208 Digestion Flashcards
(231 cards)
1
Q
3 functions of stomach
A
storage (store food and regulate its passage into small intestine), digestion (chemical and mechanical digestion into chyme), defense (destroy bacteria and other pathogens in good and pathogens trapped in airway mucus)
2
Q
acid denutures proteins (break H bonds) by ___
A
Pepsin
3
Q
Receptive relaxation
A
upon swallowing food, parasympathetic neurons to the ENS cause the fundus of the stomach to relax
4
Q
_____ of stomach enhances motility (& starts short & long reflexes)
A
distension
5
Q
Propulsion
A
weak peristaltic waves (15-25 seconds) that increase in force proceeding down to the antrum move chyme towards pylorus
6
Q
Retropulsion
A
larger particles are moved back to the body (reverse waves)
7
Q
Storage and motility of the stomach process
A
mixes food with acid and digestive enzymes, small amounts of chyme squeeze through pylorus
8
Q
G-cell short reflex
A
release gastrin in response to AA, peptides, and distension
9
Q
G-cell long reflex
A
parasympathetic neurons communicate with ENS to stimulate gastrin production during cephalic phase
10
Q
Gastrin direct action
A
stimulate gastric acid secretion from parietal cells (HCl)
11
Q
Gastrin indirect action
A
stimulate histamine release from enterochromaffin-like cells (ECL cells), which then stimulates secretion from parietal cells
12
Q
Parietal cell daily production
A
1-3L of gastric acid (HCl) with pH as low as 1
13
Q
3 stimulants of parietal cell secretion
A
gastrin (G-cells), histamine (ECL cells), ACh from ENS neurons via long and short reflexes)
14
Q
5 gastric acid functions
A
stimulate release of pepsinogen from chief cells and cleaves pepsinogen to pepsin, denatures proteins (easier for pepsin), kill bacteria and other ingested microorgs, inactivate salivary amylases, stimulate D cells to release somatostatin (stops acid production)
15
Q
Process of acid secretion in stomach
A
free H+ is actively transported across apical membrane to accumulate in stomach, water dissociates to H+ and OH- to allow more H+ to be transported to stomach, OH- combines with CO2 by CA to form HCO3- in parietal cell, HCO3- is exchanged with Cl at basolateral membrane, Cl diffuses across apical membrane through open channels into stomach
16
Q
Tubulovesicles
A
vesicles that store apical H+/K-ATPase, Cl, and K- transporters when cell is resting
17
Q
Activation of apical transporter insertion (exocytosis)
A
stimulated by histamine, gastrin, ACh
18
Q
Activation of apical transporter removal
A
by somatostatin
19
Q
Treatment of excessive acid
A
H2 receptor antagonists, proton pump inhibitors
20
Q
Activators of gastric acid secretion (long reflex)
A
G cells (gastrin), ECL cells (histamine), ACh
21
Q
Inhibitors of gastric acid secretion (long reflex)
A
D cells (somatostatin)
22
Q
Activators of gastric acid secretion (short reflex)
A
stomach lumen distension, amino acids, peptides
23
Q
Enteric hormones that inhibit gastric H+ secretion
A
CCK, secretin, GIP, GLP-1, somatostatin
24
Q
Stimulant of gastric digestive enzyme secretion
A
acid secretion via short reflexes
25
Chief cells secrete what
secrete gastric lipase and pepsinogen
26
Pepsinogen
cleaved to pepsin which breaks down proteins into peptides
27
ECL - Histamine (activates _ receptors on _ cells to stimulate _)
activates **H2** receptors on **parietal** cells to stimulate **HCl secretion**
28
parietal cell - Intrinsic factor
forms a complex with B12 so it can be absorbed
29
D cell - Somatostatin: negative feedback for _ secretion and inhibit _ release
**negative feedback for acid secretion** (G cells, parietal cells, ECL cells), **inhibit pepsinogen release** (chief cells)
30
Steps of gastric digestive enzyme secretion
**food/cephalic reflexes initiate gastric secretion of *gastrin, histamine, and acid*** - **gastrin stimulates acid secretion** by **direct action on *parietal cells*** or ***indirect action with histamine*** - **acid stimulates short reflex *pepsinogen secretion*** - ***somatostatin release by H+* modulates acid and pepsin release**
31
Mucous cells secrete
mucus and HCO3-
32
Stimulant of mucus secretion ( _ input and _ )
***para*sympathetic** input and irritation
33
HCO3- secretion stimulant
***para*sympathetic** input and **H+**
34
Peptic ulcer
sore or break in the lining of the stomach or duodenum
35
Peptic ulcer caused by
**excessive acid production** (**gastrin-secreting tumours**), nonsteroidal anti-inflammatory drugs (**NSAIDS**), **helicobacter pylori**
36
How does helicobacter pylori live survive in stomach?
