INTS12 - Endocrine Regulation of Metabolism Flashcards
(125 cards)
1
Q
Define intermediary metabolism.
A
Metabolic reactions that occur between the uptake of nutrients, their conversion into cellular components and fuel, and formation of excretory products.
2
Q
Define metabolism as a whole.
A
Chemical processes which occur in the body. Balance between anabolism and catabolism.
3
Q
Define catabolism.
A
Break down of substances.
4
Q
Define anabolism.
A
Build up of molecules.
5
Q
What are the three main macronutrients of the body.
A
Carbohydrates, lipids and proteins.
6
Q
How are the three macromolecules used in the body.
A
Carbohydrates - glucose provides energy for cells as it is a metabolic substrate.
Lipids - fats used to build cell walls.
Amino acids - built into complex proteins used in cell division and rePair
7
Q
How are the three main macromolecules stored in the body.
A
Carbohydrates - glucose stored as glucagon in liver and muscle cells.
Lipids - excess fat stored as adipose tissue in fat cells.
Proteins - amino acids cannot be stored so are converted into fatty acids for storage.
8
Q
Give general overview of how energy is produced in the body and where it is obtained from.
A
Carbohydrates broken down into glucose, used in respiration for production of ATP. Amino acids can enter respiration as acetyl coA. Lipids may also be converted into metabolic substrates which result in ATP energy production.
9
Q
Amino acids are used for energy production. True or false.
A
True in extreme cases when no glucose or other metabolic substrates are available.
10
Q
How can proteins be used for energy production in the body.
A
Broken down into amino acids and used to produce either pyruvate or acetyl coA (directly) and continues with rest of aerobic respiration process.
11
Q
How can lipids be used for energy production.
A
Lipids broken down into glycerol and fatty acids. Glycerol can enter aerobic respiration process as pyruvate. Continues with rest of aerobic respiration.
12
Q
Link between protein and urine.
A
Protein broken down into amino acids, converted to amine waste product which is then removed via urine.
13
Q
Two ways amino acids can be used in the body.
A
Protein production.
Growth and repair of muscle and lean tissue.
14
Q
Give examples of hormones involved in anabolic reactions.
A
Insulin. Sex steroids. Thyroxine. growth hormone.
15
Q
Give examples of hormones involved in catabolic reactions.
A
Glucagon. Epinephrine. Growth hormones. Thyroxine.
16
Q
How much energy is used by the brain in relation to its mass.
A
Uses 20% of energy produced by glucose in the Body. Is only equal to 2% of total body weight.
17
Q
Discuss structure of the pancreas.
A
Elongated gland containing hormone producing cells and enzyme secreting cells. Contains mainly exocrine tissues. Also contains endocrine tissue.
18
Q
Define exocrine tissue.
A
Tissue that secrete chemical substances through ducts outside the main body of itself.
19
Q
Define endocrine tissue.
A
Tissue that release chemicals directly into the bloodstream.
20
Q
Discuss the role of the pancreas as an endocrine tissue.
A
Pancreas contains islets of langerhans which secrete hormones into blood stream that regulate blood glucose.
21
Q
What symptoms may occur when blood glucose levels are low.
A
Hunger, sweating, trembling.
22
Q
What are symptoms of persistently high blood glucose levels.
A
Dehydration. Thirst. Frequent urination. Tiredness.
23
Q
What long term damage may occur as a result of high blood glucose levels.
A
Excess fluid loss leads to nerve and blood vessel damage resulting in CVD.
24
Q
Give types of cell with high energy demands.
A
Brain cells. Neurones.
25
What are the two pancreatic hormones involved in blood glucose concentration regulation.
Insulin and glucagon
26
What is the role of glucagon in blood glucose regulation.
Raises glucose levels in blood by stimulating breakdown of glycogen stored in liver and muscle.
27
What is the role of insulin in blood glucose regulation.
Insulin lowers glucose levels by stimulating body cells to absorb glucose, store it is glycogen and convert to fatty acids.
