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NPB101 > Mt3 > Flashcards

Mt3 Flashcards

1
Q

Major function of the digestive system

A

transfer nutrients from the food we eat into our body to be used as fuel and building blocks

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2
Q

What is continuos with the outside world

A

Insides of our intestines/stomach technically

Lumen content of the GI-tract is still outside of our body

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3
Q

4 major tissue layers of digestive tract wall

A
  1. Serosa, 2. Muscularis externa, 3. Submucosa, 4. Mucosa
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4
Q

Serosa

A

• Secretes serous fluid- lubricates
• Continuous with mesentery throughout much of the tract
– Supports digestive organs in proper place while allowing them freedom for mixing and propulsive movements

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5
Q

Muscularis externa

A

• Major smooth muscle coat of digestive tube
• Usually two layers
– Inner circular layer
• Contraction decreases diameter of lumen
– Outer longitudinal layer
• Contraction shortens the tube
• Contractile activity produces propulsive and mixing movements
• Myenteric plexus: part of the enteric nervous system
– inbetween muscle layers

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6
Q

Submucosa

A

• Thick layer of connective tissue
• For distensibility and elasticity
• Contains larger blood and lymph vessels
• Contains submucosal plexus nerve network
part of the enteric nervous system

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7
Q

Mucosa

A

Lines lumen: highly FOLDED surface increases absorptive area

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8
Q

Epithelial layer of mucosa

A

(or, mucous membrane)
• Cells modified for secretion and absorption
• Contains exocrine gland cells – secrete digestive juices, mucus, enzymes into lumen
• Contains endocrine gland cells – secrete gastrointestinal hormones into capillaries

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9
Q

Lámina propria of mucosa

A

Loose connective tissue

• Small blood vessels, lymphatics, and enteric neurons
• Contains gut-associated lymphoid tissue (GALT)

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10
Q

Muscularis mucosa

A

Sparse layer of smooth muscle

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11
Q

Why is it IMPORTANT that the lumen of the GI tract is continuos with the external environment

A
  1. pH in the stomach can fall as low as 2. Inside the body the range of pH that is compatible with life = 6.8 - 8.0 (homeostatic range is 7.35 - 7.45).
  2. Harsh Enzymes that hydrolyze food could destroy the body’s own tissues. Therefore enzymes are synthesized in an inactive form and are activated when they reach the lumen.
  3. Millions of microorganisms inhabit the GI-tract,and these could be lethal if they entered the body proper.
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12
Q

Digestive process

A

Ingestion, chewing, swallowing, defecation- Transfers food into the digestive tract via the mouth (skeletal muscle -> voluntary)

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13
Q

Motility

A

Muscular contractions that mix and move forward the contents within the tract, facilitating later steps in the digestive process (smooth muscle -> involuntary)

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14
Q

Propulsive movements (peristalsis)

A

Move the contents forward through the digestive tract

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15
Q

Mixing movements (segmentation)

A

1) aid digestion by mixing food with digestive juices
2) facilitate absorption by exposing food to absorbing surfaces
3) forward movement (slow and non-linear)

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16
Q

Secretion (exocrine)

A

digestive juices are secreted into the lumen by exocrine glands upon appropriate neuronal or hormonal stimulation

Secretions contain enzymes, acids, buffers, electrolytes, and water that promote digestion, adjust tonicity & provide lubrication for better movement throughout the tract.

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17
Q

Secretion (endocrine)

A

gut hormones are secreted into the blood by endocrine glands upon appropriate neuronal or nutritional stimulation.

Gut hormones are chemical messengers released into circulation and act on receptors in distal locations to regulate motility, pancreatic secretions, and other digestive tract (and non-digestive tract) functions.

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18
Q

Digestion (=chemical)

A

accomplishes the breakdown of structurally complex foodstuffs into smaller, and eventually absorbable units.

