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Human Nutrition Flashcards

Human Nutrition

Arterial Lipid Deposition

  • Grade 0 (Normal Intima): No lipid deposits in the intima layer, observed in a 36-year-old male.
  • Grade 1: Characterized by fatty streaks, as seen in a 32-year-old male.
  • Grade 2: Also presents with fatty streaks, but with varying lipid density. Examples include a 39-year-old female and a 44-year-old male, with the latter showing greater total lipid density.
  • Grade 3 (Pathologic Intimal Thickening): Accumulation of lipid-laden macrophages (but not foamy) in the upper to middle layer of the intima, observed in a 49-year-old male.
  • Grade 3 (Pathologic Intimal Thickening with Foam Cells): Foam cells with clear cytoplasm and abundant intracellular lipids accumulated in the upper to middle layers of the intima, as seen in a 29-year-old male.
  • Key structures:
    • I = intima
    • M = media
    • Arrowheads indicate internal elastic lamina
    • Bars represent 100 μm

Saturated Fat, Vegetable Oil Consumption, and Heart Disease

  • A graph illustrates the relationship between saturated fat and vegetable oil consumption versus heart disease deaths in the USA from 1900 to 2010.
  • PUFA oils and oxidation: Oils high in polyunsaturated fatty acids (PUFAs) are susceptible to oxidation, especially when heated.
  • Toxic chemicals: Heating vegetable/seed oils can release toxic chemicals, potentially increasing cancer risk.
  • Recommendation: Use oils rich in PUFAs for cooking with caution.
  • Alternative: Saturated fats are less susceptible to oxidation and may be a better alternative for cooking.
  • Reheating oil: Not recommended due to increased free-fatty acid content, which lowers the smoke point and increases volatile emissions at lower temperatures.
  • Toxic Aldehyde Release: Heating oils at 180°C releases toxic aldehydes, with different oils (coconut, butter, olive, corn, sunflower) releasing varying concentrations over time (10-30 minutes).

Lipid Transport and Processing

  • Importance of understanding lipid mechanisms: Lipids are part of the atherogenic plaque, which drives the need to understand how they're transported and processed.
  • Clinical measurements: Measuring different lipid-rich particles in the blood helps understand the pathophysiology of CAD.
  • Hydrophobic nature: Lipids are transported in the bloodstream as constituents of lipoproteins due to their hydrophobic nature. NEFAs are an exception, circulating bound to albumin.
  • Lipoproteins: Chylomicrons, VLDL, IDL, LDL, and HDL circulate in the blood, varying in lipid composition, density, size, and metabolic function.
  • Apoproteins (Apo): Orchestrate the movement, distribution, and exchange of lipids.
    • Confer water solubility.
    • Regulate the activity of key enzymes in lipoprotein metabolism.
    • Mediate particle removal by binding to specific receptors on cell surfaces.
  • ApoB-48: Found in chylomicrons, originates from the intestine.
  • ApoB-100: Enriches VLDL and LDL, originates in the liver. Functions as a receptor ligand.
  • Apo-E: Exists in three isoforms, present in almost all lipoproteins. Synthesized in the liver and functions as a receptor ligand, particularly for the LDL receptor.
  • HDL apoproteins: A-I, A-II, A-IV, and C.
    • ApoA-I and A-IV are believed to activate lecithin-cholesterol acyl transferase (LCAT).
  • ApoC: Three isoforms (CI, CII, and CIII), all synthesized by the liver.
    • ApoC-II is important for LPL activation and is present in chylomicrons, VLDL, IDL, and HDL.

Lipoprotein Composition and Characteristics

  • Chylomicrons:
    • Largest lipoproteins (80-1000 nm diameter).
    • Density < 0.950 g/ml.
    • Composition: 90% TG, 5% cholesterol, 4% phospholipids, 1% protein.
  • VLDL:
    • Diameter: 30-80 nm.
    • Density: 0.950-1.006 g/ml.
  • LDL:
    • Diameter: 20-25 nm.
    • Density: 1.019-1.063 g/ml.
  • HDL:
    • Smallest lipoproteins (9-15 nm diameter).
    • Density: 1.063-1.210 g/ml.

Chylomicrons and VLDL

  • Chylomicron Production: Produced by enterocytes, primarily deliver dietary lipids to tissues other than the liver.
    • Composition: 90% triglycerides (TG), 5% cholesterol, 4% phospholipids, 1% protein.
    • 80% of lipids are taken up by skeletal muscle and adipose tissue.
    • The remaining 20% goes to the liver as chylomicron remnants.
  • VLDL Production: Produced by the liver similarly to chylomicrons in the gut.
    • Composition: 65% TG, 13% cholesterol, 13% phospholipids, 10% protein.
    • High-carbohydrate diets increase de novo lipid synthesis in the liver and VLDL production.
    • VLDLs deliver endogenous triglycerides to peripheral tissues.
  • Lipoprotein Lipase (LPL): Removes triglycerides from chylomicrons, VLDL, and IDL.
    • Hydrolyzes TG molecules in lipoproteins passing through capillaries of adipose, skeletal muscles, and heart tissues.
    • Provides tissues with NEFAs for esterification or energy metabolism.
    • Requires Apo-CII for activation.
  • ApoC-II Acquisition: Nascent chylomicrons and VLDL acquire ApoC-II from HDL after interacting in the bloodstream.

Fate of Chylomicrons

  • Nascent Chylomicrons: Contain ApoB-48 and ApoA, travel through the lymphatic system, and enter the bloodstream.
  • ApoC-II and ApoE Acquisition: Chylomicrons acquire ApoC-II and ApoE from HDL.
  • Lipolysis by LPL: At capillary walls, LPL's lipolytic action releases fatty acids to peripheral tissues (adipose tissue and skeletal muscle).
  • Chylomicron Remnants: Formed after TG transfer to tissues. ApoC-II and ApoA are transferred back to HDL.
  • Liver Uptake: Chylomicron remnants attach to a liver binding site containing hepatic lipase (HL), transferring fatty acids, cholesterol, and cholesterol esters to the liver.
  • Removal: Remnants are removed via hepatocyte endocytosis, interacting with ApoE or ApoB/E receptors.
  • Lysosomal Degradation: Lysosomes degrade the remnant particle, and digestion products (fatty acids, amino acids, glycerol, cholesterol, phosphate) are reutilized by the cell.

VLDL, IDL, and LDL Formation and Function

  • VLDL to IDL Conversion: As triglycerides are cleaved and fatty acids are donated to extra-hepatic tissues, VLDLs become IDLs.
  • IDL to LDL Conversion: Continued removal of triglycerides leads to the formation of smaller, cholesterol-rich LDL particles.
    • LDL Composition: 10% TG, 45% cholesterol, 23% phospholipids, 20% protein.
    • LDL carries about 60% of total serum cholesterol.
  • LDL Function: Delivers cholesterol to tissues for membrane construction and steroid hormone production.
  • LDL Uptake: LDLs interact with LDL-apoB-100 receptors on hepatic and non-hepatic cells, leading to endocytosis and removal from circulation.
  • Lysosomal Degradation: Inside the cell, LDL is degraded by lysosomal enzymes, and the LDL receptor is recycled to the cell surface.
  • LDL Receptor Lifecycle: The LDL receptor has a lifespan of about 20 hours, making a round trip in and out of the cell every 10 minutes.
  • LDL and Atherosclerosis: Elevated LDL is associated with atherosclerosis and considered a risk factor for cardiovascular disease (CVD); hence, LDL is often termed