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KHI > PBL 8: Nathan Arby -Obesity > Flashcards

PBL 8: Nathan Arby -Obesity Flashcards

1
Q

Calculate BMI

A

BMI = weight (kg) / heigh (m2)

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2
Q

What are the 3 primary contributors to energy intake (macronutrients)

A

Fat: 9 cal/gram

Carbohydrate: 4 cal/gram

Protein 4 cal/gram

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3
Q

What is the role of adipose tissue in fat storage?

A
  1. Primary Source of endogenous energy; very energy dense (7700 cal/kg)
  3. Stored as Triacylglycerols (clycerol + 3 FA chains)
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4
Q

What is the role of adipose tissue in endocrine control of energy intake/expenditure?

A

Increased AT = Increased Leptin, Decreased Adiponectin

Leptin = negative feedback control for body in controlling hunter. More FA, more leptin, less hunger.

Adiponectin is inversely proportional to body fat; sensitizes insulin’s actions helpting to promote anabolism when body fat is low.

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5
Q

Which two areas of the hypothalamus are important for controlling eating and where are they?

A
  1. The Satiety Center is located in the ventromedial nucleus (VMN)
  2. The Hunter/Feeding center is location in the lateral hypothalamic area
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6
Q

Orexigenic Neurotransmitters

A

Stimulate feeding

Associated with the LHA (Hunter Center)

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7
Q

Anorexigenic Neurotransmitters

A

Inhibit Feeding

Associated with VMN (Satiety Center)

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8
Q

List Anorexigenic hypothalamic factors

A
  1. CRH
  2. Clucagon-like peptide I (GLP-1)
  3. a-Melanocyte-stimulating hormone (a-MSH)
  4. Cocain- and amphetamine-regulated transcript (CART)
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9
Q

List Orexigenic hypothalamic factors

A
  1. Neuropeptide Y (NPY)
  2. Norepinephrine (NE)
  3. Gamma-aminobutyric acid (GABA)
  4. Galanin (GAL)
  5. Ghrelin
  6. EOP
  7. Orexin-A
  8. Orexin-B
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10
Q

What signals from the gut control apetite?

A
  1. Feedback from the GI tract (nutrient absorption, e.g. glucose, amino acids, lipid levels
  2. GI distention triggers vagal afferents that supress hunger center
  3. Release of GI peptides in resposne to meal (Gastrin-releasing peptide), glucagon, somatostatin and CCK reduces meal size
  4. CCK may stimulate vagal afferents
  5. Oropharyngeal reflex responds to chewing and slallowing to meter food intake
  6. Ghrelin produced by oxyntic cells of fundus stinulated apetite by activating central appetite-stimulating pathway
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11
Q

Ghrelin

A
  1. Peptide hormone released by the oxyntic cells of the fundus of the stomach
  2. Stimulates appetite by activating the central appetite-stimulating pathway
  3. Circulatory concentration is high before a meal and reduced rapidly by ingestion of a meal or glucose
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12
Q

What Signals from Adipose Tissue control apetite?

A
  1. Leptin plasma levels reflect whole-body fat stores
  2. More fat = higher plasma leptin levels
  3. Produced by adipocytes
  4. Binds to receptors which act to inhibit expression of NPY (orexigenic) and stimulate expression of CART (anorexigenic)
  5. In addition, leptin levels reflect fed/fasting state as a short-term signal
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13
Q

Leptin

A
  1. Plasma levels reflect whole body fat stores
  2. Produced by the adipocytes
  3. Binds to receptors which act to inhibit expression of NPY (Orexigenic) and stimulate expression of CART (anorexigenic)
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14
Q

What Signals from the pancreas control apetite?

A
  1. Release of Insulin after meals which supresses appetite
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15
Q

Triglycerols

A
  1. Glycerol backbone with 3 FA chains attached
  2. Major fat in diet as they are major storage lipid
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16
Q

What is the major route of digestion for Triglycerols?

A

Hydrolysis to fatty acids and 2-monoacylglycerols

17
Q

Where and how are Triglycerols digested?

A
  1. Dietary fat enters the SI and is emulsified by bile salts.
  2. Bile salts are synthesized in the liver and secreted by the gall bladder
  3. This is stimulated by CCK which is released from intestinal cells
  4. Emulsification increases surface area of the fat on which the pancreatic lipase can work
  5. Pancreating lipaze is an enzyme that digests triglycerides, hydrolysing them to make fatty acids and 2-monoacylglycerols
18
Q

Bile Salts

A

Synthesized in the liver and secreted by the gall bladder in response to stimulation by CCK. Emulsifies the TGs, increasing surface area.

