Metabolism Flashcards

0
Q

List the 6 essential components of the diet and 1 non essential.

A

Carbohydrates, lipids, protein, vitamins, minerals, water, and fibre.

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1
Q

Describe the condition of diabetes mellitus.(1)

A

When blood glucose is too high, hyperglycaemia, over years and leads to damage to small and large blood vessels.

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2
Q

What is the main store of glycogen?

A

Liver,

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3
Q

Why are lipids an essential part of the diet? And what percentage of our energy intake should they be?

A

30% of our daily energy intake should be from fats.
Necessary for absorption of fat soluble vitamins A, D, E, K.
Structural components of cell membranes.

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4
Q

What part of the diet facilitates metabolic reactions?

A

Vitamins and minerals

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5
Q

Why are amino acids essential? What do they produce? List 3 compounds.

A

Used to synthesise nitrogen containing compounds.

Purines, pyridamines and haem groups.

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6
Q

How is the nitrogen balance altered in starvation and in pregnancy?

A

Normal: N2 intake = N2 loss
Starvation/ muscle wastage: n2< n2 loss
Pregnancy/growth: n2>n2 loss

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7
Q

Why is the nitrogen balance effected by pregnancy or growth?

A

Nitrogen released in the continuous breakdown of tissue protein. These are mostly reused. Excess is secreted in urea.
During growth there is more n2 than loss though.

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8
Q

Name the disorder caused by a low protein, high carbohydrate diet.
That causes symptoms of odema, anaemia, distended abdomen, lethargy and anorexia.
Affects hair and skin.

A

Kwashiorkor.

E.g. A young child displaced from breast feeding and going on to a diet of cassava and carbohydrate.

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9
Q

What condition can occur when a child is nutrient deficient and in particular, low in protein? Leads to no odema?

A

Marasmus

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10
Q

Describe an exergonic chemical reaction

A

When energy input is greater than the energy released

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11
Q

What is the equation for calculating BMI?

A

= weight (kg) /

Height2 (m)

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12
Q

Is energy from fuel released by oxidation or reduction?

A

Oxidation.

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13
Q

There are three components to our daily energy expenditure

A

Basal metabolic rate: energy to required to maintain life. The functioning of the body and physical digestive and emotional rest.
Energy for voluntary physical activities
Energy require to process the food we eat. Diet induced thermogenesis.

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14
Q

How do we estimate BMR? And what are the major tissues contributing to it (4).

A
Body weight(kg) x 100.
If not obese
Skeletal muscle, 30%
CNS
Liver
Heart
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15
Q

How would you calculate a rough estimate of the total daily energy required for a person who does 2 hrs excercise a day?

A

BMR + 60/70%

+30 sedentary
+100 several hours a day

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16
Q

How much energy is required to process food?

A

10%

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17
Q

BMI values. State ranges.

Normal is 18.5-24.9

A
Underweight is below 18.5
Overweight is 25-29.9
Obese 30-34.5
Severely obese 35+
Waist to hip more accurate
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18
Q

Define homeostasis and state it’s importance

A

The internal environment of the body. It must remain stable.
It counteracts changes in the internal environment.
Failure - disease

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19
Q

Define cell metabolism and state it’s importance

A

The physical and chemical processes occurring within a living cell necessary for maintenence of life.
derive energy and raw materials from food stuffs and use them in the tissues of the body.
Support the growth, constant repair, and activity of tissues.

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20
Q

Describe anabolic and catabolic metabolism

A

Catabolism is the break down of molecules to release energy. It provides reducing power as it is an oxidation reaction.
Anabolism. Uses reducing power and raw materials to make molecules for growth and maintenance. Uses energy, mostly hydrolysis of ATP

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21
Q

Name 4 catabolic pathways.

A

Glycolysis, lipolysis, fatty acid oxidation, glycosylation, fa syntheis,

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22
Q

Give 4 examples of pathways and reactions that build up molecules.

A

Gluconeogenesis, pentose phosphate pathway, e acceptors other than oxygen

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23
Q

Why do cells need a continuous supply of energy?

