MET2 Revision4

Question 1

How does obesity cause extrinsic insulin resistance? [3]

How does obesity cause intrinsic insulin resistance? [3]

What is net effect of obesity and insulin? [1]

Answer 1

Which aspects of obesity causes extrinsic insulin resistance? [3]
* Accumulation of lipids and FFA
* Chronic inflammation
* Altererd adipokiine (cytolines from FA)

How does obesity cause intrinsic insulin resistance? [3]
* Mitochondrial dysfunction
* Ox stress
* ER stress

Overall: causes hyperinsulinaemia, whcih increases lipid synthesis and insulin resistance

Question 2

How do B pancreatic cells first react to being insulin resistant? [3]

Answer 2

B cells:
* become bigger
* increase in number
* produce more insulin

Question 3

Whats difference between insulin resistance and DMT2?

Answer 3

Insulin resistance: adapt by : become bigger, increase in number and produce more insulin (compensatory hyperinsulinaemia)

DMT2: resistance AND failure

Question 4

How does islet compensation occur if there is impaired function from obesity of B-cells?

Answer 4

As the impacts of obesity occur the susceptible cells will decrease in number/function –> B-cell apoptosis

Question 5

Impaired genetic compensation: genetic component

How do most of the genes associated with DMT2 influence insulin [2]

Answer 5

impairing insulin secretion rather than insulin action

Gene risk variants are to do with the regulators of β cell turnover or regeneration

Question 6

Impaired genetic comepensation: environmental component

Which envrionmental factors within body influence DMT2 infuence? [4]

Answer 6

Increased circulating FFAs (lipotoxicity)

Hyperglycaemia (glucotoxicity)

Combination of the two (glucolipotoxicity)

Hyperinsulinemia

Question 7

What is Monogenic diabetes? [1]

Specifically how is it caused / insulin affected? [2]

Answer 7

Caused by a mutation in a single gene (one of over 40 genes): Means theres 40 types of MODY

Most cases are Maturity Onset Diabetes of the Young (MODY)

Caused by:
* prevent the insulin sensing glucose metabolism in B-cells

• Due to: impairment of insulin secretion/pancreatic βcell dysfunction

Question 8

What may cause gestational diabetes? [2]

Answer 8

excessive proinsulin that may induce β cell stress

high concentrations of hormones may affect β cell function and peripheral insulin sensitivity

Question 9

Many women with GD experience pregnancy-related complications including WHAT? [3]

Answer 9

Many women with GD experience pregnancy-related complications including
* high blood pressure,
* large birth weight babies
* obstructed labour

Question 10

What is LADA?

What are characteristics of LADA? [2]

Answer 10

Latent Autoimmune Diabetes of Adults (LADA): Features of both Type 1 and Type 2 (type 1.5)

Immunologically similar to T1 - produce DMT1 antibodies but destruction is slower than in T1.

Question 11

What HbA1c is used as cut off for diabetes? [1]

Answer 11

An HbA1c of 48 mmol/mol (6.5%) is recommended as the cut point for diagnosing diabetes

Question 12

How can you treat DMT1?

Currently? [2]
Future? [2]

Answer 12

Insulin - short acting and long acting.
- Pumps
- Injections - pens
- Short / Fast acting: Humalog
- Long acting: Glargine

Islet transplantation
- Only patients matching a strict list of criteria, including being at risk of frequent and secere hypos/hypers.

Possible future treatment: immunotherapy

SGLT Inhibitors:.
* Prevent co-reabsorption of glucose in the PCT with Na.
* Encourages glycosuria -> wee out the excess glucose. Lowers blood glucose levels. Restores GFR in diabetics
* E.g.

Question 13

MoA of Metformin [3]

Answer 13

Inhibits gluconeogenesis in the liver
Inhibits CAMP + PKA pathway.
Also increases glucose transport - increasing uptake at skeletal muscle. Opposes insulin resistance through various mechanisms.

From Drugs List:

acts by activation of the AMP-activated protein kinase (AMPK)
increases insulin sensitivity
decreases hepatic gluconeogenesis

Question 14

Which treatments for DMT2

inhibitGNG [1]
increase insulin sensistivity [2]
stimulate insulin secretion [2]

two others? [2] ?