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19
Q

Chemical digestion

A

enzymatic hydrolysis of carbohydrates, proteins, and fats into absorbable units

Dietary carbs go to polysaccharides (starch and glycogen) and disaccharides (sucrose and lactose)

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20
Q

Breakdown of proteins

A

By pepsin and pancreatic proteolytic enzymes
- small peptides
- amino acids by aminopeptidase

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21
Q

Breakdown of fats chemical

A

Triglycerides are broken down by lipase to monoglycerides and free fatty acids

LIPASE

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22
Q

Absorption

A

the transfer of small absorbable units along with water, vitamins, and electrolytes from the lumen into the blood or lymph

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23
Q

When no food is in lumen of digestive tract

A

1) the membrane potential of pacemaker cells (Interstitial Cells of Cajal, or ICC) oscillate at 3-5 times per sec (3-5 Hz): this is the Basic Electrical Rhythm (BER) in the stomach.
2) ICCs in the small intestine depolarize more frequently: 8-11 Hz: the BER in the small intestine.
3) these depolarizations spread thru gap junctions to smooth muscle cells, then signal propagated through the tract by the enteric nervous system
4) however, these depolarizations exceed spike threshold only 10-15 times per day = the migrating motility complex, which triggers contractions that are frequent enough to “sweep” residual contents from the stomach & small intestine to the large intestine (triggered by motilin = extrinsic regulation)

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24
Q

BER

A

membrane potential of pacemaker cells (Interstitial Cells of Cajal, or ICC) oscillate at 3-5 times per sec (3-5 Hz): this is the Basic Electrical Rhythm

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25
Q

What happens with food in the lumen

A

1) stretch and gastrin (hormone induced by protein in the stomach) activate neural circuits that increase the amplitude & frequency of the basic electrical rhythm (BER) depolarizations.
2) when these depolarizations exceed spike threshold (approx -35 mV), the smooth muscles spike & therefore contract.
3) stretch & gastrin thereby increase digestive tract motility. (W food SIGNALS)

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26
Q

INTRINSIC: autonomous smooth muscle cells

A

connected by gap junctions, thereby forming a functional syncytium. Single-unit smooth muscle.

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27
Q

INTRINSIC: Interstitial cells of canal (ICC)

A

actaspacesettercells and generate slow-wave potentials (Basic Electrical Rhythm; BER). If threshold is reached and action potentials are triggered, then the whole muscle sheet contracts as a unit.

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28
Q

INTRINSIC: enteric nervous system

A

(myenteric + submucosal nerve plexuses) an interconnecting network of nerve cells localized within the digestive tract wall; coordinates local activity within the digestive tract

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29
Q

EXTRINSIC: extrinsic nerves

A

(originate from outside the digestive system) from both the sympathetic and parasympathetic branch influence motility and secretion by:
– Modifying activity of the enteric nervous system
– altering gastric hormone secretion
– acting directly on smooth muscle and glands

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30
Q

EXTRINSIC: gastrointestinal hormones

A

– Long-range chemical messengers secreted into blood and act on receptors in distal locations to regulate digestive tract (and non-digestive tract) functions.

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31
Q

Role of lips and tongue

A

contain food in mouth; guide food during chewing & swallowing

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32
Q

Teeth role

A

Begin mechanical breakdown by chewing of food

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33
Q

Palate

A

roof of the oral cavity
• separatesoralcavityfrom nasal passage
• allows chewing and breathing to occur simultaneously

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34
Q

Uvula

A

soft tissue that hangs from the rear of the mouth & seals off nasal passage during swallowing

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35
Q

Salivary glands

A
  1. Sublingual
  2. Submandibular
  3. Parotid
    • Secrete saliva in response to autonomic stimulation.
    • Salivacontains:
    – mucus to moisten food and lubricate
    – lysozyme to lyse bacteria
    – Bicarbonate buffers which
    neutralize acids
    – amylase, which begins chemical
    digestion of carbohydrates by cleaving polysaccharides into maltose
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36
Q

How is salivary center in medulla activated

A

Pressure receptors and chemoreceptors in mouth

Cerebral cortex: thinking, seeing, smelling food

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37
Q

Where does the digestion of carbohydrates (polysaccharides) start

A

In the mouth

Salivary and pancreatic amylase

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38
Q

Swallowing

A

refers to the entire process of moving food from the mouth, through pharynx and esophagus, to the stomach.
• Is a sequentially programmed all-or-none reflex, initiated when bolus is voluntarily forced by tongue to rear of mouth into pharynx
• Can be initiated voluntarily but cannot be stopped once it has begun
2 stages:
A. Oro pharyngeal stage B. Esophageal stage

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39
Q

What happens at the end of the oropharyngeal stage

A

pharyngoesophageal sphincter closes & breathing resumes.

