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75 Cards in this Set
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- 3rd side (hint)
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What does insulin promote in the liver? |
1. GLUT2 to cell surface 2. glycogen synthesis via glucokinase expression and glycogen synthase activity 3. glycolysis and oxidation via pyruvate dehydrogenase and phosphofructokinase activity 4. lipid storage 5. protein synthesis |
5 main points |
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What does insulin inhibit in the liver and how? |
Insulin prevents gluconeogenesis via enzymes 1. PEPCK 2. glucose-6-phosphase (G-6-P) 3. fructose-1,6-bisphosphatase (FBPase) |
3 enzymes |
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What does insulin promote in the muscle? |
1. GLUT4 to cell surface 2. glycogen synthesis via hexokinase expression and glycogen synthase activity 3. glycolysis and oxidation via pyruvate dehydrogenase and phosphofructokinase activity 4. protein synthesis |
4 main points |
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What does insulin promote in adipocytes? |
1. GLUT4 to cell surface 2. glycogen synthesis via hexokinase expression and glycogen synthase activity 3. glycolysis to give precursors for acetyl CoA and glycerol phosphate 4. fatty acid uptake |
4 main points |
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What does insulin inhibit in adipocytes? |
Insulin inhibits the synthesis of 1. lipoprotein lipase (LPL) 2. hormone-sensitive triglyceride lipase |
2 main points |
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Summarise insulin actions on carbs |
1. GLUT4 uptake by skeletal muscle and adiopose tissue 2. stimulates glycogenolysis in liver and sk. muscle (glycogen formation) 3. inhibits glycogenolysis in liver (glycogen breakdown) 4. inhibits gluconeogenesis in liver (glucose output) |
4 main points |
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Summarise insulin action on fats |
1. GLUT4 uptake by adipocytes 2. activates glycerol phosphate, acetyl CoA, pyruvate, and FAs 3. promotes FA entry into blood 4. inhibits lipolysis |
4 main points |
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Summarise insulin action on proteins |
1. Promotes aa transport to muscle and other cells (not liver) 2. increases incorporation of aa's into protein 3. inhibits protein degradation |
3 main points |
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How is insulin synthesised by beta cells? |
1. DNA becomes linear preproinsulin, gets folded in ER 2. preproproinsulin removes signal peptide becomes proinsulin 3. C-peptide is cleaved off, becomes insulin and stored in secretary granule |
3 main points |
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Glucagon receptors are expressed on what kind of tissues? |
Adipocytes and liver |
2 different kinds, one is an organ |
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Glucagon-like peptide (GLP) controls what? Where is this receptor located, and what kind of receptor is it? |
Appetite, predominately in hepatocytes, G-protein coupled receptor (GPCR) |
More general term than hunger |
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Summarise the actions of glucagon on carbs |
1. Inhibits glycogen synthesis 2. Promotes glycogenolysis 3. Stimulates gluconeogenesis |
3 main points |
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Summarise glucagon action on fats |
1. Promotes lipolysis 2. Inhibits triglyceride synthesis 3. Enhances ketogenesis |
3 main points, one comes under starvation response |
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Summarise glucagon action on proteins |
1. Inhibits hepatic protein synthesis 2. Promotes degradation of hepatic proteins 3. Stimulates gluconeogenesis 4. No significant effect on blood aa levels |
4 main points, 2 to do with the liver, one to do with aa's |
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What does glucagon promote in the liver? |
1. glycogen breakdown via glycogen phosphorylase and P6Pase 2. gluconeogenesis ia activation of PEPCK and FBPase 3. lipid oxidation |
3 main points, inclusive of activated enzymes |
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The stimulation of:1. high blood aa and FA levels2. ANS - parasympathetic vagal stimulates insulin secretion3. glucagon4. GI hormones: gastrin, secretin, gastric inhibitory peptide,
controls what action? |
Insulin secretion |
4 main points |
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The stimulation of 1. paracrine influences from beta cells 2. high blood aa and low FA levels (UNUSUAL) 3. sympathetic NS adrenaline beta-adrenoceptor 4. infection and exercise 5. cortisol, controls what action? |
Glucagon secretion |
5 main points |
