Endocrine Part 6 Flashcards
Which of the following correctly matches the pancreatic endocrine cell with its hormone and function?
A. Alpha cell – Amylin – Suppresses insulin secretion
B. Beta cell – Insulin – Promotes glycogenolysis
C. Delta cell – Somatostatin – Inhibits other pancreatic hormones
D. PP cell – VIP – Stimulates glucose uptake
C. Delta cell – Somatostatin – Inhibits other pancreatic hormones
Rationale:
Delta cells secrete somatostatin, which inhibits the secretion of both insulin and glucagon (Slide 4). Alpha cells produce glucagon, beta cells produce insulin and amylin, and VIP is secreted by rare D1 cells. None of the other options correctly match all three parts (cell–hormone–function).
what is secreted by alpha cells and beta cells of the pancreas?
glucagon for alpha
insulin for beta
Why is the pancreas classified as both an endocrine and an exocrine gland?
A. It secretes insulin and glucagon into ducts and digestive enzymes into the blood
B. It releases digestive enzymes through ducts and hormones directly into the bloodstream
C. It produces only hormones but transports them through specialized ducts
D. It synthesizes all its secretions in the acinar cells and delivers them into circulation
It releases digestive enzymes through ducts and hormones directly into the bloodstream
Rationale:
The exocrine function of the pancreas involves the acinar cells, which release digestive enzymes into the duodenum via ducts. The endocrine function involves islet cells that secrete hormones like insulin and glucagon directly into the bloodstream (Slide 3).
hormone of the pancrease that has anabolic action and increases the updake of storage of fuels during feasting
a. glucagon by alpha cells
b. somatostatin by delta cells
c. insulin/amylin by beta cells
d. pancreatic polypeptide by F or PP cells
e. vasoactive intestinal polypeptide by D1 cells
insulin/amylin
why is insulin, dlucagon, cortisol, growth hormone, and ephinephrine so important in the body
insulin is the oly hormone that can promote storage of major body fuels (glucose, triglycerides, fats and amino acids)
cortisol, growth hormone, ephinephrine, and glucagon promote the liberation of body fuels to maintain metabolism and cell function
. What is the effect of insulin on glucagon secretion, and what is the physiological basis for this interaction?
A. Insulin increases glucagon secretion by enhancing gluconeogenesis in alpha cells
B. Insulin has no effect on glucagon because they act on different target tissues
C. Insulin suppresses glucagon secretion by promoting an anabolic state and reducing the need for fuel mobilization
D. Insulin indirectly increases glucagon levels by stimulating lipolysis in adipose tissue
Insulin suppresses glucagon secretion by promoting an anabolic state and reducing the need for fuel mobilization
Rationale:
Insulin and glucagon have opposing roles: insulin promotes fuel storage (anabolism), while glucagon mobilizes fuels (catabolism). When insulin is present in high amounts (e.g., post-feeding), glucagon secretion is suppressed, as there is no need to mobilize energy stores (Slide 8).
which of the following is not a target for insulin?
a. adipose tissue cells
b. hepatocytes
c. liver cells (hepatocytes)
d. the pancrease
the pancrease is not a target for insulin
instead, glucose in circulation in the blood will go to the pancrease to stimulate the release of insulin from the pancrease
Which of the following best describes the role of GLUT-4 in glucose metabolism?
A. GLUT-4 facilitates passive glucose transport into liver cells independent of insulin
B. GLUT-4 enables insulin-independent glucose uptake in neurons and red blood cells
C. GLUT-4 is an insulin-dependent glucose transporter primarily found in adipose and muscle tissue
D. GLUT-4 mediates glucose absorption from the gut lumen via secondary active transport
C. GLUT-4 is an insulin-dependent glucose transporter primarily found in adipose and muscle tissue
Rationale:
GLUT-4 is the only insulin-dependent glucose transporter, found in skeletal/cardiac muscle and adipocytes. It translocates to the plasma membrane in response to insulin, allowing facilitated diffusion of glucose into cells (Slide 17).
Option A incorrectly attributes GLUT-4 to liver cells; liver uses GLUT-2, which is insulin-independent.
Option B is false because neurons and RBCs use GLUT-1/3, not GLUT-4.
Option D misstates the function—intestinal glucose absorption uses SGLT transporters, not GLUT-4.expl
how does insulin work on liver, muscle and adipose tissue?