Answer 14

Inhibits GNG:
* Metformin: inhibits GNG at liver

Increases insulin sensitivity:
* Metformin
* Thiazolidinediones: Enhance GLUT4 uptake into the cell membranes (in adipocytes - so causes weight gain) via PPAR-y gene

Stimulation of insulin secretion:
* Sulfonylureas: close ATP sensitive K chance which regulates insulin secretion
* Prandial glucose regulators: same as above but faster

Others:
* GL1-P receptor agonists
* DPP-4 inhibitors: DPP-4 inhibits GL1-P

Question 15

What is the role of GLP-1 on:

• glucagon secretion [1]
• GNG [1]
• insulin secretion [1]
• insulin synthesis [1]

Answer 15

GLP-1
* Can inhibit glucagon secretion
* Can reduce gluconeogenesis.
* Can enhance insulin secretion + restore B-cell function/differentiation.
* Can increase insulin biosynthesis.

Question 16

When do you see DKA? [3]

Answer 16

DKA is a hallmark of DMT1 - it is usually seen in:
- Previously undiagnosed diabetes
- Interruption of insulin therapy
- The stress of intercurrent illness e.g. surgery or infection

Question 17

How does DKA occur?

Answer 17

In the absence of insulin there is an unrestrained increase in hepatic gluconeogenesis and peripheral glucose uptake by tissues such as muscle is reduced

High circulating glucose levels result in an osmotic diuresis (since increased glucose in urine which pull more water into urine) by the kidneys and consequent dehydration and loss of electrolytes

Peripheral lipolysis occurs leading to an increase in circulating free fatty acids (FFAs) which are then broken down to acetyl-coenzyme A (CoA), but little oxaloacetate within the liver cells and this, in turn, is converted to ketone bodies within the mitochondria. (no Kreb’s cycle)

Ketone bodies are in excess

Ketone bodies dissociate: H+

Causes metabolic acidosis w/ raised anion gap.

Vomiting leads to further electrolye loss

Question 18

What is the order of treatmnet for DKA? [3] What are complications of mismanaged treatment?

Answer 18

1. Fluids
2. Restore electrolytes - especially K+
3. Insulin intravenously.

DKA patients have high extracelullar K+ but little intracellular. Need to he careful because if give insulin first, causes intracellular uptake of K but that would causes overall reduction in K and cardiac arrythmias

Question 19

How does XS alcohol cause hypoglycaemia (especially in DMT1?)

Answer 19

Alcohol broken down by alcohol dehydrogenase -> NADH:NAD ratio increased -> less gluconeogenesis -> hypo.

Dangerous overnight when the body uses stores for energy

Question 20

What are some chronic complications of diabetes?

• Because of hyperglycaemia? [1]
• Microvascular disease? [4]
• Dyslipidaemia? [3]

Answer 20

Hyperglycaemia: Atherosclerosis and CVD events

Microvascular disease: Nephropathy, Neuropathy, Retinopathy Amputation

Dyslipidaemia: Ectopic fat deposition in muscle + liver, Exacerbation of insulin resistance

Question 21

What is difference between non-proliferative and proliferative retinopathy?

Answer 21

Both occur because of damage to BV in back of eye

Non-profilerative: ‘Cotton wool’ dilation of retina veins causes internal haem. oedema causes vision loss

Proliferative: New BV proliferate near optic disc and bleed: detachment of retina

Question 22

MoA of diabetic nephropathy?

Answer 22

PKA activation -> collagen/fibronectin proliferation -> capillary occlusion -> thickening of glomerular basement membrane. PKA activation -> increase in NADPH -> ROS

Question 23

MoA of diabetic retinopathy?

Answer 23

Hyperglycaemia -> increased PKA activity -> reduced retinal blood flow due to vasoconstriction
PKA activity -> vascular permeability angiogenesis -> macular oedema

Question 24

How can diabetes increase chance of atheromatic plaque formation through Adva?