A

The supply the cells and ensure that they undergo their normal reactions. Without energy many cells cannot function.

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24
How to we generate heat metabolically?
By using coupling reactions to convert the energy released in exergonic reactions to heat production
25
Where do we get cell nutrients from?
They circulate in the blood from the diet, synthesis in body tissues from precursors and released from storage in body tissues. Some is lost as waste in the faeces or via the kidney and lungs
26
How do we utilise cell nutrients?
Degradation to release energy, all tissues Synthesis of cell components, all tissues Storage, liver, adipose tissue, skeletal Inter conversion to other nutrients, liver, adipose, kidney cortex Excretion, liver, kidney, lungs
27
Why do we metabolise nutrients?
Energy as atp for cell function Building block molecules Organic precursor molecules, e.g. Acetlyl coa Bio synthetic reducing power e.g. NADPH
28
What type of metabolic reaction is oxidative, releases large amounts of free energy (incl some ATP) and produce intermediary metabolites?
Catabolism
29
Does the total concentration of carrier molecules in cells remain constant? And why, why not?
Yes, they cycle between oxidised and reduced forms, so cell function is maintained.
30
Describe what happens in a reduction reaction?
Remove O2 | Or add e or H atoms (h+ e-)
31
Give 2 examples of oxidation reactions
Pyruvate oxidation to acetyl coa | Using NAD reduction to NADH and pyruvate dehydrogenase
32
What kind of reaction occurs spontaneously? Which drives energy requiring reactions?
Exergonic | Negative enthalpy change (^H is -ve)
33
Hydrolysis bond are high or low energy
High
34
Define free energy change (^G)
The energy released in an exergonic reaction that is available to do work
35
How is ATP used and how does it relate to free energy
It's a high energy molecule It can't store energy very long Therfore must be rapidly resynthesised from ADP from free energy from catabolism Therefore ATP turnover is very high.
36
What does a high energy signal signal. And give 4 examples
That there is enough energy to meet the cells immediate needs NADH, NADPH, FAD2H, reduced in anabolic reactions LOW ENERGY: NAD+, NADP+, FAD, oxidised in catabolic reactions
37
Explain the role of creatine phosphate in muscle cells
Creatine phosphate acts as a immediate store of free energy in the muscle cells. Very important in the first few seconds of vigorous excercise.
38
How is creatine phosphate syntheised?
Creatine and ATP to creatine phosphate and ADP. Using creatine kinase REVERSIBLE
39
How is creatine used as an indicator of muscle mass?
It is measured in the urine as creatine is a waste product. The rate of production of creatinine is proportional to the concentration of creatine in muscle and therfore related to skeletal muscle mass
40
How can we measure kidney function
Kidneys normally effective at removing creatinine from the blood. High blood creatinine and low urine creatine conc indicates reduced kidney function
41
What is the main function of the parathyroid glands?
To secret parathyroid hormone which is essential in maintaining serum calcium levels
42
Where are the parathyroid glands located?
In the neck, normally on the posterior surface of the thyroid gland. But may be located elsewhere. Normally 4
43
Five main polypeptide hormones released from endocrine pancreas and what cells
``` Insulin, B cells Glucagon alpha cells Somatostatin delta cells (regulates islet cell secretions) Pancreatic polypeptide Ghrelin ```
44
What is the function of the exocrine pancreas
Release digestive enzymes through duodenum
45
How does the ultra structure of a B cell relate to synthesis and storage of Insukin
``` Mitochondria RER Golgi Storage vesicles To make new proteins and provide energy for protein synthesis, secretion of the hormones. ```
46
Describe how insulin is synthesised
1) insulin mRNA translated on RER and forms pre pro insulin 2) transported to ER and sorted and modified to pro insulin (A,C,B) 3) to Golgi: C peptide cleaved off. And 2 disulphide bonds connect the A & B peptides. 4) packaged into storage granules 5) released by exocytosis into the blood stream