**urease enzyme** converts **urea** **to ammonia and HCO3- to neutralize acid,** ammonia is toxic to our cells and causes formation of ulcers
37
Inputs of intestinal phase
**5.5 L of food**, fluid secretions (2 ingested, 1.5 saliva, 2 gastric) enter small intestine, 3.5L from hepatic (0.5), pancreatic (1.5), and intestinal (1.5) to form **9L total** entering the small intestines
38
Motility regulated to...
ensure proper digestion and absorption
39
__ L absorbed in __ and __ by segmental and peristaltic contractions
7.5L in duodenum and jejunum (mostly in first half of small intestine)
40
Motility promoters
***para*sympathetic** innervation, **gastrin, cholecystokinin (CCK)**
41
Motility inhibitors
**sympathetic** innervation
42
2 things that increase SA in small intestine
**plicae** (large circular folds of small intestine) and **villi** (small folds in mucosa)
43
Villi - increase _ and secrete _
**increase SA** available **for absorption,** also **secrete mucus**
44
Crypts
contain hormone and fluid-secreting cells and stem cells
45
Most nutrients are absorbed into...
capillaries in the villi
46
Fats enter...
lacteals of lymphatics
47
Hepatic portal system purpose
**liver acts as biological filter** as it contains a variety of enzymes that metabolize drugs and xenobiotics and **clear them from the bloodstream before it proceeds to circulation**
48
Intestinal secretions that enter small intestine lumen (5)
**digestive enzymes** (brush border enzymes and pancreas), **bile** (liver, store in gallbladder), **bicarbonate** (pancreas), **mucus** (goblet cells), **isotonic saline** (crypt cells)
49
Isotonic saline function
lubricate gut contents
50
Isotonic saline formation steps
Na+/K+/Cl- enter by cotransport, Cl- enters lumen through CFTR channel, Na is reabsorbed, negative Cl- in lumen attracts Na by paracellular transport and water follows
51
Pancreas islets
endocrine secretory epithelium (a = create glucagon, B = create insulin)
52
Exocrine secretory epithelium in pancreas secrete _ and _
secrete **digestive enzymes** and **NaHCO3-**
53
Stimuli for exocrine secretion
distension of small intestine, neural signals, CCK
54
Pancreatic exocrine secretory epithelium process (empty into _ duct and into _ via _)
**empty into pancreatic duct** and **into initial duodenum via sphincter of oddi**
55
Trypsinogen
converted to **trypsin by enteropeptidase** (brush border enzyme)
56
Trypsin
**activates zymogens** (many digestive enzymes)
57
Bicarbonate production (pancreas) produced in _
produced in duct cells
58
Bicarbonate role (pancreas)
neutralize acid entering from stomach
59
Channels on **apical side** of pancreatic duct cell or duodenal cell
HCO3-/Cl- exchanger, and CFTR channel
60
Channels on **basolateral side of pancreatic duct cell** or duodenal cell
NKCC2, Na/K ATPase, K+, Na/H+ exchanger
61
Cystic fibrosis impact on pancreas secretion
cause pancreatic cysts, also without Cl- channel mucus accumulates in pancreas to block secretion duct and digestive enzyme release
62
3 main cells of pancreas
**endocrine** (alpha and beta islets), **acinar cells** (enzyme secreting), **duct cells** (bicarbonate secreting)
63
Liver functions
glucose/fat metabolism, protein synthesis, hormone synthesis, urea production, detoxification, storage
64
Hepatic portal **vein inputs**
bilirubin, nutrients, drugs, foreign substances from GIT
65
Bile duct **outputs**
bile salts, bilirubin, water, ions, phospholipids secreted into duodenum
66
Hepatic **artery inputs**
bilirubin, metabolites of hormones and drugs, nutrients from metabolites and drugs of peripheral tissues
67
Hepatic **vein outputs**
glucose, plasma proteins, urea, vitamin D, metabolites for excretion are metabolites to peripheral tissues
68
Liver weight
1.5 kg
69
Common hepatic duct (takes _ made in _ to _ for storage)
takes bile made in the liver to the gallbladder for storage
70
**Common bile duct** (takes bile from _ to _ of small intestine)
**takes bile from** the **gallbladder** **to** the **lumen of** the **small intestine**
71
Hepatic artery brings _ from _ to _
brings **oxygenated blood** containing metabolites **from peripheral tissues to the liver**
72
Hepatic portal vein