28
Give conditions caused by lack of insulin and how it is caused.
Lack of insulin leads to fatty acids being released from adipose tissue. Fats are broken down into ketone bodies to use as an energy source as without insulin, no stimulation for glucose to be used as an energy source. Ketone bodies accumulation leads to lowered blood pH which can result in coma and death.
29
Discuss effects of insulin.
Increased rate of glucose uptake in adipose tissue and muscle.
Increased rate of glucose used as metabolic substrate.
Increased amino acid transport into muscle, liver - increased protein synthesis.
Inhibits rate of lipolysis in adipose but stimulates fatty acid and triglycerides synthesis in adipose and liver.
30
Is insulin anabolic or catabolic.
Anabolic.
31
Is glucagon anabolic or catabolic.
Catabolic.
32
What is the role of catecholamin epinephrine.
Catabolic hormone carrying out glycogenesis, lipolysis and gluconeogenesis.
33
Link between growth hormone and insulin.
Growth hormone counteracts the effects of insulin on blood glucose. Growth hormone reduces glucose uptake by muscle and liver for storage as it stimulate metabolic use.
34
What is cortisol and its main role.
Glucocorticoid hormone released as a stress hormone, promoting the release of glucose into the blood and playing a role in lipid metabolism.
35
Define subcutaneous fat.
Jiggly fat visible under the skin.
36
Define visceral fat.
Fat surrounding the organs which is not visible from outside. Associated with metabolic disease.
37
Link between cortisol and specific type of fat.
High levels of cortisol drives expansion of visceral fat depots but stimulates lipolysis in subcutaneous fat.
38
Link between cortisol and protein metabolism.
Cortisol is stress hormone which stimulates proteolytic, resulting in the release of amino acids into the blood.
39
Define glycolysis.
Metabolic conversion of glucose into pyruvate.
40
Define glycogenesis.
Production of glycogen from glucose.
41
Define glycogenolysis.
Breakdown of glycogen into glucose.
42
Define gluconeogenesis.
Formation of glucose from non carbohydrates sources.
43
What is the main role of the beta pancreatic cell.
Release of insulin in response to increase blood glucose concentration, resulting in the decrease of blood glucose concentration.
44
What effect does insulin have on proteins.
Increased amino acid transport and protein synthesis
45
What effect does insulin have on lipids.
Decreased lipolysis and increased lipogenesis.
46
Which cell in the pancreas inhibits the effect of beta cells and how.
Delta cells release somatostatin which inhibits the release of insulin by beta cells.
47
What cell in the pancreas stimulates the effects of beta cells and in what way.
Alpha cells release glucagon which stimulates the release of insulin from beta cells.
48
Which nervous system has a stimulatory effect on beta cells.
Parasympathetic nervous system
49
Which nervous system has an inhibitory effect on beta cell insulin release.
Sympathetic nervous system, as it ensures that glucose is available for the fight or flight response.
50
What is the role of alpha pancreatic cells.
Release of glucagon which is secreted in response to low blood glucose, in order to increase blood glucose concentration.
51
What effects does glucagon have in the liver.
Increases hepatic gluconeogenesis and glycogenolysis. Also amino acid transport into liver is increased, as is lipolysis, aiding gluconeogenesis.
52
Which cells in the pancreas have an inhibitory effect on alpha cells and how.
Beta cells release insulin. Delta cells release somatostatin. Both inhibit release of glucagon from alpha cells.
53
Discuss role of GLP1 and GIP on beta cells.
Hormones stimulate insulin release from beta cells.
54
Give brief description of insulin release process by a beta cell.
Glucose enters pancreatic beta cell via GLUT2 protein. Aerobic respiration occurs producing ATP, which activates ATP sensitive K+ channels, preventing efflux on K+ ions. Accumulation of K+ inside cell, depolarises membrane which opens voltage gated Ca2+ channels, resulting in influx of Ca2+. Increased Ca2+ results in vesicular fusion with membrane, releasing insulin.
