Unit 2 - G. H. Lipid Digestion, Absorption, and Metabolism Flashcards

1
Q

Digestion of Lipids in the Mouth

A
  • minute amount of triglyceride digested by enzyme lingual lipase
  • Lingual lipase = originates from glands at back of tongue
  • removes fatty acid from C-3
  • Products = diacylglycerol (DAG) + F.A.
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2
Q

Digestion of Lipids in the Stomach

A
  • lingual lipase also found in the stomach
  • gastric lipase hydrolyzes 10-30 % of triglycerides with short/medium chains and at optimum pH of 5-6
  • Free F.A. from mouth digestion inhibits gastric lipase
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3
Q

Digestion of Lipids in the Intestines

A
  • majority of digestion of triglycerides, cholesterol esters and phospholipids happens in small intestines
  • Chyme (partially digested contents of the stomach) enters duodenum and stimulates release of CCK.
  • CCK causes: release of 5 enzymes and HCO31- from pancreas; and release of bile from gall bladder
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4
Q

Differences in Digestion between adults and infants

A
  • infants have a higher pH in the stomach so gastric lipase is more active.
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5
Q

Intestine enzymes secreted active

A
  • pancreatic lipase

- cholesterol esterase- hydrolyzes cholesterol ester into cholesterol and free fatty acid

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6
Q

Intestine enzymes secreted inactive

A
  • trypsinogen - activated (trypsin) by eneterokinase
  • procolipase - activated by active trypsin = colipase that displace bile salts from the surface of triglyceride droplet; anchor pancreatic lipase for triglyceride hydrolysis
  • proPLA2 - activated by active trypsin = PLA2 that hydrolyzed phospholipid into lysolecithin and 1 free fatty acid.
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7
Q

Lipid absorption

A
  • hydrolyzed lipid products + flat soluble vitamins (A,D,E,K) + bile salts = forms a micelle to be carried into intestinal cell
  • Inside cell the lipid components are delivered to the ER, reassembled, then packaged into chylomicrons
  • chylomicron interacts with Lipoprotein lipase located on the lining of blood vessels in muscle, adipose, cardiac and other tissues
  • Lipoprotein lipase hydrolyzes the TG portion of the chylomicron to glycerol and f.a.
    • Some f.a. attach to albumin and remain in circulation
    • Most are used for fuel, ATPs (via oxidation to acetyl CoA)
    • Some are reconverted to trigs and put into storage in adipocytes
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8
Q

lipolysis

A
  • During Fasting, insulin decreases and glucagon increases => leads to cAMP increased => leads to protein kinase A increase => activates HSLp (hormone sensitive lipase)
  • HSLp hydrolyzes a fatty acid from stored triglyceride from adipose tissue and releases products into the blood stream (where F.A. attaches to albumin to be transported and oxidized)
  • stored TG in adipose tissue of a person of normal weight will provide enough fuel to maintain basal metabolism for about 3 months (obese individual, a year).
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9
Q

Complete oxidation of fatty acids

A
  • F.a. are degraded in the mitochondria of cells in most tissues in the body. Exceptions: brain and other nervous tissue, and the adrenal medulla.
  • f.a. enters a cycle, and exits 2 carbons shorter (2 carbons = acetyl CoA)
  • Acetyl CoA is then processed through TCA cycle and ETC producing ATP

Beta-oxidase = conversion of fatty acids to acetyl CoA

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10
Q

Formation of Ketone Bodies

A
  • if acetyl CoA does not enter citric acid cycle, it can undergo various reactions that make Ketone Bodies
  • acetone, acetoacetic acid, and 3-hydroxybutyric acid
  • Ketone bodies are exported from the liver to skeletal muscle, the heart and the brain to be oxidized, decreasing the need for glucose via GNG, and thereby sparing body protein.
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11
Q

Triglyceride synthesis in the liver

A

2 ways:
1. During fed state, increased glucose enters hepatocytes and is converted via glycolysis to DHAP, which then is reduced to glycerol-3-phosphate. Addition of 3 f.a. to glycerol-3-phosphate results in a TG.