47
Describe the structure of insulin
Big polypeptide 2 polypeptide chains , aloha and beta chains ith insulin rceptors on cell surfaces Linked by 2 disulphide bonds to connect the cysteine residues 3rd disulphide bond in the aloha chain Short half life
48
How is insulin secretion controlled?
By its metabolites, glucose, amino acids, and fatty acids Gastrim secretion from the GI tract Neurotransmitters adrenaline and noradrenalin and acetyl choline inhibits insulin secretion
49
How does insulin resistance occur?
B cells try to compensate by increasing insulin production Eventually unable to maintain and respond effectively which leads to impaired tolerance Finally B cell dysfunction causes relative insulin deficiency leading to type 2 diabetes
50
How is cortisol released
Controlled by acth ACTH release controlled by corticotrophin releasing factor Controlled by hypothalamus in response to stress Negative feedback on pituary and hypothalamus from glucocorticoids Transported In blood by CBG corticosteroid binding globulin
51
Where is the pituary gland located and what is it connected to?
Base of brain suspended from hypothalamus | Connected to anterior pituary
52
Where are the adrenal glands located? | Brief description
Pair of multifunctional endocrine glands Cap upper poles of kidneys 2 regions, adrenal cortex and the medulla
53
Describe the adrenal cortex and what it secretesw
Capsule Zona glomerulosa: secretes mineralocorticoids. E.g. Aldosterone, regulates Ions e.g. Na and k levels Zona fasiculata, secretes glucocorticoids, e.g. Cortisol and costicosterone. Regulates carbohydrate metabolism increases serum sugars Zona reticularis: adrenal androgens, adrenaline noradrenaline dopamine,
54
Describe ACTH
39aa polypeptide POMP is its precursor and also produces B endorphins and alpha msh (melanocytes) Means that higher levels of acth increases above (darker skin) Short half life so released in pulses Can interact with other zones receptors
55
What does ACTH bind to to stimulate cortisol release
Uses cAMP as a messenger | Receptor used is MC2
56
How does cortisol interact with target cells?
``` Cross membrane as a steroid, Bind to cytoplasmic receptors Bonds to dna in the nucleus Changes transcription rate STARVED STATE Causes an increase in gluconeogenesis, lipolysis and proteolysis ```
57
Describe to role of the hypothalamus in control of pituitary function
``` Releases inhibiting or releasing hormones Travel via hypophyseal portal vessels TRH CRH SRH somatostatin ```
58
Name the TROPHIC hormones that are released from pituitary gland and what they effect. Also what stimulates their release
Thyrotrophin releasing hormone (TRH) stimualtes TSH release affects thyroid gland Corticotrophin releasing hormone (CRh) Stimulates ACTH release which affects adrenal gland (cortisol) Somatostatin releasing hormone (SRH). Stimulates GH release (somatotropin) affects liver production of somatomedins Somatostatin inhibits LH (ovary and testis hormone production) FSH (affects ovary and testis function)
59
How would you test for cushings disease/syndrome?
Dexamethasone test. Suppresses secretion of ACTH Therfore can identify if the high cortisol levels are caused by An excess secretion of ACTH in pituitary gland, (disease) An ectopic ACTH secretion caused by a tumour (syndrome)
60
How would you identify and test for addinsons disease
Low glucocorticoids, e.g, cortisol Tired, weak and dehydrated. Fluid loss due to Na imbalances. Pigmentation Low blood pressure Hypoglycaemic Test using synacthin. Similar to acth Supposed to increase cortisol levels by acting on cortisol receptors
61
Describe the three hormones secreted from the thyroid gland and from which cells
Thyroxine (T3) from follicular cells. The active form Tri iodthyronine (T4) also produced in the follicular fells and is the stable form. Much more released Calcitonin produced in parafollicular cells and is involved in calcium metabolism
62
How are t3 and T4 synthesised and released into the blood stream (7 steps)