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Glucagon secretion controls hypoglycaemia, which inhibits |
Somatostatin |
Found in pancreatic gamma cells |
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Polyuria, polyphagia, and polydipsia, are referred to as what? |
Increased urine, appetite, and thirst, respectively, in diabetes mellitus patients. |
T2DM symptoms |
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Define: 1. glycolysis 2. glycogen 3. glycogenolysis 4. glucagon 5. gluconeogenesis 6. glycogenesis 7. glucose |
1. converts glucose to pyruvate by splitting glucose molecules 2. storage molecule of glucose 3. breaking down of glycogen 4. hormones released from alpha cells to keep body in 'fed state' between meals 5. production of new glucose 6. glycogen formation 7. sugar molecule |
lysis = breaking down of x molecule |
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What are the irreversible steps in glycolysis? |
1. hexokinase (muscle/adipocytes) or glucokinase (liver) 2. phosphofructokinase (PFK) 3. pyruvate kinase (PK) |
3 steps |
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Name the key enzymes involved in 1. glycolysis which insulin stimulate, and 2. inhibit in gluconeogenesis |
1i. phosphofructokinase 1ii. pyruvate kinase 2i. PEPCK 2ii. G6P 2iii. FBPase |
INSULIN STIMULATING GLYCOLYSIS AND INHIBITING GLUCONEOGENESIS - 2 enzymes, then 3 enzymes |
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Name the key enzymes involved in 1. glycolysis which glucagon inhibit, and 2. stimulate in gluconeogenesis |
1i. phosphofructokinase 1ii.pyruvate kinase 2i.PEPCK 2ii.G6P 2iii. FBPase |
GLUCAGON INHITIBING GLYCOLYSIS AND STIMULATING GLUCONEOGENESIS - 3 enzymes, then 2 enzymes |
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How are fatty acids synthesised in TCAC? |
pyruvate -> acetyl CoA -> citrate -> malonyl CoA -> condensation, reductions and dehydration -> palmitate |
6 steps, starting with pyruvate and ending with palmitate |
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Name the steps for glycogenolysis in the liver |
glucagon in beta AR -> Gs activates adenylate cyclase, cAMP, PKA -> PKA phosphorylates PK -> PK phosphorylates glycogen phosphorylase (GP) -> active GP (GPa) catalyses breakdown of G1P -> G1P converted to G6P -> glucose released into blood |
7 steps: first being glucagon sitting in beta adrenoceptorors, and the last step is glucose being released into blood stream |
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Name the steps for glycogenolysis in muscles |
PKA -> PK, releases Ca2+ -> GP, AMP released -> glycogen -> G1P -> G6P |
5 steps, starting with PKA, ending with G6P |
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How are ketone bodies formed, and what are the 3 ketones, where are they produced, and how are they used? |
Ketone bodies are formed as a byproduct of Acetyl CoA and fatty acids. The 3 ketones are acetone, beta-hydroyxybutarate, and aacetoacetate. They are produced in the liver, and used in fat metabolism during starvation responses |
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What are symptoms of ketosis? |
fruity smell to breath (due to acetone), and metabolic acidosis (ketoacidosis) |
First one is blown off during respiration and is highly volatile, the second one is due to too much acid in the body |
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Why does ketosis occur? |
Too much Acetyl CoA is formed and is more than the citric acid cycle can handle as oxaloacetate is a limiting (used in gluconeogenesis) |
excess beta oxidation of acyl CoA yields ...? |
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Colloid is an extracellular storage site of what? |
Thyroid hormone |
Starts with a 'T' |
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C cells produce calcitonin, which is used to regulate what? |
Calcium metabolism, but it does not influence TH production |
Starts with a 'C' |
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x is the main constituent of colloid |
thyroglobulin, TH exist on the colloid as part of the protein |
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What is the active form of thyroid hormone, and how many forms of it are there? |
T3 is the active form, but there is T3, T4 (predominant form in plasma), and reverse T3 (inactive) |
3 forms |
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Name the hormones and their cell types released from the anterior pituitary gland |
1. thyroid hormone and thyrotrophs 2. growth hormone and somatotrophs 3. prolactin and lactotrophs 4. leutinising hormone+ follicular stimulating hormone and gonadotrophs 5. acetocortictrophic hormone and corticotrophs |
5 different cell types |
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The HTP axis includes which 3 organs, and what hormones? |