blood is rich in absorbed nutrients from the GIT and contains Hb breakdown products from the spleen - **blood leaves the liver in the hepatic vein**
73
Sphincter of oddi controls release of _ and _ secretions into _
**controls** the **release of bile and pancreatic** secretions **into** the **duodenum**
74
Bile
a non-enzymatic solution secreted from hepatocytes
75
3 main components of bile
**bile salts** (bile acid/AA), **bile pigments** (bilirubin), **cholesterol**
76
90% of digested fats
triglycerides
77
Bile salts role in fat digestion
a coarse emulsion of **large fat droplets** (small SA) **in chyme are broken down to smaller stable particles**
78
Lipase
enzymes that **break triglycerides into MG and 2 FA,** are unable to pass through the salt layer of micelles
79
Colipase moves _
enzymes that moves salt layer of micelles so lipase can get in to digest TG
80
Steps of fat digestion and absorption (starting with bile salts)
**bile salts** from liver **coat fat droplets** - **pancreatic lipase and colipase break down fats into MG and FA** stored in micelles - **MG and FA move out of micelles and enter cells by diffusion** through enterocyte membrane - **cholesterol is transported into cells** - **absorbed fats combine with cholesterol and proteins in intestinal cells to form chylomicrons** - chylomicrons are **removed by the lymphatic system**
81
Enterohepatic circulation ( _ is recycled _ times per meal)
the amount of bile stored in the gallbladder is not enough for one meal, **bile is recycled up to 5 times per meal**
82
Amount of bile excreted in feces
5%
83
Gallstones (due to)
hardened deposits in gallbladder due to **excess cholesterol** **or** excess **bilirubin**
84
Gallstone symptoms
upper abdominal pain, jaundice caused by inability to secrete bile
85
Gallstone treatment
removal of gallbladder
86
Amylase
break down **glucose polymers to disaccharides** (cleaves maltose)
87
Disaccharidases
intestinal brush border enzymes that break down DSAC (maltase, sucrase, lactase) to glucose, fructose, galactose
88
Glucose/galactose absorption in small intestine
enter with Na on SGLT and exit with GLUT2
89
Fructose absorption in small intestine (enter on _, exit on _)
enter on GLUT5 and exit with GLUT2
90
Enterocytes and glucose
normally glucose is phosphorylated when enters cell to be used for energy, but **enterocytes use glutamine as energy** source **so glucose is not phosphorylated to allow basolateral transport** to continue
91
Egg vs plant protein digestion
98% vs 70-80%
92
Source of 30-60% digested proteins
dead cells, enzymes, mucus
93
Endopeptidases (proteases)
attack peptide bonds in the AA chain to cleave into 2 smaller peptides
94
Endopeptidase release as what
as zymogens
95
Endopeptidase examples
pepsin, trypsin, chymotrypsin
96
Exopeptidases
release **single AA** from peptides one at a time (**aminopeptidases**, **carboxypeptidases**)
97
Aminopeptidases
remove AA from **amino**-terminal end of peptide, are brush border enzymes made by intestinal cells
98
Carboxypeptidases
**remove AA from carboxy-terminal** end of peptide, are made in pancreas (pancreatic carboxypeptidase A1, A2, B)
99
Single AA absorption by
**Na+ cotransporter** (apical), and **Na+ exchanger** (basolateral)
100
Di and tripeptide absorption
enter with **oligopeptide transporter** (H+ cotransporter) on apical, then are **digested to single AA by peptidases** and **exit with Na-AA exchanger** (basolateral)
101
Absorption of some peptides of 3 AA
transcytosis after binding to receptor on luminal surface
102
Peptides as allergen in babies
peptide absorption is high when infants, as villi are small, may play role in food intolerances or allergies
103
Fat soluble vitamin absorption
absorbed with fats (K, A, D, E)
104
Water soluble vitamin absorption
absorbed by mediated transport (C, most B)
105
Vitamin B12 absorption
absorbed **in ileum** after forming complex **with intrinsic factor** (parietal cells)
106
Mineral absorption by _ transport
active transport (Fe and Ca are regulated)
107
Regulation of Fe absorption
when Fe levels are high, **hepcidin hormone is released** and will **remove ferroportin transporter** from basolateral side of enterocytes