1) thyroglobulin synthesised in the follicular cells and stored in the colloid in the lumen of the follicular cell 2) Iodine and sodium imported into cells 3) iodine transported into the lumen 4) oxidisation of iodide 5) attach to tyrosine rings on the thyroglobulin. Either 1 (MIT) or 2 (DIT) iodines attach to each ring. 6) coupling of DIT and MIT to form t3 and T4 in ratio 1:10. Still attached to the thyroglobulin 7) whole molecule transported back into the follicular cell where the thyroglobulin is removed 8) t3&4 then transported out of the cell into the capillaries
63
How is thyroid activity controlled
Hypothalamus releases TRH, by stress/cold/ Travels down the hypothalamic pituitary portal system in blood Anterior pituitary in Thyrotrophs release TSH stims follicular cells to release t3&4
64
Effects of thyroid hormones on the body
Increase metabolic rate of tissues, slowly, increase O2 uptake Increases BMR, heat production (increased UCP) Increased mobilisation of fatty acids, proteins etc Affects growth and development Increased heart muscle, Increases nerve cell function, (absence leads to cretinism) (Stimulates production of nt and hormone receptors (tachycardia) FSH and lh
65
How does t3 affect target cells
Within target cells affecting nucleus as binds to protein receptors Increases rate of transcription of specific genes which makes specific proteins Increases cell activity so increased energy use Needs to be active 3. Therfore remove 5' iodine from t4
66
What are the roles of calcium in the body
Nerve conduction Muscle contraction Hormone secretion Messengers inside cell
67
How is calcium tied with phosphate
Form hydroxyapatite crystals to be used in bone | Regulated by PTH and calcitrol
68
How is serum calcium levels regulated.
Parathyroid hormone. Decreases urinary loss, increases release and reabsorbtion from bone, increases calcium abosobtion in small intestine Vitamin d. Activated to calcitrol in kidney. Increases ca uptake from gut Calcitonin (lowers)in animals.
69
How is PTHrP produced and what problems can it cause?
Produced by tumours Leads to hypercalcaemia Because increases release of calcium from bone, reduces excretion and reduces reabsorbtion
70
Kidney damage, (stones) constipation, dehydration, tired, depressed, abdominal pain (moans and groans) renal calucci. Indicated what disorder?
Chronic hypocalcaemia Caused by low calcium levels In children rickets can occur as bones are broken down Also more calcium is abosobed in kidney and more take. From the gut by calcitrol Thin sry hair and skin Hoarse voice
71
Give signs and symptoms of hypercalcaemia
``` Hyper excitability of nervous muscular junctions Pins and needles Find it hard to sit still Muscle spasms (tetany) Paralysis Weight loss ```
72
Describe the metabolic changes in pregnancy
First 20 weeks, increased nutrient stores, increase insulin ratio Then metabolism adapts to increased demands from foetus Release fatty acids from maternal stores Reduced disposal of nutrients after meals
73
In pregnancy what can altered metabolism lead to
Gestational diabetes. Due to needing more insulin to promote storage of nutrients Increased rate of insulin synthesis, B cell hypertrophy and hyperplasia Can't release enough insulin leads to gestational diabetes as pancreas can't cope
74
Explain how glycogen and tag stores differ and their limits
Glycogen Quick release of glucose in muscles, lots of branching. Glycogen phosphorylase Liver stores used to replenish blood glucos Not affected by blood supply unlike plasma glucose Tags: lipolysis is slow and limited by albumin availability to transport Therfore fatty acid uptake is slow to muscle cells and mitochondria More oxygen and atp is needed than in glycogen metabolism
75
Describe the metabolic response to sprinting and anaerobic respiration
Controlled by noradrenaline (nervous system) and adrenaline (endocrine) Creatine phosphate converted to creatine and ATP Muscle glycogen to glucose 6 phosphate G 6 P metabolised in glycolysis to ATP Anaerobic glycolysis Lactate and H ion build up Fatigue
76
Describe energy utilisation during marathon or aerobic exercise