hypothalamus, anterior pituitary gland, and thyroid. Thyrotropin releasing hormone (TRH), thyroid stimulating hormone (TSH), and thyroid hormones (T3 and T4) |
3 organs, 3 different hormones, all related to thyroid |
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3-monoiodotyrosine (MIT), and 3,5-diiodotyrosine bind through condensation reactions. The product of x MITs and y DITs will give which TH? |
For T4, 2 DITs For T3, 1 MIT + 1 DIT For reverse T3, 1 DIT + 1 MIT |
Order of DIT and MIT will determine whether rT3 or T3 will be formed |
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What is the difference between thyroid hormone synthesis, and thyroid hormone secretion? |
Synthesis is how it is made, secretion is how it is released |
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What is a major characteristic of secreted TH? Where does majority of T3 come from? |
It is lipophilic, T4 can readily become iodinated in cells to become T3 (mainly in the liver). T3 then can diffuse out of cell back into circulation or can act in the cell |
Think characteristics of lipids |
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The HPA axis is controlled by what kind of feedback loop? |
Negative |
Positive or negative |
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Why does fasting switch off the HPA (hypothalamus-pituitary-adrenal) axis? |
The body doesn't want a high metabolic rate as it uses too much TH, hence turning off HPA axis switches to a lower oxidative metabolism |
Think of what the body does to reserve energy |
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Define Hashimoto's and Grave's disease |
Hashimoto's disease is due to hypothyroidism, Grave's disease is due to hyperthyroidism |
Opposites of each other |
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What are some of the causes of Hashimoto's disease? |
1. failure of thyroid to produce TH -> immune system attacks the gland and destroys follicular cells, therefore no thyroglobulin production 2. hypothalamus not producing TRH and pit. gland not releasing TSH |
2 major causes |
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What are symptoms of hypothyroidism? |
1. reduced metabolic rate 2. poor resistance to cold 3. excessive weight gain (not enough oxidative metabolism) 4. easily fatigued 5. slow weak pulse 6. slow mentation and reflexes (lethargic) |
6 major symptoms |
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What are long term effects of hypothyroidism? |
1. Myxoedema, get infiltration of interstitial space with excessive mucopolysaccharides, results in swelling of extremeties and gives 'tragic facial expression' 2. Cretinism, due to lack of TH, individual cannot reach full GH potential as GH relies on other hormones. Low TH stunts GH. Can be fixed early in life, get mental retardation as it prevents synapses and neurons from being myelinated, effects HPG axis |
2 major long term effects, one including GH |
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What are treatments for hypothyroidism? |
1.thyroxine therapy (hormone replacement) 2. iodine administration (easier than thyroxine to treat as it only needs to be consumed in diet) |
2 major treatments |
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What are the causes of Grave's disease? |
1. Autoimmune 2. Secondary to excess TRH and TSH 3. hypersecreting thyroid tumour in follicular cells, can sometimes give goitre (sometimes not, may not cause hyperplasia of follicular cells) |
3 major causes |
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What are the symptoms of hyperthyroidism? |
1. elevated basal metabolic rate 2. excessive sweating and heat intolerance 3. weight loss despite increased appetite 4. muscle weakening (tremors) 5. excessively alert, irritable, anxious, emotional 6. heart palpitations 7. exopthalmos (bulging eyes due to contractions of receptors on orbital muscles, which contain TH receptors) |
7 major symptoms |
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How does hyperthyroidism lead to tremors and muscle weakness? |
1. catabolic state leads to atrophy 2. defect in contractile mechanisms within muscles due to change in muscle fibres 3. uncoupling of oxidative phosphorylation leads to inefficient ATP |
3 different ways |
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What are treatments for hyperthyroidism? |
1. surgical removal of part of the gland 2. administration of radioactive iodine 131, kills follicular cells 3. large dose of potassium iodine (suppresses iodine production?) 4. anti-thyroid drugs (stops iodine binding to thyroxine in follicular cells) |
4 different methods |
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Name the 3 zones in the adrenal cortex |