(in summary you build up everything)
KNOW: NET EFFECT IS ANABOLISM
- liver:
- increased gluconeogenesis
- increased glycolusis
- increased fat and protein synthesis - muscle
- increased amino acid uptake and protein synthesis
- increased glyconeogenesis and glucose uptake - adipose tiddue
- increased GLYCOLYSIS and glucose uptake
- increased fatty acid uptake and fat synthesis
how does insulin work on the target cells? (state the correct order)
1. insulin binds to receptor
2. phosphate groups are attatched to specific intracellular proteins
3. tyrosine kinase receptors form dimers
4. downstream effects (transport systems, enzyme activity, genen expression)
1, 3, 2, 4
why is glut 4 insulin sensitive?
Why is GLUT-4 considered insulin-sensitive, unlike other glucose transporters such as GLUT-1 or GLUT-2?
A. GLUT-4 is continuously present on the cell membrane and increases glucose uptake in response to rising blood glucose alone
B. GLUT-4 gene expression is directly stimulated by insulin to increase transporter synthesis during fasting
C. GLUT-4 is stored in intracellular vesicles and translocates to the plasma membrane only in response to insulin signaling
D. GLUT-4 activity is enhanced by insulin-stimulated glycolysis in the mitochondria of pancreatic alpha cells
GLUT-4 is stored in intracellular vesicles and translocates to the plasma membrane only in response to insulin signaling or when insulin is present
Rationale:
GLUT-4 is insulin-sensitive because under basal conditions it is sequestered inside vesicles within adipose and muscle cells. When insulin binds its receptor, it triggers a signaling cascade that causes GLUT-4 to translocate to the plasma membrane, allowing glucose uptake (Slide 17).
what is the process of gluconeogenesis during long periods of time (beyond 24 hours)
it is a process where the body makes glucose using non-carbohydrate soruces such as amino acids and fatty acids
where in the body is glucose stored as glycogen?
a. liver
b. pancrease
c. skeletal muscle
d. muscle
e. adipose tissue
glucose is stored as glycogen in the liver and in the muscles
where does fatty acid/triglyceride synthesis and protein synthesis occur?
a. liver
b. pancrease
c. skeletal muscle
d. muscle
e. adipose tissue
fatty synthesis in the liver and adipose tissue
protein synthesis in the mucsles and the liver
Which of the following best describes insulin’s effect on target tissues during the fed state?
A. Stimulates gluconeogenesis in the liver and lipolysis in adipose tissue
B. Promotes glycogenolysis in the liver and proteolysis in muscle
C. Inhibits glycolysis and promotes fatty acid oxidation in adipocytes
D. Enhances glycogen synthesis in liver and muscle, and lipogenesis in adipose tissue
Enhances glycogen synthesis in liver and muscle, and lipogenesis in adipose tissue
Rationale:
Insulin promotes anabolism—it increases glycogen storage in liver and muscle, and enhances fat synthesis in adipose tissue (Slide 19). It inhibits gluconeogenesis, lipolysis, and proteolysis (Slide 24). The other options describe catabolic processes more characteristic of glucagon or insulin deficiency.
What is the most likely metabolic state during insulin deficiency?
A. Increased protein synthesis, glycogenesis, and glucose uptake
B. Increased gluconeogenesis, lipolysis, and ketogenesis
C. Decreased glucagon secretion and increased glycogen synthesis
D. Increased glycolysis and triglyceride storage
Increased gluconeogenesis, lipolysis, and ketogenesis (muscle breakdown)
Rationale:
In insulin deficiency, the body enters a catabolic state dominated by glucagon, leading to muscle breakdown, fat breakdown, gluconeogenesis, and ketogenesis (Slides 20, 30). The other choices describe insulin-dominant (anabolic) states.
glucose uptake into fat and muscle is impaired since GLUT 4 is dependant on Insulin (which is secreted from the pancrease after stimulation of glucose in the blood)
hat is the primary role of glucagon in human metabolism, and which of the following best describes its major physiological effects?
A. To promote glucose uptake and storage by stimulating glycogenesis in muscle and adipose tissue
B. To maintain blood glucose during fasting by stimulating glycogenolysis and gluconeogenesis in the liver
C. To facilitate amino acid uptake into cells for protein synthesis after a meal
D. To lower blood glucose by increasing GLUT-4 translocation in skeletal muscle and adipose tissue
To maintain blood glucose during fasting by stimulating glycogenolysis and gluconeogenesis in the liver
Rationale:
Glucagon is the “hormone of fasting”, secreted by alpha cells to raise blood glucose when levels are low. Its primary actions are in the liver, where it promotes glycogen breakdown (glycogenolysis) and new glucose production (gluconeogenesis) (Slide 22–24).
how are the liver, adipose tissue, and muscle affected by fasting?