108
Regulation of Ca+ absorption (when high = _, when low = _)
when **Ca+ levels are high,** transporter **transcription is decreased,** when Ca+ levels are **low,** **transcription** of basolateral Ca+ channels **is increased**
109
Location of water absorption
small intestine
110
Steps of water and ion absorption ( _ enters cell, _ pumps _ into ECF to create gradient)
Na+ enters cell by multiple pathways - **Na+/K-ATPase pumps Na+ into ECF** to create osmotic gradients - **water and K+ move paracellular** pathway **to follow gradient**
111
Intestinal Phase regulation
distension, acidity, and digestive products in the small intestine through short and long reflexes and endocrine signaling to reduce motility and secretion in the stomach and increase in the stomach
112
Intestinal motility primary influence
ENS neurons (myenteric plexus)
113
Fed state small intestine motility
**mainly segmental contractions** with some peristaltic, **caused by slow waves brought to threshold initiated by distension** of stomach, small intestine, and **increased *para*sympathetic input** (long reflexes)
114
Fasting state small intestine motility
MMC caused by motilin, may be stimulated by alkaline pH
115
Small intestine phase secretions
secretin (produced by **S cell**), cholecystokinin (by **I cells**), GIP (by **K cells**), GLP-1 (by **L cells**)
116
Pancreatic secretions begin...
during cephalic (***para*sympathetic** neurons) and gastric (**gastrin** and ***para*sympathetic** neurons) phases, and due to **enteropancreatic reflex**
117
Enteropancreatic reflex ( _ reflexes activate _ cells)
once substances enter the small intestine, **long reflexes activate pancreatic cells**
118
Secretin secretion
**acid entering the duodenum** from the stomach **activates S cells to release secretin**
119
Secretin roles (3)
**stimulate bicarbonate secretion** from pancreas (regulate pH in small intestine), **stimulate bile secretion** from liver, **inhibit gastric acid secretion and gastric motility** (restrict gastric emptying into small intestine)
120
Cholecystokinin (CCK) secretion
presence of FA and AA in chyme stimulate I cells to release CCK
121
CCK roles
**regulate pancreatic enzyme secretion** (stimulate acinar cells to increase digestive enzyme secretion to duodenum), **regulate bile secretion** (cause gallbladder contraction to squeeze out bile, also relax oddi sphincter to allow bile flow into duodenum), **inhibits gastric acid production and emptying**
122
% pancreatic enzyme secretion in **cephalic phase**
25%
123
% pancreatic enzyme secretion in gastric phase
10-20%
124
% pancreatic enzyme secretion in intestinal phase
50-80%
125
GIP secretion
glucose presence activates K cells to cause release of GIP
126
GLP-1 secretion ( _ presence activates _ cells)
glucose presence activates L cells to cause release of GLP-1
127
GIP and GLP-1 roles
will activate pancreatic B-cells to cause insulin release to function in glucose homeostasis, also inhibit gastric acid secretion and motility
128
Enterogastric reflex
acid, enzymes, and digested food results in **hyperosmotic chyme** that** inhibits gastric emptying** as an endocrine cell reacts to osmolarity and releases a hormone to negatively regulate gastric functioning
129
Main role of large intestine
store and concentrate fecal matter
130
Ileocecal valve
1.5L of chyme proceed through to enter the large intestine
131
2 causes of ileocecal valve relaxation
**gastroileal reflex** - food in stomach causes contraction of ileum and **relaxation of the ileocecal valve**
132
Remaining substances at end of large intestine
0.1L (75% undigested food, 15% bacteria, small amount water)
133
Appendix role
likely is a **storage reservoir of good bacteria**, when diarrhea occurs the baccteria stored in the appendix is able to repopulate the large intestine
134
Large intestine secretions
**mucus from goblet cells**
135
Large intestine digestions
traditionally believed that zero digestion occurred, **some actually does through fermentation process**
136
Fermentation process
indigestible complex CHO, fats, and proteins are broken down by the 100 trillion bacteria in the large intestine
137
