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Terms in this set (23)
Triglyceride digestion: What is Triglyceride?
-Most fatty acids in the body and in food are in the form of triglycerides
Triglyceride Digestion: Role of Bile
- breaking up (emulsify) dietary lipids into lipid droplets (micelles).
- Due to the amphipathic nature of bile, the fat globules disperse in the aqueous environment forming small lipid spheres (droplets) called micelles.
-The small fat droplets have more surface area, which aids in the next step of fat digestion - the breakdown of triglycerides by the enzyme pancreatic lipase.
Triglyceride Digestion: Role of Pancreatic Lipase
- responsible for almost all fat digestion, hydrolyzes the ester bonds that attach FAs to the glycerol molecule.
- Results - 2 free FAs and 1 monoglyceride.
Lipoproteins: relationship between size, density, and lipid to protein ratio
- High lipid-to-protein ratio = larger size and lower density
- Low lipid-to-protein ration = smaller size and higher density
Exogenous pathway - Chylomicrons
-Exogenous (dietary) lipids absorbed into enterocytes - circulated as chylomicrons
*Chylomicrons contain mainly the newly formed triglycerides, cholesterol.
*Enter the lymphatic system, and eventually enter the bloodstream.
Role of Lipoprotein lipase
-LPL hydrolyzes the ester bonds, and the free-fatty acids are taken up mainly by adipose tissue and muscle. (4) Chylomicron remnants are taken up by the liver.
Fatty acid absorption - changes in the enterocyte: Formation of chylomicrons
-Once inside the enterocytes, the free fatty acids and monoglycerides are reassembled by a process called reesterification. (1,2)
- TG are encased with phospholipids and proteins, forming a lipoprotein called a chylomicron. (3)
-Endogenous pathway VLDL and LDL
-As VLDLs circulate, interact with the enzyme lipoprotein lipase (LPL). (2) LPL hydrolyzes the ester bonds, and the free-fatty acids are taken up. (3) Change in VLDL density, becomes Low Density Lipoprotein (LDL)
-VLDL more lipid (92%) relative to protein (8%), therefore VERY LOW DENSITY
*Made up primarily of triglycerides and function to delivery fatty acids to muscle and adipose tissue.
Clearing LDLs from the blood
-LDLs transport cholesterol in the blood and are taken up by cells that have LDL receptors.
-Cholesterol is used by cells to synthesize many substances and to synthesize cell membranes.
Role of HDLs
- HDLs transport cholesterol from cells back to the liver. = reverse cholesterol transport
- This function, referred to as reverse cholesterol transport, protect against atherosclerotic lesions.
Factors that influence levels of circulating lipoproteins
Look at slide 45 on Note Packet 9
•What does the research suggest about the role of diet and heart disease
- High carbohydrate intake was associated with higher risk of total mortality
- Total fat and individual types of fat were related to lower total mortality.
- Total fat and types of fat were not associated with CVD, heart attacks or CVD.
What is the impact of lipoproteins on atherosclerosis, myocardial infarctions and cerebral vascular accidents
-Results in a condition called atherosclerosis
-.• Cardiovascular Disease: If blood vessels that circulate blood to cardiac muscle involved - myocardial infarction (heart attack)
Physical factors that govern food intake - hunger and satiety
- Hunger: physiological need for food
- Satiety: physiological response to having eaten enough
-Hunger and satiety are physical cues that initiate and terminate eating.
- an intense desire for a specific food
- Attributed to emotional states, triggered by memories, sensory stimuli (e.g., smell, sight, hearing about a specific food), hormonal fluctuations associated with menstruation and pregnancy.
- Generally believed not caused nutrients lacking in your diet.
- more than a dislike of a food
- Often are associated with an unpleasant experience
- Highly palatable foods can activate the brain's reward center, increase the release of a NT - dopamine.
- Dopamine stimulates pleasure centers in the brain, which in turn may increase the desire to eat more highly palatable foods.
- Studies suggest over time, overeating highly palatable foods can modify the brain, leading to food cravings (in much the same way that drugs can become addictive)
Role of the hypothalamus, catabolic and anabolic neuropeptides
- Hypothalamus: area of the brain regulates food intake (hunger, satiety, and appetite) and energy expenditure (EE).
- Neurons within the hypothalamus release either anabolic neuropeptides (ANP) or catabolic neuropeptides (CNP).
- ANP promote weight gain by increasing hunger ( EI) and decreasing energy expenditure (¯EE)
- CNP promote weight loss by decreasing hunger (¯EI) and by an increasing energy expenditure (EE)
Peripheral signals that influence hunger/satiety
-• Neural - Gastric distention (triggers satiety)
- Hormonal signals -derived from the GI tract
• Ghrelin - hunger
• CCK - satiety
- Increase blood glucose and insulin levels trigger satiety
•Set point theory of body weight regulation
- It appears that there is physiologic feedback whereby the body tries to maintain stable energy reserve (body fat)
Obesity and genetics in humans
In humans, obesity is rarely caused by a single gene (few known cases), but rather numerous genes that make people obesity prone, obesity resistant, and somewhere in between.
Defect in obese mouse
-obese mouse lacked a circulating satiety factor that made the mouse obese
-• When leptin injected into ob mouse - corrected obesity by reducing hunger and increasing energy expenditure.
•Role of leptin in regulating body fat
-Leptin circulates in the blood and acts on the hypothalamus to regulated food intake and energy expenditure.
- Fat mass falls, leptin levels decrease, stimulating hunger and suppressing energy expenditure until the fat mass is restored.
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