55
What are the effects of hexokinase vs. Glucokinase
Hexokinase has lower Km so higher affinity for substrate at lower concentrations. Increased reaction velocity which remains high.
Glucokinase - velocity and substrate conc are directly proportional so has higher Km than hexokinase so lower affinity.
56
Which behaves as a glucosensor better, hexokinase or glucokinase and why.
Glucokinase as it has a lower affinity for glucose so will only drive glycolysis at rates proportional to changes in glucose concentration.
57
What happens when ATP binds to ATP sensitive K+ channels.
Prevents the efflux of K+ ions out of the cell as the ion channel changes to closed conformation.
58
Define diabetes.
Group of metabolic disorders associated with chronically elevated blood glucose levels.
59
Give general overview of type I diabetes. How can it be fixed.
Lack of insulin in the body preventing the uptake of glucose by cells. Timely insulin injections.
60
Give general overview of type II diabetes. Give on method of controlling.
Insulin receptors become desensitised preventing binding of insulin and so uptake of glucose. Increased insulin can increase sensitivity of insulin receptors.
61
Define exogenous
Originating from outside of the body
62
Define endogenous
Originating from internal origin of the body
63
What medications can be used to treat type II diabetes.
Metformin/thiazolidinediones - increase insulin receptor sensitivity.
GLP1 agonists - similar to GLP1 so stimulate insulin release from beta cells.
Sulfonylureas - bind to ATP sensitive K+ channels.
64
How are GLP1 agonists good medications for treatment of type II diabetes.
Increase insulin release from beta cells, increasing sensitivity of insulin receptors to insulin.
Can block ATP sensitive K+ channels, preventing efflux of K+ depolarising membrane, allowing Ca2+ channels to open, influx of Ca2+ and insulin release
65
Define diffuse endocrine system
Encompasses endocrine cells that are not present in primarily endocrine organs. Commonly used to describe gastrointestinal tract.
66
Why is the GI tract considered a diffuse endocrine system.
Not an endocrine organ but contains many endocrine cells.
67
Where do hormones from the GI tract signal to.
Peripheral and central nervous system to regulate various biological processes.
68
What is the role of gastrin in digestion and where is it released from.
Released by stomach in gastrointestinal tract to stimulate release of gastric acid - aiding digestion.
69
What are the roles of cholecystokinin and secretion in digestion.
Stimulate release of pancreatic juice, needed for macronutrient digestion.
70
Give general overview of incretins and how they work.
Hormones released by large intestine. Released after food intake to further increase insulin secretion by pancreatic beta cell.travel in circulation to beta cells.
71
Why do obese subjects have higher insulin and glucose levels.
Obesity commonly associated with insulin resistance meaning increased insulin levels required to suppress glucose levels. However, insulin effect is reduced therefore glucose generally remains quite high,
72
What are the two major incretins in the body.
Glucose dependent insulinotropic peptide 1 - GIP
| Glucagon like peptide 1 - GLP1
73
When were the roles of incretins first discovered. How
Experimental procedures which involved the administration of glucose both orally and intravenously. Oral administration resulted in greater insulin release as it passes through gastrointestinal tract, resulting in further hormones being released to increase Insulin levels.
74
Define energy homeostasis.
Regulation of food intake and energy expenditure.
75
What are the major regions in the brain that control energy expenditure
Hypothalamus and brain stem.
76
What is the vagus nerve.
Cranial nerve which sends input to the brain stem regarding appetite and food intake.
77
Link between adipose tissue, brain and apple regulation.
Adipose tissue releases hormone leptin which signals to the hypothalamus to regulate appetite.
78
What responses are coordinated by the hypothalamic circuitry to restore energy homeostasis
Modulation of pituitary hormone release - e.g. thyroid hormones to regulate metabolism
Signalling via autonomic nervous system - e.g. signalling to promote lipolysis
Signalling to higher brain centres e..g cerebral cortex to cause changes in behaviour regarding food and appetite
79
How does the hypothalamus regulate appetite.