NET EFFECT: catabolism
FASTING=Low glucose supply
liver: increased glycogen breakdown and gluconeogenesis and ketone syntehsis
adipose: more fatty acid breakdown
muscle: glycogen breakdown, fatty acid uptake as a fuel source, and protein breakdown
Which of the following best summarizes the contrasting actions of insulin and glucagon in the liver during fed and fasting states?
A. Insulin promotes gluconeogenesis and ketogenesis, while glucagon enhances glycogen synthesis and lipid storage
B. Insulin inhibits glycogenolysis and stimulates glycogenesis; glucagon promotes glycogenolysis and gluconeogenesis
C. Both insulin and glucagon stimulate lipogenesis but differ in their effects on protein metabolism
D. Insulin and glucagon both promote glycolysis, but insulin is more efficient during the fasting state
Insulin inhibits glycogenolysis and stimulates glycogenesis; glucagon promotes glycogenolysis and gluconeogenesis
Rationale:
In the fed state, insulin dominates and signals the liver to store glucose as glycogen (glycogenesis) and inhibit glucose release (glycogenolysis and gluconeogenesis). In contrast, during fasting, glucagon takes over and tells the liver to break down glycogen and make new glucose from non-carbohydrate sources (gluconeogenesis) to maintain blood glucose (Slide 24–25).
Which of the following best explains the mechanism behind hypoglycemia in insulin overdose?
A. Excess insulin enhances glucagon secretion and ketogenesis
B. Insulin suppresses gluconeogenesis and stimulates glucose uptake into cells
C. Excess insulin inhibits lipogenesis and promotes lipolysis
D. Insulin increases glycogenolysis and glycolysis in the liver
Insulin suppresses gluconeogenesis and stimulates glucose uptake into cells
Rationale:
High insulin levels increase glucose uptake via GLUT4 and inhibit gluconeogenesis and glycogenolysis, leading to low blood glucose (hypoglycemia) (Slide 27). The other choices are either incorrect or describe glucagon-mediated or catabolic responses.
Which combination of hormone actions is most consistent with the fasting state?
A. ↑ Insulin, ↑ Glycogenesis, ↑ Protein synthesis
B. ↑ Glucagon, ↑ Lipolysis, ↑ Gluconeogenesis
C. ↑ Insulin, ↓ Gluconeogenesis, ↑ Lipogenesis
D. ↓ Glucagon, ↑ Glycolysis, ↑ Glucose uptake
↑ Glucagon, ↑ Lipolysis, ↑ Gluconeogenesis
Rationale:
During fasting, glucagon is the dominant hormone. It promotes lipolysis, gluconeogenesis, and glycogen breakdown to maintain blood glucose levels (Slide 23). Insulin is low during fasting, so the anabolic actions in other choices are not applicable.
how does hypersecretion of insulin affect the body? why do we care about glucose?
hypersecretion of insulin causes hypoglycemia, or low glucose levels since there is more glucose being stored, rather than being used for fuel
glucose is critical for our brains to function (increases sympathetic activity) and lopw glucose causes autonomic and hormonal changes
low glucouse causes a person to feel more tired
why does hyposecretion of insulin cause hyperglycemia, diabetes mellitus and ketoacidosis?
causes hyperglycemia and diabetes mellitus since glucose is not being stored into the liver and the muscles
causes ketoacidosis (maikng glucose with ketones) and hyp
Why does insulin deficiency lead to diabetic ketoacidosis (DKA)?
A. Low insulin enhances GLUT-4 expression in muscle, increasing glucose storage and ketone production
B. Insulin deficiency leads to unchecked glucagon activity, increasing lipolysis and ketogenesis
C. Without insulin, glucose enters cells rapidly, stimulating excessive fatty acid synthesis and ketone accumulation
D. Insulin deficiency causes hypoglycemia, triggering cortisol-mediated ketone body suppression
Insulin deficiency leads to unchecked glucagon activity, increasing lipolysis and ketogenesis
Rationale:
In DKA, the absence of insulin results in glucagon dominance, leading to increased lipolysis, free fatty acid release, and conversion into ketone bodies in the liver (Slide 30–31). This causes acidosis, dehydration, and hyperosmolarity.