Answer 24

Hyperglycaemia and dyslipidaemia:
* endothelial cell dysfunction
* increased adhesion of monocytes and platelets

AGE modification of oxidised low-density lipoprotein (LDL) and their receptor (LDLR)
* enhanced LDL uptake into atherosclerotic plaques
* pro-inflammatory cytokine production

Glycation of apolipoprotein, LDL or LDLR
* impaired cholesterol efflux from atherosclerotic plaques
* impaired cholesterol clearance

Question 25

For DMT1 treatment, name a short acting and long term acting insulin injection [2]

Answer 25

- Short / Fast acting: **Humalog** - Long acting: **Glargine**

Question 26

Which of the following drug treatments for diabetes utilise the followng mechanism of actions? *Inhibits liver gluconeogenesis and enhances insulin sensitivity* * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Answer 26

Which of the following drug treatments for diabetes utilise the followng mechanism of actions? *Inhibits liver gluconeogenesis and enahnaces insulin sensitivity* * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * **Metformin** * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Question 27

Which of the following drug treatments for diabetes utilise the followng mechanism of actions? * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Answer 27

Which of the following drug treatments for diabetes utilise the followng mechanism of actions? * **Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide** * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone *Bind and close K+ channel in beta cells to* *depolarise the cell and release insulin*

Question 28

Which of the following drug treatments for diabetes utilise the followng mechanism of actions? ​ *Activate PPARγ to reduce insulin insensitivity and better glucose use via gene expression changes* * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Answer 28

Which of the following drug treatments for diabetes utilise the followng mechanism of actions? ​ *Activate PPARγ to reduce insulin insensitivity and better glucose use via gene expression changes* * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors *** Thiazolidinediones e.g Pioglitazone or Rosiglitazone**

Question 29

Which of the following drug treatments for diabetes causes weight loss? * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Answer 29

Which of the following drug treatments for diabetes causes weight loss? * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * **SGLT2 Inhibitors**: excreting glucose * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Question 30

Which of the following drug treatments for diabetes causes weight gain? [2] * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Answer 30

Which of the following drug treatments for diabetes causes weight gain? [2] * **Sulfonylureas** - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * **Thiazolidinediones** e.g Pioglitazone or Rosiglitazone

Question 31

Which of the following has similar action to prandial glucose regulators? * Sulfonylureas - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Answer 31

Which of the following has similar action to prandial glucose regulators? * **Sulfonylureas** - e.g. gliclazide, glibenclamide and tolbutamide * Metformin * SGLT2 Inhibitors * Thiazolidinediones e.g Pioglitazone or Rosiglitazone

Question 32

What is the most important factor from diet in reducing CVD? [1]

Answer 32

**Total calorie intake** is most important thing in reducing CVD: particularly **saturated** **fats**

Question 33

What happens to arachidonic acid during inflammation? [1] Due to the action of which enzyme? [1]

Answer 33

**Escapes from membrane**: metabolised to potent **inflammatory mediators** by **phospholipase** **A2** (PLA2) eg. Prostaglandins (which is in turn further metabolized by cyclooxygenases (COXs) and lipoxygenases (LOXs) and cytochrome P450 (CYP) enzymes)

Question 34

How are omega-3s anti-inflammatory? [3]

Answer 34

Metabolised to **anti-inflammatory lipid mediators**: * **Resolvins** * **protectins** * **maresins**. (increasing macrophage phagocytosis of debris and countering proinflammatory molecules)

Question 35

Why are flavonoids beneficial for stroke and MI? [2]

Answer 35

* **Antioxidants** * Inhibit inflam enzymes: e.g **NADPH oxidase** (which generates ROS) Important part of Mediter. diet

Question 36

Under normal B12 and Folate levels what is homocysteine converted to? [1] Deficient B12 and Folate levels what is homocysteine converted to? [1] What pathology does this lead to? [1]

Answer 36

When the body has **Folate** and **vit B12** (necessary co factors for) * **methionine synthase enzyme**: converts homocysteine --> methionine. BUT: without Folate and B12: * **homocysteine** -> **homocysteine** **thiolactone** (damages endothelium = ATHEROSCLEROSIS

Question 37

Chronic deficiency in folate causes low **[]** and high blood **[]** levels

Answer 37

Chronic deficiency in folate causes **low methionine** and **high blood homocysteine** levels

Question 38

When chronic folate deficiency: homocysteine is converted to toxic **[]** which damages endothelium.

Answer 38

When chronic folate deficiency: homocysteine is converted to toxic **thiolactone** which damages endothelium.

Question 39

Name 4 things that can trigger endothelium inflammation [4]

Answer 39

Hyperlipidaemia &LDL smoking Hyperglycaemia & diabetes. Hypertension and angiotensin II. Oxidised LDL & atherosclerosis -> positive feedback cycle.