Integrates many signals received from multiple centres.
80
Define neuropeptides.
Short chain polypeptides that can behave as neurotransmitters.
81
Role of the arcuate nucleus in the brain. How does its location aid it’s role.
Crucial in regulation of appetite. Located in the median eminence so can detect hormones and signals in circulation.
82
Structural Link between ARC and PVN in Brian and how this aids their roles.
Neurones extend from the arcuate Nucleus to the paraventricular nucleus which allows the incorporation of various signals and stimulate the appropriate response.
83
Give the role of structure of the 3rd ventricle in the brain.
Cerebrospinal fluid containing ventricle located in the middle of the brain, that runs down the middle of the hypothalamus
84
What is POMC and its role in the ARC.
Proopiomelanocortin is a large precursor protein that is cleaved to form alpha melanocyte stimulating hormone (aMSH). This binds to receptors and suppresses food intake.
POMC is released from the arcuate nucleus.
85
How can the ARC make you feel hungry.
Release neuropeptide Y and agouti-related protein from the arcuate nucleus. Stimulation of these neuropeptides results in increased appetite.
86
What is the link between aMSH and obesity.
Lifelong obesity cases commonly see a mutation in the aMSH protein gene.
87
Discuss signalling in the gut-brain axis.
Bidirectional biochemical signalling as the gastrointestinal tract can signal to the central nervous system and vice verse. Results in overall appetite regulation and responses carried out that relay information obtained.
88
What type of information can be relayed to the brain from the gastrointestinal tract.
Energy required which translates to appetite regulation. Macronutrient content. Located of ingested food in gut.
89
Discuss direct signalling from between GI tract and brain.
Hormones released by gastrointestinal tract that bind to receptors on neurones in central nervous system, which feed information to the brain of appetite regulation.
90
Discuss indirect signalling between the GI tract and the brain.
Hormones can bind to receptors on vagus nerve neurons, which alters their activity, which then feeds information to the brainstem and eventually higher regions on the brains
91
What is the role of grehlin
Hormone that is increased during periods of fasting. Acts on central nervous system to drive hunger.
92
What is the role of GLP-1 and PYY3-36
Released from enteroendocrine L cells following a meal, in order to suppress food intake.
93
What is the role cholecystokinin.
Suppresses food intake at high concentrations of pancreatic enzymes, whose release it controls.
94
Name hormones involved in the regulation of short term appetite.
Grehlin
Cholecystokinin
GLP1
PYY3-36
95
Discuss the apical and basal side of an L cell, and relate to role.What is an L cell.
Enteroendocrine cell releasing GLP1 and PYY3-36 in intestinal lumen.
Apical - contact with intestinal lumen so can sense nutrients as they pass.
Basal - contains hormone contains granules whose contents can be released into circulation, upon sensing nutrient shortages or excesses.
96
Link between GLP1/PYY3-36 and grehlin and how does this happen.
Upon release of GLP1 and PYY3-36 to suppress food intake, grehlin circulation is reduced preventing stimulation of food intake. GLP1 and PYY3-36 directly modulate activity of neuronal circuits in the brain which then signal to the stomach, inhibiting grehlin release.
97
Define orexigenic vs. Anorexigenic.
Orexigenic - appetite stimulating hormone
| Anorexigenic - appetite reducing hormone
98
Discuss orexigenic hormone levels before and after meals, with example.
Levels increase before a meal in order to drive hunger. Falls following a meal. Example - grehlin.
99
Discuss anorexigenic hormone levels before and after a meal.
Low before a meal as you do not want to drive a feeling of satiety before eating. Increase during and after a meal, in order to suppress food intake. Example - cholecystokinin
100
Define adipokines.
Hormones released from adipocytes - cells of adipose tissue.
101
Define adipocytes.
Cells of adipose tissue.
102
Is adipose tissue an endocrine organ.