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40
Q

Esophageal stage

A

Peristaltic (propulsive) waves move bolus into stomach

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41
Q

Where is the stomach

A

J-shaped chamber located between the esophagus and the small intestine

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42
Q

3 sections of the stomach

A

A. Fundus-located above the gastroesophageal sphincter
B. Body- the middle portion
C. Antrum- bottom portion
• Thick layer of smooth muscle
• Connected to small intestine by the pyloric sphincter
o is a key regulator of gastric emptying

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43
Q

3 major functions of stomach

A

A. until it can be emptied into small
intestine. This occurs in the body of the stomach.
B. Create gastric secretions: including HCl and enzymes that begin chemical digestion of protein
C. Gastric motility converts pulverized food to chyme– a thick liquid mixture of pulverized food and gastric secretions

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44
Q

Gastric filling

A

gastric volume can expand ~20-fold during a meal, by expansion/ flattening of deep folds.

• This expansion of gastric volume is a
vagally-mediated process called
receptive relaxation.

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45
Q

Gastric secretions

A

Two distinct areas of secretory gastric mucosa •Oxyntic mucosa (body and fundus)
•Pyloric gland area (PGA) (antrum)

In oxyntic mucosa, 3 types of gastric EXOCRINE secretory cells, associated with gastric pits

•Mucous cells secrete thin, watery mucus pit
•Chief cells secrete enzyme precursor, pepsinogen
•Parietal (oxyntic) cells secrete
a) HCl
b) intrinsic factor (important for VitaminB12 absorption: essential for normal function of red blood cells)

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46
Q

What protects stomach from itself

A

HCl activates pepsingogen in the lumen

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47
Q

What cells secrete pepsinogen

A

Chief cells

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48
Q

Functions of HCl (secreted by parietal cells)

A

– Activates pepsinogen to active enzyme pepsin and provides acid medium for optimal pepsin activity
– Denatures protein
– Along with salivary lysozyme, kills most of the microorganisms ingested with food

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49
Q

Enterochromaffin

A

like (ECL) cells:secrete histamine (activates parietal cells

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50
Q

G cells secrete

A

Gastrin (hormone goes into bloodstream)
Stimulates parietal, chief, and ECL cells
- Gastrin increases gastric motility and promotes movement of leftover, undigested/unabsorbed material out of ileum into large intestine

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51
Q

D cells secrete

A

hormone somatostatin into bloodstream Somatostatin inhibits parietal and ECL cells

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52
Q

Gastric mixing and gastric emptying

A

strong peristaltic contractions occur in the antrum that:
• mix food with gastric secretions to produce chyme
• Propel chyme toward spyloric sphincter, where a small amount is pushed into the duodenum
• In response to chyme, sphincter closes and remaining chyme is tumbled back into the antrum.

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53
Q

Factors arising in the stomach that control gastric mixing and gastric emptying (pyloric function):

A

A. Volume of the chyme- distention directly stimulates stretch receptors on the smooth muscle, stimulates enteric and parasympathetic nervous system as well as the stomach hormone gastrin to increase motility.
B. Fluidity of the chyme- liquids do not require extensive mixing and churning; contents must be rendered fluid before they are evacuated

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54
Q

Factors arising in the duodenum that control gastric EMPTYING (via neural and hormonal factors)