Zona glomerulosa, Zona fasiculata, Zona reticularis |
Zona ...? |
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Name the 6 major sex steroids |
Progesterone, pregnenalone, androgens, oestradiol, testosterone, oestrogen |
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What are the 3 kinds of adrenal steroids secreted? |
1. aldosterone (mineralocorticoids) 2. cortisol + corticosterone (glucocorticoids) 3. DHEA and androstenedione (androgens) |
A...C...D |
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HPA axis refers to what part of the adrenal gland, and is regulated around what? |
Adrenal cortex, cortisol |
Outer part of adrenal glands |
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What are the actions of glucocortocoids? |
1. fuel metabolism 2. permissive effects 3. water metabolism 4. resistance adaptation to stress 5. nervous system 6. reduce response to inflammatory stimuli and immunosuppression |
6 actions |
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Define Addison's disease |
Chronic failure of adrenal cortex |
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What are the symptoms of Addison's disease? |
Loss of glucocorticoids, loss of aldosterone, (CV failure due to lack of water balance) |
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Define Cushing's syndrome |
Excess glucocorticoid production |
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What causes Cushing's syndrome? |
1. ACTH secreting pit. gland tumour (not very common) 2. adrenal tumour (more common) 3. over medication with anti-inflammatory steroids eg prednisolone) 4. adrenalectomy 5. no ACTH 6. autoimmune |
6 major causes |
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What are the symptoms of Cushing's syndrome? |
1. protein depletion
2. poor healing, immune deficiency 3. thin hair and skin 4. body fat redistribution = obesity 5. insulin resistant diabetes (prone to T2D as hormone chronically elevating BGL) |
5 major symptoms |
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What organ becomes a secondary site for gluconeogenesis in a starvation response? |
Kidneys |
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What hormones get completely switched off during a starvation response? |
Insulin and thyroxine |
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What processes happen during overnight fasting? |
Increased glycogenolysis, gluconeogenesis, and lipolysis |
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During a starvation response, the body switches from x mechanism to y |
Enhanced gluconeogenesis of protein stores to ketogenesis from fat |
Sugar to fat |
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What happens in a prolonged starvation response? |
1. Decreased gluconeogenesis in the liver 2. enhanced gluconeogenesis in kidney 3. increased ketogenesis in liver |
3 main responses, 2 in the liver and one in the kidney |
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In gluconeogenesis in the kidney, how does it create glucose? |
It uses glutamine as a subtrate to go to pyruvate -> glucose -> increased glucose output from kidneys |
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Hunger and satiety are triggered by which hormones? |
Ghrelin and leptin, respectively |
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What is leptin produced by? |
Adiopcytes, it is also proportional to the total body adipose tissue |
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Anorexigenic best describes what? |
Leptin, loss of appetite |
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Orexigenic best describes what? |
Ghrelin, stimulates appetite |
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What are the anorexigenic neurones, and what do they do? |
POMC and CART, are stimulated by leptin, and inhibit food intake |
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What are the orexogenic neurones, and what do they do? |
NPY and AGRP, are inhibited by leptin, and stimulate food intake |
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Satiety signals: |
1. vagal afferents (neural) 2. CCK 3. peptide YY 4. GLP-1 |
Anorexigenic |
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Fasting signals: |
1. hypoglycaemia 2. ghrelin |
Orexigenic |
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GLP is released from where? |
The gut, in response to intestinal nutrients as insulin increases |
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What are the peripheral effects of GLP-1? |
1. reduces blood glucose levels 2. increases insulin secretion 3. inhibits glucagon secretion 4. slows gastric emptying and gut motility (keeps food in your stomach, convinces you that you don't need to eat anymore food) |
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