No but has endocrine function.
103
Define cytokines.
Hormones released by the immune system cells in adipose tissue.
104
Link between adipose tissue, inflammation and diabetes.
Excess adipose tissue results in pro-inflammatory state leading to obesity and also, which results in insulin resistance, driving diabetes.
105
Discuss link between adipose tissue and inflammation.
Adipose tissue releases hormones like interleukin 6 which drives expansion and activation of T cells and B cell activation. Inflammatory responses are up regulated.
106
Discuss role of leptin, including its release.
Hormone leptin is released from adipose tissue. Binds to Ob-Rb receptor in hypothalamus. Leptin reduces food intake.
107
Link between leptin levels and adipose tissue levels.
Leptin increases as adipose tissue increases.
108
Which two organs do adiponectin act on.
Muscle and liver.
109
Discuss effect of adiponectin on muscle.
Adiponectin binds to adipo R1 receptor, increase insulin sensitivity of the muscle cells.
110
Discuss the feat of adiponectin on liver tissues
Adiponectin binds to adipo r2 receptor. Increases insulin sensitivity and decreases gluconeogenesis.
111
Link between adipose tissue levels and adiponectin release.
Increase adipose tissue means decreased adiponectin release.
| Decreased adipose tissue means increased adiponectin release.
112
Give physiological effects of decreased leptin.
Decreased leptin results in the hypothalamus thinking that there are no fat stores in the body, hence a feeling of starvation.increased felonies of hunger are apparent which can lead to over eating and gain of body weight.
113
Give examples of adipose tissue hormones.
Leptin. Adiponectin. Interleukins. Estrogen. Visfatin. Resistin. Tumour necrosis factor
114
Give overview of roles of calcium in the body.
```
Neuromuscular excitability
Muscle contraction
Blood coagulation
Bone strength
Intracellular second messengers molecule
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115
Define hypercalcemia
Increase of calcium levels
116
Which hormone is used to regulate calcium levels and where is it released from.
Parathyroid hormone released from 4 parathyroid glands
117
What are the two organs that PTH directly acts on.
Bone and kidney.
118
What effects does PTH have on bone.
PTH binds to PTH receptors on osteoblasts, suppressing their activity of forming bone using up calcium. Factors are released which activate osteoclasts, breaking down bone, releasing calcium into circulation.
119
What effects do PTH have on kidney.
Promotes calcium reabsorption, by preventing loss of calcium, in urine.
Promotes second hydroxylation of vitamin D3 which is then directed to the gastrointestinal tract to increase calcium absorption
120
Which organ does PTH have an indirect effect on. How.
Gastrointestinal tract. Activated vitamin D3 from kidney is passed to gastrointestinal tract to have its effect of increasing calcium absorption.
121
Discuss role of liver in calcium absorption.
First hydroxylation of cholecalciferol occurs in liver forming 25-hydroxycalciferol. Passes to kidney where PTH has an effect to form the second hydroxylation step. This then passes to gastrointestinal tract which increases Calcium abosorption.
122
Discuss effects of primary hyperparathyroidism. How does it occur.
Commonly formed by growth of parathyroid glands by adenoma.
Endocrine cells of parathyroid gland expand resulting in more PTH being released, which is not responsive to the feedbacks circulation. Continue to increase calcium levels even if already high. Sensory receptors of calcium levels in parathyroid hormone are affected.
123
Discuss effects of secondary hyperparathyroidism
Occurs as a result of an inability of the PTH to stimulate second hydroxylation of vitamin D3 preventing it from being activated and so prevents calcium absorption in gastrointestinal tract. PTH is high but calcium remains low.
124
Discuss effects of vitamin D deficiency on calcium levels.
Without vitamin D, gastrointestinal tract cannot be stimulated to absorb calcium meaning calcium levels would remain low,
125
Discuss effects of tertiary hyperparathyroidism
Negative feedback loop is disrupted. Consistently high levels of both calcium and PTH which cannot besuppressed