Fermentation process products
**lactate and short chain FA** (used by colonocytes for energy), absorbable vitamins (**vitamin K**), produce gases
138
3 kinds of motility in large intestine
slow segmental contractions, haustral rolling/churning, mass peristaltis
139
Duration of large intestine motility
18-24 hours
140
Haustral rolling/churning
thickened bands of longitudinal muscle layer taeni coli create pouches (haustra), churning causes rolling of fecal matter from one haustra to the next
141
Mass peristalsis
is the gastrocolic reflex stimulated by the presence of food in stomach, moves feces quickly to collect in rectum and stimulates the defecation reflex 2-3 times per day
142
Secretin target
pancreatic duct cells, cholangiocytes, G cells, ECL cells, parietal cells
143
Physiological response of secretin
**bicarbonate secretion** from pancreatic duct cells, **bile production** in liver, **inhibit gastric secretion** and motility
144
CCK target
pancreas acini, gallbladder, sphincter of oddi
145
Physiological response of CCK
**digestive enzyme secretion**, **bile secretion**, **inhibit gastric acid secretion** and gastric motility
146
GIP and GLP-1 target
stomach, beta islets in pancreas
147
Physiological response of GIP and GLP-1
stimulate insulin secretion, inhibit gastric acid secretion and gastric motility
148
Motilin target (_ muscle)
smooth muscle
149
Physiological response of motilin
MMC
150
Short reflex of defecation response
local **peristaltic waves** initiated by **stimulation of stretch receptors in rectum**
151
Long reflex of defecation response
**stimulation of *para*sympathetic** motor neurons cause relaxation of internal sphincter (smooth), contraction of external sphincter (skeletal), and forceful peristaltic contractions
152
Completion of defecation reflex
voluntary relaxation of external sphincter and aided by increased abdominal pressure
153
Diarrhea
increase in the frequency, volume, and fluid content of the feces **due to increased secretion, reduced absorption, or increased motility**
154
4 kinds of diarrhea
**osmotic** (decreased absorption from increased solute in intestine), **secretory** (bacterial toxins cause immune system to flush), **inflammatory** (bacterial toxins cause inflammation and decreased absorption), **motility-induced** (nervous feeling increase autonomic input)
155
Secretory diarrhea example
**cholera produce toxin** that **keeps CFTR channels open** to create a negative charge in the lumen, this **draws Na into the lumen which creates a gradient for water** to enter the small intestine and cause diarrhea
156
Use of penicillin-based antibiotics and C. difficile
use can alter the normal bacterial flora causing remaining bacteria to have reduced competition for space and nutrients, leaving a person prone to C. difficile infection
157
C. difficile produce toxins that cause development of __
Colitis
158
Colitis symptoms
watery diarrhea, fever, nausea, abdominal pain
159
Colitis treatment
fecal transplant through colonoscopy (spray donor fecal matter into patient), poo pills (take pill with donor fecal matter that releases into large intestine)
160
Vomiting
contents of stomach and small intestine are forcefully expelled through the mouth, associated with nausea
161
Stimulants of vomiting center
balance disturbances, direct input from drugs/toxins/metabolites carried in the blood, input from sensory receptors in the stomach and intestines carried by afferent fibers
162
3 responses of vomiting center
**retrograde contractions** (small intestine to stomach), **contraction of abdominal and inspiratory muscles** (increase gastric pressure), **relaxation of esophageal sphincters** (contents move from high gastric pressure to lower pressure)
163
% lymphoid tissue in gut
80% (GALT)
164
M cells role in _, sample _
(microfold cells) major role in immune responses/functioning as they continually **sample lumen contents with receptor-mediated endocytosis**
165
**GIT immune response process** ( _ cells transport detected _ to macrophages, lymphocytes, and dendritic cells. _ are released to attract more immune cells to attack, _ can also trigger increased _ secretion (diarrhea) to flush pathogens.