Hormonal control (low insulin and high adrenaline GH glucagon and cortisol) and some noradrenaline Muscle glycogen stores used for 60 mins Use blood glucose. Remain constant due to gluconeogenesis and liver glycogen Fatty acid oxidation
77
What is the first line of defence against super oxide radicals
Superoxide dismutase, transfers it to hydrogen peroxide and then catalase oxidises it to water and oxygen :) If not enough then radicals oxidise proteins, lipid and dna - damage as highly reactive
78
How are ROS formed
In mitochondria | By protein carriers prematurely reducing oxygen to O2- ions
79
Name two other radicals? How formed? How eliminateD?
Hydroxyl radicals, 'OH - x Rays, gamma rays, uv light - damage cell membranes, alter haemolysis in RBC, damage dna, can't be eliminated by an enzyme system NO' From arginine to NO' Oxidised to form ONOO- peroxynitrate :( inflammation Oxidising agents e,g antimalarials
80
How do we eliminate ROS
Cellular defence NADPH (from pentose phosphate pathway). Reducing agent Glutathione (GSH) antioxidant and acts as a reducing agent: front line defence as abundant Antioxidants C E A Flavenoids, coloured fruit and veg Minerals: selenium and zinc
81
What can oxidative stress lead to? Which three areas are damaged? What diseases can it cause? How does stress occur?
Damage dna, lipids in cell membrane (plaque formation), proteins Occurs if too many ROS or antioxidant levels too low Leads to: atherosclerosis, Parkinson's, Alzheimer's, inflammatory reaction
82
Describe oxidative burst
When a neutrophils or monocytes produces a massive restlessness of ROS - destroys cell and the bacteria or fungus Produced by NADPH oxidase
83
List the main lipid classes
``` Cholesterol Cholesterol esters Phospholipids Tags Fatty acids ```
84
Describe cholesterol and its uses
Found in membranes Precursor to bile salts, steroid hormones, Syntheised in the liver and also from the diet
85
How are lipids transported
In carrier proteins Fatty acids in albumin (limited) Others in lipoprotein particles Outside membrane, cholesterol, phospholipids, apoproteins Insoluble inside: tags, cholesterol esters,
86
Describe chylomicrons. Where synthesised, what do they transport, how do they release their load and when should you expect to see them in the blood?
Low density Transport dietary tags from the intestines to tissues They are syntheised in enterocytes lining the intestine They release the tags at the capillary endothelial cells. Lipase breaks them down (cleaves) releasing tags Glycerol released into circulation for glycolysis Fatty acids used for b oxidation Appear 4-6 hrs after meal
87
Describe VLDL | Where synthesised, what do they transport, how do they release their load.
Carry tags synthesised in the liver to adipose tissue for storage VLDL syntheised in the liver Capillary endothelium binds the VLDL, cleaves the VLDL releasing TAGs Broken down to fatty acids and glycerol Some VLDL remnants used in HDL formation
88
Describe LDL | Where synthesised, what do they transport, how do they release their load.
``` Syntheised in liver Transport liver cholesterol to tissues. Apo B100 used to transport High lol high risk of atherosclerosis Cells have LDL receptors. Bind lol, and release by endocytosis Cholesterol ester released and cleaved to cholesterol and fatty acids Controlled by cholesterol concentration in the cell ```
89
Describe HDL | Where synthesised, what do they transport, how do they release their load.
Syntheised in tissues Transports excess cholesterol to the liver for disposal as bile salts :) Cholesterol delivered via the capillaries to the HDL particles
90
Describe Hyperlipoproteinaemia
Raised levels of lipoprotein Most types leads to increased risk of coronary artery diseases Caused by over production or under removal, due to defective enzymes (lipase), receptors, or apoproteins Genetic or caused by lifestyle and diet
91
Describe the pharmokinetics of a drug. What the body does to the drug, and their metabolites in the body
Absorption Distribution Metabolism Elimination
92
Why can't we just excrete drugs