A

A. Fat is only digested and absorbed within the
small intestine. When fat is present in the small
intestine further emptying is inhibited
B. Acid- highly acidic chyme from the stomach is
neutralized by sodium bicarbonate (secreted from pancreas) in the duodenum. Un- neutralized acid in the duodenum inhibits gastric emptying

C. Hypertonicity– increased osmolarity in the duodenum indicates a back-up of nutrients and delays gastric emptying.
D. Distention– too much chyme in the duodenum inhibits gastric emptying

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55
Q

Neural responses

A

mediated through both intrinsic nerves (short reflex) and autonomic nerves (long reflex)

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56
Q

Enterogastric reflex

A

involves both intrinsic nerves (short reflex) and autonomic nerves (long reflex)

short reflex is mediated by the enteric nervous system, which acts locally to inhibit gastric motility and secretion without involving the brain. The long reflex involves the autonomic nervous system, where signals are sent to and from the brain to adjust gastric function in response to conditions in the small intestine.

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57
Q

Hormonal responses involve

A

release of hormones from duodenal mucosa collectively known as “enterogastrones”
–Cholecystokinin (CCK), stimulated by fat in the duodenum. CCK inhibits antral contractions and induces contraction of the pyloric sphincter.
–Secretin, stimulated by unneutralized acid in the duodenum. Secretin is released by S cells and slows gastric emptying.

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58
Q

CCK

A

stimulated by fat in the duodenum. CCK inhibits antral contractions and induces contraction of the pyloric sphincter

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59
Q

Secretin

A

stimulated by unneutralized acid in the duodenum. Secretin is released by S cells and slows gastric emptying

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60
Q

Cephalic phase of gastric secretion

A

the first phase of gastric digestive activity, which is triggered by the sight, smell, taste, or even the thought of food. During this phase, sensory signals from the brain (via the vagus nerve) stimulate the stomach to prepare for food intake by increasing the secretion of gastric acid (HCl) and digestive enzymes, even before food enters the stomach.

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61
Q

Gastric phase of gastric secretion

A

occurs once food enters the stomach and is characterized by a strong stimulation of gastric acid and enzyme secretion. This phase is triggered by the presence of food, which causes the stomach to stretch (distention) and activates chemoreceptors that detect the presence of proteins and peptides. In response, the vagus nerve and local reflexes stimulate the secretion of gastrin from G cells, which in turn increases the production of gastric acid (HCl) and digestive enzymes, facilitating the breakdown of food. This phase is the MOST ACTIVE phase of gastric secretion.

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62
Q

Intestinal phase

A

when chyme (partially digested food) enters the small intestine, particularly the duodenum. This phase functions to regulate the amount of gastric secretion and motility based on the conditions in the small intestine. The presence of acidic chyme, fats, or protein in the duodenum triggers the release of hormones like secretin and cholecystokinin (CCK), which inhibit gastric acid secretion and slow gastric emptying to allow for proper digestion and absorption in the small intestine. Additionally, the enterogastric reflex, both intrinsic and autonomic, further inhibits gastric activity to protect the intestine from being overwhelmed

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63
Q

Why are accessory organs like the pancreas and liver needed

A

Need secretions of accessory organs to complete digestion and neutralize acid in chyme

64
Q

Pancreas

A

mixed gland that contains both endocrine and exocrine tissue.
The exocrine pancreas includes:
-duct cells- release sodium bicarbonate (NaHCO3) into duodenum to neutralize acidic chyme
-acinar cells- release digestive enzymes into duodenum (work better at a neutral or alkaline pH)

65
Q

Pancreatic acinar cells release

A

——- pancreatic amylase (carb digestion)
——- pancreatic lipase (only enzyme secreted throughout entire human digestive system that can significantly digest fat)
——- Proteolytic enzymes (secreted as
inactive forms)
• Trypsinogen - converted to the
active form trypsin by enteropeptidase in the luminal (brush border) membrane of small intestine
• Chymotrypsinogen – converted to active form chymotrypsin by trypsin
• Procarboxypeptidase – converted to active form carboxypeptidase by trypsin

66
Q

Why are protein-degrading (proteolytic) enzymes (pepsin, trypsin, chymotrypsin and carboxypeptidase) secreted as inactive precursors?