**M cells transport detected antigens** to macrophages, lymphocytes, and dendritic cells. **Cytokines are released** to attract more immune cells to attack, **cytokines can also trigger increased Cl- secretion** (diarrhea) to flush pathogens
166
**Feeding state** (nutrients converted to _, _, _, _, and _)
see high amounts of **anabolism** where absorbed nutrients are **converted to glucose, FA, ketones, TG, and glycogen**
167
Fasting state
see high amounts of **catabolism** where glucose, FA, and ketones are used as energy for cells
168
Hunger center
lateral hypothalamus
169
What area was originally believed to be the satiety center?
ventromedial hypothalamus
170
Path of appetite
**GIT** inputs into ARC (**arcuate nucleus**), ARC feeds into PVN (**paraventricular nucleus**) and LH (**Lateral hypothalamus**), PVN and LH feed into **NTS** (**nucleus tractus solitarii**) which releases outputs
171
2 theories of long term regulation of feeding behaviour
**glucostatic theory** (glucose metabolism in the hypothalamus regulates food intake), **lipostatic theory** (signals from the body's fat stores regulate food intake)
172
Evidence for lipostatic theory
identification of ob/ob mice, found that the gene encoded a protein that tells the brain fat reserves are normal (leptin is the coded protein) and ob/ob mice lack leptin protein
173
Leptin
released from adipocytes and regulates body mass by acting directly on neurons of the hypothalamus that decrease appetite and increase energy expenditure
174
Response to elevated leptin
acts on arcuate nucleus to 1. inhibit lateral feeding 2. activate PVN to cause humoral and visceromotor response
175
Humoral response (increased _ and _ released from __ _ to increase the __ _ )
**increased TSH and ACTH** is released from the **anterior pituitary** **to increase the metabolic rate** throughout the body
176
Visceromotor response
**increase sympathetic output** to increase body temperature
177
Anorectic peptides
**prevent** feeding behaviour when acting on lateral hypothalamus
178
Response to decreased leptin
1. **reduced activation of a-MSH and CART neurons** (**reduced activation of PVN to decrease TSH/ACTH/metabolic rate**, activate ***para*sympathetic output**), 2. **activate NPY and AgRP neurons** (stimulate feeding center, **inhibit PVN further)**
179
Orexigenic peptides
stimulate feeding behaviour when acting on hypothalamus
180
Why did leptin supplements fail to treat obesity?
decreased sensitivity to leptin in obese individuals due to reduced ability of leptin to cross BBB or due to reduced receptor expression
181
Short term regulation of feeding behaviour depends on
how long it has been since the last meal and how much we consumed at that time
182
Short term regulation is a balance between...
**satiety signals generated during digestion** (fed state), and **orexigenic signals generated during fasting** (fasting state)
183
4 signals of short-term regulation
ghrelin, gastric distension, CCK, insulin
184
Ghrelin released by...
cells in the stomach in response to emptying
185
Ghrelin stimulates...
**NPY/AgRP containing neurons** **in the arcuate nucleus** that stimulate feeding behaviour
186
Result of ghrelin injection
food intake is stimulated
187
Result of mice lacking NPY/AgRP neurons
do not respond to ghrelin
188
Gastric distension response
**sensed by mechanosensory neurons**, information is **sent to NTS (medulla)** which **projects to the PVN and ARC to** **decrease feeding behaviour**
189
CCK response (_ meal frequency)
**released by I cells** in duodenum **in response to fats and AA** entering the small intestine **to *inhibit* meal frequency and size**
190
Gastric distension and CCK act on...
the NTS (medulla) to stimulate satiety feeling
191
Result of increased insulin **during cephalic and gastric phase**
cause a **drop in blood glucose to drive hunger through activation of NPY/AgRP neurons**
192
Result of increased insulin **during intestinal phase**
increased BG causes **increased insulin that acts as a *satiety signal* by activating a-MSH/CART** **neurons** in the arcuate nucleus
193
Why is marijuana prescribed?
means to stimulate appetite in patients with chronic diseases associated with reduced appetite
194
Why does marijuana increase appetite in humans?
