions is primarily the function of enzymes, which are proteins (though some RNAs can also act as catalysts). Lipids do not typically function as enzymes.

Hormone-sensitive lipase (HSL) is the primary enzyme responsible for the hydrolysis of stored triacylglycerols in adipocytes during lipolysis. It initiates the breakdown of triacylglycerols into diacylglycerols and fatty acids. Subsequent lipases complete the hydrolysis to monoacylglycerols and finally glycerol and free fatty acids, which are then released into the bloodstream. HSL is catabolic, not anabolic, and does not transport fatty acids or synthesize cholesterol esters.

The carnitine shuttle system is essential for transporting long-chain fatty acids from the cytoplasm into the mitochondrial matrix, where beta-oxidation occurs. Fatty acids need to be activated to fatty acyl-CoA in the cytoplasm, then conjugated with carnitine to cross the inner mitochondrial membrane. It`s not involved in acetyl-CoA transport out of mitochondria, carnitine synthesis from fatty acids, or inhibiting beta-oxidation in low fatty acid conditions.

Pancreatic lipase is the primary enzyme responsible for hydrolyzing dietary triacylglycerols (triglycerides) in the small intestine. It cleaves the ester bonds at positions 1 and 3 of the glycerol backbone, releasing 2-monoacylglycerol and free fatty acids. While other lipases exist for phospholipids and cholesterol esters, pancreatic lipase specifically targets triacylglycerols as its main substrate.

Lipoxygenases (LOXs) are a family of enzymes that catalyze the synthesis of leukotrienes from arachidonic acid. Cyclooxygenases (COXs) are responsible for the synthesis of prostaglandins and thromboxanes. Phospholipase A2 releases arachidonic acid from membrane phospholipids, making it available for both COX and LOX pathways. Acyltransferases are involved in esterification reactions, not eicosanoid synthesis from arachidonic acid.

Lipid rafts are membrane microdomains enriched in cholesterol and sphingolipids, particularly sphingomyelin. These lipids tend to have saturated fatty acids, which allows for tighter packing and decreased membrane fluidity compared to surrounding regions rich in glycerophospholipids with unsaturated fatty acids. Triacylglycerols are storage lipids, not structural components of membranes. Lipid rafts are lipid-rich, not protein-based structures.

Statins primarily lower cholesterol levels by inhibiting HMG-CoA reductase, the rate-limiting enzyme in the mevalonate pathway of cholesterol biosynthesis in the liver. By reducing cholesterol synthesis, statins lead to a decrease in LDL cholesterol levels in the blood. They do not primarily act by inhibiting intestinal absorption, increasing bile acid excretion, or increasing lipoprotein lipase activity, though some of these effects might be secondary.