A

If these enzymes were secreted in their active forms, they could begin breaking down proteins within the cells or tissues of the stomach, pancreas, and other organs that produce them, leading to self-digestion or damage

67
Q

What acts on small peptides in the brush border of small intestine epithelial cell

A

Aminopeptidase

Gives us individual amino acids

68
Q

Páncreas- regulation of secretion

A

Chyme in the duodenum stimulates pancreatic secretions via intestinal hormones, aka enterogastrones.
Increase in CCK release

-Pancreatic enzyme secretion from acinar cells
- Gastric emptying/secretion ⍖
- Gall bladder contraction ⍏ Sphincter of Oddi relaxation (both promote bile release)

69
Q

Secretin from S cells

A
  • HCO - secretion from duct ⍏
  • Gastric emptying ⍖
  • Gastric HCl secretion ⍖
    (stomach parietal cells)
70
Q

Liver receives blood from 2 sources

A

• The hepatic artery provides oxygenated blood
• The hepatic portal vein ensures that venous blood from the digestive tract is first carried to the liver.
• Blood leaves the liver by the hepatic vein

71
Q

2 important liver functions

A

• This ensures that all absorbed monosaccharides and amino acids are routed to the liver first for processing.
• Also allows for detoxification of absorbed foreign compounds by the liver first, before they access the general circulation.

72
Q

Major contribution of liver to digestive system

A

Secretion of bile (stored in gall bladder)

biliary system includes the liver, the bile ducts, and the gall bladder.

73
Q

Bile secretion during meals

A
  • secreted from the liver (and/or released from gall bladder) and enters the duodenum
74
Q

Bile release between meals

A

sphincter of Oddi closes and bile is diverted into the gallbladder for storage (until next meal)

75
Q

Bile salts after meal digestion

A

~95% of bile salts are resorbed in the distal small intestine and carried to the liver.

76
Q

Bile consists of

A

• Bileacids/salts
• Cholesterol
• Phospholipid(Lecithin)
• Bilirubin (RBC breakdown product)
• Aqueous mixture or bicarbonate, ions, water
95% of bile acids are reabsorbed after lipid digestion is complete

77
Q

Role of bile

A

Aids in fat digestion by emulsification: increases surface area for lipase
Helps neutralize stomach acid Cholesterol balance

78
Q

What causes bile to be secreted

A

CCK
Contracts smooth muscle in gall bladder and causes relaxation of sphincter of odi

79
Q

Small intestine

A

Primary site of digestion and absorption

Three segments
1. Duodenum(~5%of length)
2. Jejunum(35-40%)
3. Ileum(55-60%)

80
Q

Motility in small intestine

A

primarily via segmentation, which both mixes and propels chyme. Propulsion occurs because the frequency of contractions gradually decreases along length of small intestine (duodenum ~12/min; ileum ~9/min).

• Mixing food with digestive juices
• Facilitate absorption
• Forward movement (slow and non-linear)

81
Q

Inner surface circular folds

A

Increases surface area 3x

82
Q

Villi on surface of circular folds

A

Increases surface area by additional 10x

83
Q

surface of villi contain microvilli (brush border)

A

increases surface area by an additional 20x

84
Q

All together, the folds, villi and microvilli increase the surface area

A

by 600 times.
If spread out flat, the surface of the
small intestine would cover an entire tennis court!
Needed for ABSORPTION

85
Q

What happens in the intestinal lumen

A

carbohydrate and protein digestion is accomplished by pancreatic enzymes, with fat digestion enhanced by bile secretions

86
Q

Brush border

A

small intestine does produce digestive enzymes, but these act on the surface of the cells lining the brush border. The brush border contains 3 types of enzymes:
a. enteropeptidase
b. the disaccharidases: maltase, sucrase, and lactase which complete the digestion of carbohydrates
c. The aminopeptidases, which complete the digestion of proteins