Question 40

What is metabolic syndrome a combination of? [4]

Answer 40

Syndrome of increased CVD risk because of: * Insulin resistance/ Type II diabetes * Abdominal obesity * Dyslipidaemia (particularly hypertriglyceridaemia) * Hypertension These factors cluster together more frequently than expected by chance !

Question 41

Which cels in the GI tract sense the luminal envrionment? [1] Describe how their structure is adapted to their role

Answer 41

**Enteroendocrine Cells**: **Apex**: Long processes into lumen + microvilli: for sampling the luminal nutrient environment. **Basal side**: stores many vesicles, containing appetite regulating hormones. close to nerve endings - hormones bind to nerve receptors to signal orexigenic or anorexigenic pathways

Question 42

Role of the following of on firing of ECC vesicles? 5HT [1] Leptin [1] Ghrelin [1]

Answer 42

5HT - **increases firing** Leptin - **decreases firing** Ghrelin - **decreases firing**

Question 43

How does VN work in appetite regulation with regards to chemoreceptors and mechanoreceptors? [2] Where does VN stimulate in the brain with ^ information? [1]

Answer 43

**Chemoreceptors**: activated by mediators released from EEC cells (nutrients / hormones / pH etc) **Mechanoreceptors**: detect stretch (gastric distention causes satiety) Goes to **NTS**

Question 44

How does leptin affect: NPY / AgRP neurones [1] POMC / CART neurones [1] Is it a short or long term acting hormone? [1]

Answer 44

How does leptin affect: NPY / AgRP neurones: **inhibits** POMC / CART neurones: **activates** Is it a short or long term acting hormone: **long term**

Question 45

PYY has what effect on satiety? [1]

Answer 45

PYY leads to enhanced satiety

Question 46

Which cells release PYY? [1] Where is PYY predominately found? [1] What effect does PYY have on NPY [1] and POMC neurones [1]

Answer 46

Which cells release PYY? [1]: **L cells in GI tract** Where is PYY predominately found: **Colon --> rectum** What effect does PYY have on NPY: **inhibits** and POMC neurones: **activates**

Question 47

GLP-1 is released in response to? [1] Effect of GLP-1 on blood glucose? [1] What is GLP-1 like in obese patients? [1]

Answer 47

GLP-1 is released in response to? [1] **Food intake** Effect of GLP-1 on blood glucose? [1] **Decreases blood glucose levels** What is GLP-1 like in obese patients? [1] **Reduced in obese patients**

Question 48

Effect of pancreatic polypeptide (PP) on appetite? [1] Effect of oxontymodulin on appetite? [1]

Answer 48

pancreatic polypeptide (PP): **anorexigenic** (decreases appetite) Oxontymodulin: **anorexigenic**: decreases ghrelin levels in plasma

Question 49

Ghrelin is [suppressed / increased] in proportion to the calories ingested

Answer 49

Ghrelin is **suppressed** in proportion to the calories ingested

Question 50

AGRP/NPY neurones in arcuate nucleus of hypothalamus are activated by which hormone? [1] What biochem effect does this have? [1]

Answer 50

AGRP/NPY neurones in arcuate nucleus of hypothalamus are activated by which hormone? [1] **Ghrelin** What biochem effect does this have? [1] **Causes a release of Y1 receptors**

Question 51

Label A-E xx

Answer 51

A: **GLP-1** B: **PYY** C: **Ghrelin** D: **Leptin** E: **Insulin**

Question 52

Role of malonyl-coA? [1] [] malonyl-coA supresses food intake [] malonyl coA increases food intake

Answer 52

Malonyl-CoA is the **substrate for fatty acid synthase**, but it is a key determinant for the **entry of fatty acids into the mitochondria,** and appears to play a pivotal signaling role in appetite regulation. **Increased** malonyl-coA supresses food intake **Decreased** malonyl coA increases food intake

Question 53

Role of Malonyl CoA? [1] The ratio of which two molecules determines if malonyl CoA works

Answer 53

Malonyl CoA is a relay in energy homeostasis Determined by AMP/ATP ratio (energy levels), and AMPK CPT1c relays the signal

Question 54

Explain how overall food intake decreases in response to increased energy levels? [1] Explain how ^ occurs [3]

Answer 54

**Increased M-CoA** - stimulates FA synthesis -->> therefore suppresses appetite **More ATP over AMP** -> increased denovo FA synthesis -> increased M-CoA -> **stimulation of POMC/CART** + **suppression NYP/AgRP** -> decreased food intake

Question 55

Effect of serotonin on appetite? Effect on POMC and AgRP neurones?

