Lipids Flashcards
What are the types of lipids found in food, rich food sources, and their energy value?
Saturated = butter, animal sources
Monounsaturated = olive oil, avocados, peanuts, almonds
Omega 3 PUFA = fish, shellfish flaxseed, hemp seed, walnut, grape-seed, soybean
Omega 6 PUFA = chicken, whole grain wheat, vegetable oils
Terminology pertaining to triglyceride formation and breakdown
Esterification, lipolysis, lipogenesis, beta-oxidation
Where do dietary trans-fats come from? (production and sources)
Processed foods (e.g. margarine) or ruminant derived foods. Produced via partial hydrogenation of sat FA
Describe the digestion, absorption and transport of dietary lipids
Lingual lipase from serous gland. Gastric lipase from chief cells. CCK triggers bile and pancreatic enzyme secretion. Bile emulsifies fat to convert into micelles. Pancreatic enzymes act on micelles: pancreatic lipase (triglycerides to glycerol and FFA), pancreatic phospholipase (phospholipids to FFA, glycerol and phosphoric acid), pancreatic cholesterol esterase (cholesterol esters to cholesterol and FFA)
The water soluble micelles diffuse their contents at the brush border into the enterocytes (distal duodenum and jejunum), moving down a concentration gradient. Long chain FA re-esterified and combine with cholesterol and protein to form chylomicrons. These enter the lymphatic system via lacteals. Short and medium chain FA absorbed directly into the portal vein.
Lipids are transported in the circulation via lipoproteins. Describe the characteristics, composition and role of the four main lipoproteins
Chylomicrons = mostly triglycerides. Transport triglycerides from GIT to cells and liver
VLDL = mostly triglycerides. Transport triglycerides from liver to cells
LDL = mostly cholesterol. Transport cholesterol from liver to cells
HDL = mostly protein. Transport cholesterol from cells to liver and excretion
Explain the chemical characteristics and specific physiological function of dietary FA
Provide energy Insulate and protect body structures Component of membranes (phospholipids), strength (cholesterol and SCFA) and fluidity (PUFA) Fat soluble digestion and absorption Precursor of sex hormones Precursor of eicosanoids
What are EFAs? Why are they essential? Describe the omega and delta naming methodologies for these FA
EFSa essential because the body doesn’t produce them endogenously. Lack of ∆12 and ∆15 desaturase enzymes
Delta naming from the carboxyl end 18:1∆^15
Omega naming from the methyl end 18:1n-3
Explain the function of EFAs
EFAs important structures within cell membranes = DHA/EPA keep the membrane fluid
DHA/EPA essential in foetal development = assist in development and function of brain, retina, nervous system
DHA/EPA essential throughout life = regulation of nerve transmission, signalling in gene expression, formation of eicosanoids
What are eicosanoids? How are they made?
Hormone-like structures formed from EFA. Responsible for numerous cell functions
n-6 PUFA are pro-inflammatory = cause constriction of BV leading to increased BP
n-3 PUFA are anti-inflammatory = cause dilation of BV leading to decreased BP
What are 5 enzymes involved in the digestion of lipids?
Lingual lipase, gastric lipase, pancreatic lipase, pancreatic phospholipase, pancreatic cholesterol esterase
Explain the entero-hepatic circulation? What is its purpose?
Responsible for recycling of bile. 95% is reabsorbed in the distal ilium into the hepatic portal vein
How can the entero-hepatic circulation be used to modulate circulating cholesterol?
Fibre can bind cholesterol and excrete it. This decreases the amount reabsorbed. Liver must generate now bile from cholesterol. Lowers circulating cholesterol
What are the sources of circulating cholesterol
Endogenous synthesis in the liver, intestines, gonads, adrenal glands
Explain briefly endogenous cholesterol syntheses
37 step process. Starting molecule is acetyl CoA
Synthesis is increased when plasma cholesterol is low and when BGL is increased
What exactly is measured when “blood cholesterol” is measured in a routine blood test?
Lipoproteins
What is the apolipoprotein in lipoprotein? How is it made?
A “marker” on the surface of the lipoprotein. Assists in cell recognition and facilitates movement across membranes. Synthesised via DNA expression in the liver
Describe cholesterol uptake in the peripheral cells
Receptor pathway = B100 LDL receptor recognises the LDL apolipoprotein. LDL is taken up via endocytosis and its content is used by the cell. B100 synthesis is increased when cholesterol concentration in the cell is low and blocked when high. When the system is dysregulated or when there is too much circulating LDL, LDL can build up in the blood
Describe plant sterols, where they are found, and their role in reducing dietary cholesterol absorption
Plant sterols are chemically similar to dietary cholesterol from animal products but cannot be converted to steroids in the body.
Found in the cell wall of whole grains, fruits, legumes and leafy vegetables
Reduce dietary cholesterol absorption by competing with cholesterol. Plant sterols are incorporated to micelles during lipid digestion, thus reducing the amount of dietary cholesterol in micelles. 2-3g/day needed
Explain the mechanism by which oats can reduce circulating cholesterol
Oats contain B-glucans, a type of soluble fibre. Binds to bile and increases excretion. Lack of reabsorption leads to increased synthesis from cholesterol = decreased plasma cholesterol
What is the difference between MCT and LCT metabolism?
MCT absorbed directly into the portal vein bound to albumin. Can be used more rapidly for energy production
LCT absorbed into lymphatic system via lacteals in chylomicrons
Describe how EFAs are involved in the inflammatory response of the body
Precursors of eicosanoids. Pro vs anti-inflammatory
What is the diet-heart hypothesis: how was it developed; what does it state?
DIetary cholesterol and saturated fat raise blood cholesterol. High blood cholesterol associated with atherosclerosis and thus coronary heart disease. Therefore saturated fat and cholesterol increase risk of CVD
However, study was funded by the sugar industry and involved feeding cholesterol to rabbits (vegetarian)
Briefly (but precisely) describe how atherosclerosis develops
Scavenger pathway = LDL not taken away by HDL can become oxidised. This oxidised LDL can burrow under the endothelium and become engulfed (scavenged) by macrophages. This turns the LDL into foam cells. These cells often become trapped in the walls of blood vessels and contribute to atherosclerotic plaque formation => hardening of the blood vessel wall => less flexibility to adapt to changes in blood volume => hypertension
Narrowing of blood vessel => risk of clot => ischemia => stroke
High BGL can damage the endothelium, making cholesterol deposit take place easier
Is dietary fat the culprit in the development of atherosclerosis? Explain your answer
No. Dietary fat is broken down via digestion and absorption. Lipoproteins have to be reformed. Increased BGL may actually be the culprit as it can damage the blood vessel endothelium, allowing easier deposition of oxidised LDL
What are the Australian recommendations for fat intake?
20-35% EER, no more than 10% sat + trans, 0.2% n-3 PUFA (SDT)
What are the essential fatty acids? Explain why specifically they are essential. Explain why the EFAs status (i.e. having sufficient supply for good physiological function) may be problematic in vegan diets
EFAs cannot be synthesised in the body as we lack ∆12 and ∆15 desaturase enzymes
ALA and LA can be elongated or have more double bonds added, but the rate of this is limited by enzymes (genetic variance can result in decreased rates). This is a concern for vegan diets since the only source of DHA and EPA is oily fish and algae