87
Q

Carbohydrate digestion

A
88
Q

Protein digestion

A
89
Q

Small intestine fat digestion

A
90
Q

Ileum into cecum

A

One-way flow - of contents from ileum into cecum (first part of large intestine). Necessary to keep colonic bacteria from entering the ileum

91
Q

Large intestine

A

primarily for drying and storage, includes:
• Cecum (blind-ended pouch below ileocecal valve)
• Appendix (finger-like projection of lymphoid tissue
• Colon (ascending, transverse, descending, & sigmoid)
• Rectum (“straight”, connected to anal canal)

92
Q

Haustral contractions

A

slowly shuffle contents of large intestine to aid absorption (primarily of water and salt)
• Gradually change location, forming haustra

93
Q

Mass movement in large intestine

A

large contractions in ascending and transverse colon that rapidly drive contents forward (generally 1/3 to 3/4 length of colon in few seconds)
• Typically occurs after a meal, when the presence of
chyme in the stomach triggers the gastrocolic reflex.

94
Q

Defecation reflex

A

initiated by mass movement of feces into the rectum, which stimulates stretch receptors
• Causes the internal anal sphincter (smooth muscle) to relax and the rectum and sigmoid colon to contract
• IF the external anal sphincter is also relaxed, defecation occurs.
• Since the external anal sphincter is made of skeletal muscle, the sphincter is under voluntary control.

95
Q

Constipation

A

occurs if defecation is delayed too long and too much water is absorbed from the feces (become dry and hard)

96
Q

Appendicitis

A

can occur if hardened feces get lodged in the appendix, obstructing normal circulation and mucus secretion.

97
Q

Circulating form of carb; glucose… stored as

A

Glycogen
Glucose is essential fuel for brain
First energy source

98
Q

Protein use

A

Stored as body proteins and majorly stored in muscle
DO NOT want to tap into stores bc then you degrade function and structure

99
Q

Brain can only

A

use glucose for fuel (exception: ketoacids produced by liver in “starvation”)
and..
brain cannot store glucose reserves!

100
Q

Absorptive state

A

Anabolic rxn> catabolic rxn (break down)

-Fed state
-Glucose is plentiful and serves as major energy source

101
Q

Postabsorptive state

A

Catabolic (break down) rxn > anabolic (build up)

-Fasting state
-Endogenous energy stores are mobilized to provide energy (esp. glucose for brain)

102
Q

Islets of Langerhans

A

clusters of hormone-producing cells within the pancreas that regulate blood glucose levels. They consist of alpha cells, which secrete glucagon to raise blood glucose, and beta cells, which release insulin to lower blood glucose. Delta cells produce somatostatin, inhibiting both insulin and glucagon secretion, while PP cells release pancreatic polypeptide, which may help regulate appetite and pancreatic functions

103
Q

B cell

A

Release insulin

104
Q

Alpha cell

A

Secrete glucagon

105
Q

Delta cell

A

Secrete somatostatin

Pancreatic site of somatostatin synthesis and secretion, modulates insulin/glucagon secretion.

106
Q

Insulin is major

A

ABSORPTIVE state hormone

107
Q

Glucagon is major

A

Post-absorptive state hormone

108
Q

A major job of insulin

A

Enhance glucose uptake via GLUT4 in many tissues of the body (but not all)

Insulin-dependent glucose uptake is most important in skeletal muscle and adipocytes
NOTE:
Brain does not need insulin for glucose uptake (Neurons: GLUT3, Blood brain barrier: GLUT1)
Contracting skeletal muscles insert GLUT4 in membrane w/o needing insulin
Liver doesn’t need GLUT4 for uptake (GLUT2) but still needs insulin to store it as glycogen
LOOK AT SLIDES

109
Q

Increase in insulin and carb metabolism

A

Decreases [gluc] in blood

110
Q

Increase in insulin and fat metabolism

A

Lowers [fatty acids] in blood

111
Q

Protein metabolism and increase insulin

A

Lower [amino acids] in blood

112
Q

Parasympathetic stimulation of islet B cells

A

Rest and digest
Increase insulin secretion

113
Q

Sympathetic stimulation and islet B cells

A

Inhibit!
Want blood sugars to stay high; need nutrients to stay in blood for use

114
Q

Glucagon-Like Peptide (GLP-1) and Glucose-dependent Insulinotropic Peptide (GIP)