Answer 55

Serotonin (5HT): **anorexigenic**: augmentation of brain 5HT **inhibits food intake**, depletion promotes weight gain They **increase signalling** (simulate) activity in the **POMC** neurones (via the 5HT2CR) They **decrease** signalling in the **AgRP** neurones (via the 5HT1BR)

Question 56

What class of drug is metformin? [1]

Answer 56

**biguanide**

Question 57

Explain the effect of DKA on insulin levels

Answer 57

Insulin normally drives potassium into cells Without insulin, potassium is not added to and stored in cells. Serum potassium can be high or normal in diabetic ketoacidosis, as the kidneys continue to balance blood potassium with the potassium excreted in the urine, **however total body potassium is low** because no potassium is stored in the cells. When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, and this can lead to fatal arrhythmias.

Question 58

Name a risk of severe hypokalaemia? [1]

Answer 58

fatal arrhythmias.

Question 59

Label the types of diabetic retinopathy [2]

Answer 59

A: **Non-proliferative** - cotton wool spots B **proliferative**

Question 60

What type of diabetic retinopathy is depicted? [1]

Answer 60

**Nonproliferative** Funduscopic features of nonproliferative diabetic retinopathy include retinal hemorrhages and hard exudates (yellow patches)

Question 61

What type of diabetic retinopathy is depicted? [1]

Answer 61

**Proliferative** The key funduscopic feature of proliferative diabetic retinopathy is neovascularization, seen here around the optic disk.

Question 62

A 65-year-old man presents to his GP with vision loss, headaches and cold intolerance. He also mentions he has unintentionally gained 5kg in the last 3 months. On examination, he is found to have a bitemporal hemianopia and a pulse of 50 bpm. A thyroid function test is ordered. Which of the following test results is most likely to belong to this patient? TSH: Low T4: Low T3: Low TSH: high T4: low T3: low TSH: high T4: normal T3: normal TSH: low T4: high T3: high

Answer 62

A 65-year-old man presents to his GP with vision loss, headaches and cold intolerance. He also mentions he has unintentionally gained 5kg in the last 3 months. On examination, he is found to have a bitemporal hemianopia and a pulse of 50 bpm. A thyroid function test is ordered. Which of the following test results is most likely to belong to this patient? **TSH: Low T4: Low T3: Low** TSH: high T4: low T3: low TSH: high T4: normal T3: normal TSH: low T4: high T3: high This man most likely has a pituitary adenoma causing secondary hypothyroidism. In addition to thyroid function tests, he would also need an MRI of the head to confirm the presence of an adenoma. His thyroid function tests would be expected to show TSH: Low T4: Low T3: Low. In this case secretion of TSH is most likely suppressed due to compression of TSH secreting cells (thyrotrophs) by a pituitary mass.

Question 63

Which one of the following diabetes medication classes has been shown to be weight-neutral/weight-losing in patients with T2DM? SGLT-2 inhibitors Sulphonylureas Insulins Thiazolidinediones (glitazones)

Answer 63

Which one of the following diabetes medication classes has been shown to be weight-neutral/weight-losing in patients with T2DM? **SGLT-2 inhibitors** Sulphonylureas Insulins Thiazolidinediones (glitazones)

Question 64

A 49-year-old woman is investigated following an osteoporotic hip fracture. The following results are obtained: Free T4 29pmol/L (normal 9-18) TSH < 0.05 mu/L (normal 0.5-5.5) Which one of the following autoantibodies is most likely to be present? TSH receptor stimulating autoantibodies Anti-thyroid peroxidase autoantibodies Anti-nuclear antibodies Anti-thyroglobulin autoantibodies

Answer 64

A 49-year-old woman is investigated following an osteoporotic hip fracture. The following results are obtained: Free T4 29pmol/L (normal 9-18) TSH < 0.05 mu/L (normal 0.5-5.5) Which one of the following autoantibodies is most likely to be present? **TSH receptor stimulating autoantibodies** Anti-thyroid peroxidase autoantibodies Anti-nuclear antibodies Anti-thyroglobulin autoantibodies