  1. TG can also be synthesized from monoglycerides, diglycerides and free f.a. delivered to the liver in chylomicron remnants. These TG are then packaged into VLDL, and released into the circulation where the majority are delivered to adipose tissue
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12
Q

Triglyceride synthesis in adipose tissue

A
  • During fed state, increased glucose and free F.A. are taken up into adipose.
  • similar synthesis as in liver only without the use of chylomicron
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13
Q

Adipose tissue

A
  • adipocyte + fibrous connective tissue = adipose tissue

WAT (white adipose tissue):

  • really light yellow color
  • due to carotenoids
  • predominant type
  • store TG’s derived from dietary fats or synthesized from carbohydrates through lipogenesis

BAT (brown adipose tissue):

  • large number of mitochondria
  • abundance of blood vessels
  • primarily found in fetuses, infants and young children (accounts for up to 6% of an infants body weight)
  • also maintains body temperature in neonates (and hibernating animals).
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14
Q

Hypertrophy vs. Hyperplasia

A

Hypertrophy = increased cell size
- seen in adipocytes of persons considered to be overweight (BMI of 25-29.9) or moderately obese (BMI of 30-34.9)

Hyperplasia = increase in cell number

  • occurs as part of the growth processes that occur during infancy and adolescence
  • also occur during adulthood when the TG storing ability of adipocytes has reached their maximum size (generally, with BMI > 40)
  • makes it harder to loose weight
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15
Q

Fat distribution patterns

A

Central obesity:

  • fat stored around the organs of the abdomen.
  • Associated with increase risks of: heart disease, stroke, diabetes, HT, gallstones, and some types of cancer.
  • Abdominal fat is most common in men and to a lesser extent, in women past menopause
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16
Q

biochemical explanation for fat distribution

A
  • involves activity of enzyme lipoprotein lipase (LpL)= promotes storage of TG in both adipose and muscle tissue.
  • women: estrogen stimulates LpL activity in adipocytes in the breast, hips, buttocks and thighs, promoting fat storage in these areas
  • In men, LpL is produced in abundance in abdominal fat cells.
  • LpL more active in adipose tissue of obese people compared to lean individuals
  • activity of LpL also increases with weight loss
17
Q

Factors affecting food intake

A
  • energy balance and body weight (results in appetite/decreases basal metabolic rate and stimulates the following)
  • dependent upon interaction nervous system and hormones:
    • brain neurotransmitters
  • -gut peptides
18
Q

Brain neutoransmitters

A

Neuropeptide Y (NPY)
- stimulates feeding (for carbohydrates in particular) and decreases physical activity
- lvls increase during food deprivation (why appetite increases during dieting)
Serotonin
- another neurotransmitter involved in appetite.
- ↓ in serotonin associated with ↑ intake of carbohydrates

19
Q

Gut peptides

A
  • primarily orchestrated by hypothalamus
  • neural signals from the mouth, stomach and small intestine during/ following eating

amylin (decreases food intake):

  • co-secreted with insulin from the pancreas during food intake
  • As stomach fills, it becomes distended, stimulating stretch receptors in stomach wall that provide neural signals to the hypothalamus that inhibit appetite

glucagon-like peptide-1 (GLP-1) (decreases food intake):

  • increases secretion of insulin from the beta cells of the pancreas
  • decreases secretion of glucagon by the alpha cells.
  • results in a lowering of blood glucose levels
  • decreases food intake by increasing satiety
  • actions are very short-lived due to its rapid degradation by the enzyme dipeptidyl peptidase-4 (DPP-4).

Peptide YY (decrease appetite):

  • secreted by the cells in the ileum and colon
  • decreases appetite in response to food consumption upon PYY binding to Y2 receptor in hypothalamus

Ghrelin

  • hormone mainly produced by the stomach
  • stimulates appetite
  • levels are normally increased during fasting
  • levels decrease after food intake, decreasing appetite