A

Both GLP-1 and GIP are part of a complex system that enhances insulin secretion after meals, improving glucose control and contributing to the regulation of postprandial blood sugar levels
INCRETIN hormones

115
Q

What controls insulin secretion

A

Beta cells sense glucose

116
Q

INCRETIN effect

A

oral ingestion of glucose leads to a greater insulin secretion compared to the same amount of glucose given intravenously. This enhanced insulin secretion is mediated by incretin hormones, primarily glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP), which are released from the intestines in response to food intake.

hormones are released into the bloodstream, where they stimulate insulin secretion from the pancreas in a glucose-dependent manner (meaning insulin is only secreted when blood glucose levels are elevated). This effect helps improve glucose control after meals by ensuring adequate insulin is released to manage the rise in blood sugar.

117
Q

GIP from

A

Duodenum K cells

118
Q

GLP-1 from

A

Ileum L-cells

119
Q

Increase in glucagon

A

Increase in glucose in blood
Carbohydrate metabolism

120
Q

Fat metabolism and glucagon increase

A

Increase in [fatty acids] in blood

121
Q

Low glucose is major regulator of

A

Glucagon secretion

122
Q

Low circulating [fatty acids] also stimulate

A

Glucagon secretion

123
Q

High protein effect on insulin and glucagon

A

Increases secretion of both

124
Q

Prominent feature of diabetes

A

Elevated blood glucose levels
-urine acquires sweetness from excess blood glucose that spills into urine

125
Q

Basic defect in type 1 vs type 2

A

1; autoimmune destruction of B cells; none or almost no insulin secretion
2; reduced sensitivity of insulin’s target cells; may be normal or exceed normal insulin secretion
Both have genetic component

126
Q

Carb metabolism and diabetes

A

Reduction in glucose uptake by cells
Excessive hunger, thirst, and urination bc glucose levels in filtrate exceed kidney’s ability to reabsorb it

127
Q

Lipid metabolism and untreated diabetes

A

No insulin- body doesn’t know it has lots of sugar so it switches to fat as an alternative energy source
Ketosis

128
Q

Untreated diabetes and protein metabolism

A

Increased protein degradation, muscle wasting, weight loss

Decreased amino acid uptake, increased blood amino acids, increased gluconeogenesis, adding more glucose that we dont need
Aggravation of hyperglycemia

129
Q

Therapies for Type 1

A

Insulin
No cure
Pancreas or islet transportation

130
Q

Treatment for T2D

A

Target B cells to produce more insulin (T2 has faulty B cells)
Improve/restore insulin signaling in target cells (cells are not able to respond to insulin; less responsive )
Decrease liver glucose production

131
Q

Obese BMI

A

> 30; increased risk of T2

132
Q

Do our bodies control how much nutrients are absorbed

A

NO
If we eat excess nutrients then we absorb it no matter if we need it or not, so it is stored and could end up doing more harm than good

133
Q

Where does energy used by cells come from

A

All energy used by cells of the body comes from ingested food.
• We do not change the rate of nutrient absorption depending on fuel reserves.

134
Q

External work

A

Energy expended to MOVE the BODY in relationship to the environment
Exercise

135
Q

Internal work

A

energy expending activities that must go on all the time to sustain life + skeletal muscle activity other than external work

136
Q

Heat

A

only ~50% of energy in food is transferred to ATPs. The remaining 50% is lost to heat. Next, when cells expend ATP, an additional 25% lost to heat. So… only 25% of consumed energy is available for work.