Question 65

During a routine physical examination, a 65-year-old woman with diabetes mellitus has her balance checked. She is first asked to stand with her feet together (eyes open) and does this well. When she closes her eyes, she begins to fall and is caught by the examiner. Additional neurological findings include absent ankle jerk reflexes and absent perception of vibration at her toes bilaterally. A lesion to which of the following is the most likely cause of her balance difficulty? Peripheral nerves Vestibular system Upper motor neurons Cerebellum Basal ganglia

Answer 65

During a routine physical examination, a 65-year-old woman with diabetes mellitus has her balance checked. She is first asked to stand with her feet together (eyes open) and does this well. When she closes her eyes, she begins to fall and is caught by the examiner. Additional neurological findings include absent ankle jerk reflexes and absent perception of vibration at her toes bilaterally. A lesion to which of the following is the most likely cause of her balance difficulty? **Peripheral nerves** Vestibular system Upper motor neurons Cerebellum Basal ganglia

Question 66

Which of the following is most associated with this skin condition? Polycystic ovarian syndrome Graves' disease Small cell lung cancer Addison's disease Methotrexate use

Answer 66

Which of the following is most associated with this skin condition? **Polycystic ovarian syndrome** Graves' disease Small cell lung cancer Addison's disease Methotrexate use This is a typical appearance of acanthosis nigricans; symmetrical, dark, 'velvety' plaques which arise on the neck, axillae and groin creases in conditions associated with raised insulin, such as: Obesity Type 2 diabetes Polycystic ovarian syndrome Cushing's disease

Question 67

Which of the following are released from the stomach: A: GLP-1 B: PYY C: Ghrelin D: Leptin E: Insulin

Answer 67

Which of the following are released from the stomach: A: GLP-1 B: PYY **C: Ghrelin** D: Leptin E: Insulin

Question 68

Which of the following is the action of PYY? Inhibits excitatory appetite neurones Stimulates excitatory appetite neurones Inhibits inhibitory appetite neurones None of the above

Answer 68

Which of the following is the action of PYY? **Inhibits excitatory appetite neurones** Stimulates excitatory appetite neurones Inhibits inhibitory appetite neurones None of the above

Question 69

Which of these transmitters is stimulatory for appetite? NPY POMC a-MSH CART

Answer 69

Which of these transmitters is stimulatory for appetite? **NPY** POMC a-MSH CART

Question 70

Which structure in the hypothalamus is a key player in appetite control? Preoptic nucleus Supraoptic nucleus Arcuate nucleus Lateral nucleus

Answer 70

Which structure in the hypothalamus is a key player in appetite control? Preoptic nucleus Supraoptic nucleus **Arcuate nucleus** Lateral nucleus

Question 71

Which peptide hormone released by cells in the ileum and colon suppresses appetite? Insulin Leptin Ghrelin PYY (peptide tyrosine tyrosine)

Answer 71

Which peptide hormone released by cells in the ileum and colon suppresses appetite? Insulin Leptin Ghrelin **PYY (peptide tyrosine tyrosine)**

Question 72

Release of which of the following substances is inhibitory for appetite? Ghrelin AgRP (Agouri-related peptide) NPY (Neuropeptide Y) CART (cocaine- and amphetamine regulated transcript)

Answer 72

Release of which of the following substances is inhibitory for appetite? Ghrelin AgRP (Agouri-related peptide) NPY (Neuropeptide Y) **CART (cocaine- and amphetamine regulated transcript)**

Question 73

Alpha-MSH and Beta-endorphin may be produced from which neurotransmitter? CART (cocaine- and amphetamine regulated transcript) POMC (pro-opiomelanocortin) NPY (Neuropeptide Y) AgRP (Agouri-related peptide)

Answer 73

Alpha-MSH and Beta-endorphin may be produced from which neurotransmitter? CART (cocaine- and amphetamine regulated transcript) **POMC (pro-opiomelanocortin)** POMC can be cleaved into other neurotransmitters such as alpha-MSH and beta-endorphin. **These also act to suppress hunger**. NPY (Neuropeptide Y) AgRP (Agouri-related peptide)