19
Q

Pancreatic Lipase

A

Major enzyme of triglyceride digestions. Hydrolyses the TG to give fatty acids and 2-monoacylclycerols

20
Q

How are dietary lipid absorbed?

A
  1. Fatty Acids and 2-MGs are packed into micelles which are then emulsified by bile salts
  2. Micelles also contain other lipids such as cholesterol, phospholipids and fat soluble vitamins.
  3. Travel to microvilli on surface of intestinal epithelium where all components except bile salts are absorbed.
21
Q

What is the fate of bile salts after absorption of the micelle?

A

Reabsorbed when they reach the ileum and recirculated through the enterohepatic circulation

22
Q

Synthesis of Chylomicrons

A
  1. Within intestinal epithelial cells, FAs and 2-MGs condensed by enzymatic reactions in smooth ER to reform TGs
  2. TGs are packaged together with proteins and phospholipids in the golgi apparatus to make chylomicrons
23
Q

Chylomicrons

A

Lipoprotein particles that do not readily combine and stick together in aqueous solutions. These contain TGs, cholesterol, fat soluble vitamins and apopproteins (from RER)

24
Q

How are chylomicrons transported in the blood?

A
  1. Secreted into the chyle of the lymphatic system and enter the blood through the thoracid duct approx 1-2 hours after meal
  2. Accept proteins from HDL -ApoE
  3. APoE recognized by receptors on liver, allowing chylomicron entry
25
Q

How are chylomicrons digested in the liver?

A
  1. ApoC11 activated LPL in capillary endothelial cells
  2. LPL produced by adipose cells, muscle cells and lactating mammary glands
  3. Digest chylomicrons > release FAs
  4. FAs become soluble in blood throuigh complex forming with protein albumin
26
Q

What is the fate of FAs released from chylomicrons?

A
  1. Storage as TGs in adipose tissue
  2. Hydrolysis in muscle and other tissue for energy
  3. Glycerol released can be used by liver for TG synthesis in fed state
  4. Remants disposed of by liver
27
Q

Synthesis of TGs

A
  1. FAs from chylimicrons enter adipose cell and form fatty acyl CoA
  2. React with glycerol-3-phosphate derived from glucose in the adipocyte to make a TGs
  3. TGs remain stroed in adipose tissue until needed for energy
28
Q

How is TG use stimulated in the fasting state?

A
  1. Decrease in insuin and increase in glucagon causes cAMP levels to rise in adipose tissues
  2. Stimulated lipolysis
  3. Hormone sensitive lipase cleaves a fatty acid from TG and allows FA to be released into blood
29
Q

How is excess dietary carbohydrate converted to fatty acids?

A
  1. FA synthesis initially requires conversion of glucose to acetyl CoA via glycolytic pathway
  2. Acetyl CoA synthesized in mitochondrai and condenses with oxaloacetate to form citrate for transport to cytoplasm
  3. Acetyl CoA carboxylated to produce malonyl CoA to key regulatory enzyme acetyl CoA caboxylase
  4. FA synthase catalyses complicated set of reactions to condense malolyn CoA to palmitate
  5. Palmitate can be modified to produce other FAs
30
Q

How are the FAs synthesised from Carbohydrates converted into Tiacylglycerols?

A
  1. Glycerol 3-phosphate produced from phosphorylation of glycerol is required

TAGs produced are pakacged with other lipids into type of lipoprotein known as VLDL

31
Q

What is the fate of VLDSs following synthesis?

A
  1. Released into the circulation by liver
  2. Lipoprotein lipase acts on VLDLs in addition to chylomicrons to release FAs for uptake into adipose tisue an storage as TAGs
32
Q

What are the major controls of the carbohydrate > fatty acid pathway?

A
  1. Acetyl CoA carboxxylate (key regulatory enzyme in FA synthesis) subject to mutiple controls.

ACTIVATION BY CITRATE
INHIBITION BY PALMITOYL CoA

ENZYME DEPHOSPHORYLATED WHEN INSULIN:GLUCAGON IS HIGH (leading to increased actvity)

Increased insuklin after meal increases both glycolysis and FA synthesis.

33
Q

Outline the pathway for oxidation of fatty acids in tissues such as muscle and liver.

A
  1. Fatty acid binding proteins (FaBPs) transport fatty acids across the plasma membrane and bind them in the cytosol
  2. Fatty Acyl CoA Synthetase activated FA to FA-CoA
  3. Carnitine transports activated fatty acyl group into mitochondrion
  4. B-oxidation generates NADH, FADH2 and acetyl CoA
  5. In liver, acetyl CoA is converted to ketone bodies
34
Q
A

KHI (8 decks)

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