137
Q

Metabolic rate

A

rate of energy use (due to internal work, external work, and heat)
= energy expenditure/unit of time

generally expressed in terms of kilocalories/hour

138
Q

Calorie

A

basic unit of heat
• is the amount of heat required to raise 1 g of H20 by 1oC
• is too small to be convenient, so the Kilocalorie or Calorie is used Calorie = 1,000 calories

When nutritionists refer to the amount of calories in food, they are actually referring to kilocalories or Calories

139
Q

Energy expenditure

A

A person’s metabolic rate varies depending on their activity level.
Therefore basal metabolic rate
is typically measured under standard basal conditions when:
• Person is at physical rest
• Person is at mental rest
• Comfortable room
temperature
• At least 12 hours after a
meal

MORE ACTIVE= require MORE ENERGY

140
Q

Gain weight

A

Energy input exceeds energy expenditure
(As adipose tissue)

141
Q

Lose weight

A

Energy expenditure exceeds energy intake
(From adipose tissue stores)
Fats are the long term storage

142
Q

9 yr old, messed up hypothalamus

A

Removal of the tumor damaged the part(s) of the hypothalamus that regulate energy balance.
• No longer receive correct inputs from the periphery about fuel storage.
• The result is that her brain ‘thinks’ her body is starving and she is constantly ravenous
• She gained 150 pounds in less than 3 years.

143
Q

VMH-lesion

A

Brain can’t receive signal to stop eating, BUT the signal is still present

144
Q

How does body accomplish homeostatic regulation of energy balance

A

• Brain receives information from the periphery about energy needs and energy availability.
• These signals are integrated in key regions of the hypothalamus and brainstem, which recruit downstream effector systems in the brainstem and elsewhere to change feeding behavior and metabolism.

145
Q

Db/db

A

Affects receptor of signal to stop eating

146
Q

Ob/ob

A

Affects the circulating factor

147
Q

Adiposity signals

A

Provide chronic information about energy AVAILABILITY

148
Q

Leptin

A

a hormone released from adipose tissue, in proportion to total adiposity

By signaling to the brain about the body’s fat stores, it helps control appetite and energy expenditure, contributing to the maintenance of a healthy body weight.

Leptin ‘tells the brain’ how much body fat there is.

149
Q

Insulin

A

hormone released from pancreas, also in proportion to total adiposity

150
Q

CCK and satiety

A

helps to signal the brain when the body has had enough food, promoting feelings of fullness and preventing overeating
Should stop eating now :)

151
Q

GLP1 and satiety

A

From small intestine

helps to signal the brain when the body has had enough food, promoting feelings of fullness and preventing overeating

152
Q

Leptin is adiposity signal

A

When fat mass increases, the leptin signal gets larger than usual. In response, the hypothalamus ‘sends out orders’ to eat less and to increase energy expenditure (BMR)
Fat mass is REDUCED
DECREASED FOOD INTAKE
Maintain stable body weight

153
Q

Leptin when fat mass DECREASES

A

fat mass decreases, the leptin signal gets smaller than usual. In response, the hypothalamus ‘sends out orders’ to eat more and to reduce energy expenditure (BMR).
LESS LEPTIN SIGNAL= MORE eating

154
Q

Obesity still??

A

Leptin resistance :(
Less efficient response to Leptin

threshold at which leptin elicits a catabolic response is increased
Fat mass NOT reduced

Telling it to stop but needs sm more Leptin to get message across so the decrease in food intake doesn’t occur :(((

155
Q

Adiposity and satiety signals

A

Work TOGETHER
Feed off of each other
fat mass is depleted, adiposity signaling is low relative to ‘expectation’.
• Sensitivity to satiety signals is reduced.
• Allows for consumption of bigger meals
and regain of lost fat.

excess fat mass has occurred, adiposity signaling is high relative to ‘expectation’.
• Sensitivity to satiety signals is increased.
• Allows for consumption of smaller meals
and loss of excess fat.

156
Q

Nutrients as key players.

A

Glucose-sensing neurons in the hypothalamus
and brainstem respond to severe
hypoglycemia to increase appetite.
• There is not much evidence that this occurs
during the normal postprandial state.
• Some evidence that certain amino acids and
fatty acids can act directly to regulate energy balance

NPB101 (6 decks)

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