Indigestion & Digestion

Week 12: Tuesday, November 11th: Energy: Digestion & Dysregulation; Thursday, November 13th: Energy: Ingestion & Dysregulation

eating is also known as _______

indigestion

breaking down food mechanically and chemically is known as _______

digestion

when we stop eating and signals distribute the molecules we ate into cells, this is known as _______

post digestion

energy expenditure is the process of using muslces to make _______

ATP

what does the brain/neurons use for energy?

glucose 

after we eat, blood glucose is stored as _______ in the liver, muscles, and other tissues

glycogen 

after we eat, fat in our blood is stored as _______ in adipose tissue

triglycerides

after we eat, proteins are stored where?

throughout the body

which part of the nervous system controls eating?

parasympathetic nervous system

which nerve controls our digestion?

vagus nerve

adjusting food intake and energy expenditure is control by the hypothalamus and adipose tissue mass to _______

maintain body weight 

_______ being released from the GI tract to stimulate the hypothalamus is a body → brain hunger signal

ghrelin

_______ being released from the hypothalamus to the body is a brain → body hunger signal

neuropeptide y

_______ being released from the GI tract to stimulate the hypothalamus is a body → brain satiety (fullness) signal

cholecystokinin (CCK)

_______ being released from the hypothalamus to the body is a brain → body satiety (fullness) signal

alpha melanocyte stimulating horomone

_______ released from the adipose tissue to stimulate the hypothalamus is a body → brain adiposity (fat satiety) signal

leptin

_______ released from the pancreas to stimulate the hypothalamus is a body → brain adiposity (fat satiety) signal

insulin

sensations, thoughts, imagination, and emotions are what types of stimuli that activate the vagus nerve from the brain to the gut?

neural stimuli

_______ are physical stimuli that respond to the GI tube stretching when food enters our stomach

mechanoreceptors

_______ are chemical stimuli that response to changes in pH or the presence of fatty acid or peptide chains

chemoreceptors

during digestion, our stomach breaks down proteins using _______

gastric acid

during digestion, our small intestine receives:

1. insulin from our _______ to break down glucose

2. bile from our _______ to break down fat

3. enzymes from our _______ to break down all molecules

liver, gallbladder, pancreas

_______ release digestive endocrine chemicals

entroendocrine cells

_______ are entroendocrine cells in the stomach that release gastrin

G cells

_______ are entroendocrine cells in the stomach and small intestine that release somatostatin

D cells

_______ are entroendocrine cells in the small intestine that release secretin

S cells

_______ are entroendocrine cells in the small intestine that release CCK

I cells

_______ are entroendocrine cells in the small intestine that release gastric inhibitory peptide (GIP)

K cells

during the digestion of proteins, peptides, and fats:

1. protein enters the stomach and signals G cells to release _______ (what chemical?)

2. gastrin stimulates _______ (what substance?) release from parietal cells

3. HLC denatures proteins, then activates _______ (what enzyme?) and signals S cells to release secretin

4. Peptides activate _______ (what cells?) to release CCK

5. CCK and secretin stimulate the Islets of Langerhans in the pancreas to release _______ (what substance?)

6. CCK stimulates the _______ to release bile into the small intestines

1. gastrin

2. HLC (gastric acid)

3. pepsin

4. I cells

5. a basic solution

6. gallbladder

during digestion inhibition:

1. _______ inhibits gastric secretion and movement

2. D cells release _______ to regulate digestive actions via inhibtion

3. the Islets of Langerhans regulate digestion by releasing _______ and _______ to neutralize the stomach

1. GIP

2. somatostatin

3. water and HCO3- (bicarbonate ion)

during glocose metabolism:

1. glucsoe stimulates _______ (what cells?) to release GIP

2. GIP stimulates the Islets of Langerhans to release _______

3. insulin decreases blood glucose levels (hypoglycemia) by stimulating organs to intake _______ (what molecule?)

4. the Islets of Langerhans releases _______ (an insulin antagonist) and somatostatin

1. K cells

2. insulin

3. glucose

4. glucagon

the _______ of the pancreas regulaes energy storage adn metabolism

Islets of langerhans (endocrine)

_______ cells in the pancreas release glucagon, and _______ release insulin

alpha cells, beta cells

the absorptive phase of glucose regulation and inhibition is regulated by _______, which directs:

1. amino acids → _______ and _______

2. glucose → muscles, tissues, liver, and brain for _______

3. triglycerides → _______

insulin

1. muscles, liver

2. ATP

3. adipose tissue

during the absorptive phase of glucose regulation and inhibition, excess glucose is:

1. stored as glycogen in liver and muscles via _______ (what process?)

2. stored as fat in adipose tissue via _______ (what process?)

1. glycogenesis

2. lipogenesis

where is glucsoe transformed in to triglycerides before its storied in adipose tissue?

the liver

during the postabsorptive phase of glucose regulation and inhibition, what two processes occur for other molecules to be turned back into glucose?

glycogenosis and glycoenolysis

assited by stress and growth hormones, glucagon regulates nutrient mobilization to induce high blood sugar, which is also known as _______

hyperglycemia

insulin binds to _______ (what receptors?) on cells, then inserts _______ from the cytosol into cell membranes for glucose entry

tyrosine kinase receptors, glucsoe transporter molecules

specific glucose transporter molecules are found on specific cells:

1. GLUT 1 → _______

2. GLUT 2 → _______

3. GLUT 3 → _______

4. GLUT 4 → _______

1. all cells

2. liver and pancreas

3. neurons

   1. fat tissue and muscles

broken or overstimulated beta cells causes no insulin release, which is also known as _______ (what disease?)

Type 1 diabetes

broken tyrosine koanse receptors causes unrecognition of insulin, which is also known as _______ (what disease?)

Type 2 diabetes