**indirectly activates NPY/AgRP neurons in ARC and CB1 receptors in LH** to increase appetite
195
Why does marijuana increase appetite in mice?
enhances their sense of smell
196
% of energy outputs
50% heat (unregulated, thermoregulation), 50% work (membrane transport, mechanical work, chemical work)
197
Measurement of energy input
bomb calorimeter where heat released from burned food is measured
198
One kcal =
amount of energy needed to raise the temperature of 1L of water by 1 degree
199
Why do bomb calorimeters lightly overestimate energy input?
we do not completely digest and absorb most foods
200
Energy output =
work + heat
201
2 ways to measure energy output
direct (chamber to measure heat released), indirect (measure O2 consumption of CO2 production)
202
Basal metabolic rate
an individuals lowest metabolic rate, usually measured as resting matabolic rate
203
Factors affecting overall metabolic rate
age and sex (male 1 kcal/hour/kg, female 0.9 kcal/hour/kg), amount of lean muscle mass, activity level-metabolic activity above BMR, diet and diet-induced thermogenesis, hormones (influence O2 consumption and heat production of body tissues), genetics
204
Single most important BMR determinant
thyroid hormones
205
Metabolism
sum of all chemical reactions in body
206
3 categories of chemical reactions
extract energy from nutrients, use energy for work, store excess energy for later
207
Skeletal muscle in fed state
take up glucose for energy use and stores it as glycogen (70% glycogen stores), AA are taken up for protein turnover
208
Liver in fed state
**convert glucose to glycogen** (24% body stores), **convert glucose to FA** (transport to adipocytes), **AA used for synthesis and conversion to keto acids** (energy or FA synthesis)
209
Adipocytes in fed state
take up dietary TG from chylomicrons, excess glucose taken up and converted to TG, store TG made in liver
210
Glycogen % total energy reserve
1%, sustain quiet activity for few hours
211
TG % total energy reserve
75-80%, decreased levels compromise cellular function
212
Proteins % total energy reserve
20-25%, can sustain activity for two months
213
Skeletal muscle in fasted state
convert glycogen to G-6-P (glycogenolysis) for own use, form pyruvate and lactate
214
Liver in fasted state
glycogen converted to glucose and used throughout body (glycogenolysis), **produce new glucose** from pyruvate, lactate, glycerol and some AA (**gluconeogenesis**), **converts FA to ketone bodies** for energy
215
Adipocytes in fasted state
lipolysis occurs, FA and glycerol enter blood to be used as energy in most cells
216
Processes occuring in fed state
Glucose primarily used by cells for energy. Glycogenesis, lipogenesis, AA uptake and protein synthesis
217
Processes occurring in fasting state
FA primarily used by cells for energy. Glycogenolysis, lipolysis, gluconeogenesis, ketogenesis, protein degradation
218
Main hormone of fed state
**insulin** (from pancreatic B-islet cells) Promotes anabolism
219
Main hormone of fasting state
**glucagon** (from pancreatic a-islet cells)
220
Stimulants of insulin secretion
**increased** plasma glucose, AA, GIP, GLP-1, and ***para*sympathetic** activity
221
Insulin impact on most tissues
increase glucose uptake, AA uptake, protein synthesis, decrease protein breakdown
222
Insulin impact on adipose tissues
increase FA and TG synthesis, decrease lipolysis
223
Insulin impact on liver and muscle
increase glycogen synthesis, decrease glycogenolysis
224
Insulin impact on liver
increase FA and TG synthesis, decrease glycogenolysis
225
Steps of insulin release from B-islet cells
high concentration of **glucose outside the cell moves in via facilitated diffusion** - glucose **converts to pyruvate and enters mitochondrial matrix** - **oxidative phosphorylation releases ATP into cytosol** - **ATP binds to ATP-selective K channels** **to** cause them to close and **block K movement out of cell** - cell membrane depolarizes -**voltage-gated Ca+ channels open and Ca+ enters the cel**l - **Ca+ triggers insulin release through exocytosis**
226
Steps of insulin's action
binds to tyrosine kinase receptor - receptor phosphorylates IRS - phosphorylation activates second messenger pathways that alter protein synthesis and existing proteins - membrane transport is modified - cell metabolism is changed
227
Tyrosine kinase receptor causes
insertion of glucose transporters, increase/decrease of metabolic enzyme activity
228
Glucagon stimulation
**decreased** plasma glucose, **sympathetic activity**
229
Glucagon receptor
G-protein coupled receptor, will adenylate cyclase pathway which causes changes in enzymatic activity
230
Effects of Glucagon in liver
increased glycogenolysis, gluconeogenesis, ketone synthesis, and protein breakdown, decreased glycogen synthesis, protein synthesis
231
Effects of glucagon in adipose tissue
increased lipolysis, decreased triglyceride synthesis