Most are lipid soluble so get reabsorbed in kidney tubule | Therfore alter them so that they are soluble in water
93
What is a prodrug and give an example
A drug that is activated by the body E.g, codeine to morphine Normally drugs are deactivated by metabolism in the body
94
Describe the drug metabolism pathways
Phase 1: expose reactive groups so it can be eliminated rapid,y , some skip this step. Occurs in liver microsomes, GI tract, kidney for e.g Uses an enzyme system: cytochrome p450 and NADPH as a cofactor Phase 2: conjugation in the liver using cytosolic enzymes. The altered drug combines with water soluble group e.g. Glucuronic acid
95
How can environmental factors affect enzyme inhibition and induction
Grapefruit and cranberry juice and cimetidine can inhibit metabolism of other drugs- poly therapy problems Enzyme induction: metabolism of one agent induces enzymes in liver. And increases metabolism of other drugs. E.g. Alcohol
96
Describe the metabolic response to alcohol.
Alcohol oxidised to acetyl aldehyde in liver using NAD+ to NADH and acetyl dehydrogenase Further oxidised to acetate (can form acetic acid) in liver using aldehyde dehydrogenase and producing NADH. Then to acetyl coa to generate energy.
97
How can we treat alcoholism
Disulfiram: inhibits aldehyde dehydrogenase Causes build up of acetyl aldehyde Causes a very bad hangover. Controlled conditions
98
Describe metabolism of paracetamol
Metabolised by phase 2 conjugation Normal dose: phase 2, glucuronidation (add glucuronide sulphate) or sulphation Toxic dose: saturate pathway so use alternative pathway Phase 1: NAPQI toxic metabolite Phase 2: conjugation with glutathione (used in antioxidants, depleted=liver failure from ROS damage) Treatment: rapidly with n-acetyl cysteine antioxidant
99
Describe the metabolic effects of alcohol abuse. Direct and indirect
Leads to build up of NADH which means that there is not enough NAD for glycolysis . Excess NADH used for: -pyruvate to lactate shift - lipid synthesis: glycerol or fatty acids - electron transport chain: therfore inhibiting normal oxidation of fats in B oxidation or the citric acid cycle therfore they build up and can produce ketone bodies. Excess fats also secreted into the blood stream: atherosclerosis Build up of acetyl aldehyde can lead to cirrhosis and hepatitis: liver damage. Damages cells in GI tract- loss of appetite, diahorrea, low folic acid (anaemia) Non direct: poor diet, vitamin and mineral deficient, low carb and protein intake
100
What is the function of glucagon?
Opposes insulin Promotes increased glucose levels in blood Increases proteolysis, gluconeogenesis from amino acids, glycogen lysis, ketogenesis, Controlled by adrenaline and noradrenaline
101
How do steroid, thyroid and lipid hormones affect target cells?
Cross cell membranes To nucleus, bind to dna and stimulate or inhibit protein synthesis Produce mRNA
102
How do peptide, amine and water soluble hormones affect target cells
Can't cross cell membranes so bind to receptor Activate a messenger pathway Exerts a metabolic response
103
Describe the control of appetite
Appetite centre: arcuate nucleus of the hypothalamus Primary neurones sense metabolites in the blood( FA and glucose) and respond Excitory pathway- stimulate appetite Inhibitory pathway - reward system or suppress appetite
104
Describe the excitory pathway in appetite control
Neurotransmitter control: release neuro peptide Y Agouti related peptide (AgRP) Stimulates appetite
105
Describe the inhibitory pathways in appetite control
POMC cleaved Produces B endorphins: reward system activates And alpha melanocytes stimulating hormone: suppress appetite
106
Describe ghrelin and its effect
Feedback from gut to hypothalamus when stomach empty Stimulates primary neurones to release neurotransmitters Stimulates excitory pathway: stimulate apetite
107
Describe the hormones that stimulate the apetite inhibitory pathway
Leptin: released from adipocytes. If deficient then severe overeating. Induces uncoupling in mitochondria- heat produced instead of atp Insulin: suppress Amylin: form B cells in pancreas, inhibits the excitory response.