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WEEK 6 OBESITY Flashcards

1
Q

What is overweight and obesity defined as?

A
  • When energy intake is more than energy expended through physical activity
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2
Q

What is the most common calculation for weight status in adults and what is the formula?

A
  • BMI
  • BMI= weight in kg/height (m^2)
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3
Q

What is the prevalence in Australia (2017) of overweight and obesity in children?

A

1.9 billion adults 18 years+ overweight & 650 million adults obese
- 1 in 5 children (20%) from 2-4 yrs
- 11% had overweight and 9 % had obesity

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4
Q

Does childhood obesity affect a similar proportion of males and females?

A
  • YES
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5
Q

Why is obesity known as a wicked problem?

A
  • Because it is difficult or impossible to solve
  • We need to know what matters, what works (in the real world) and what translates.
  • Must think in new and different ways
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6
Q

What are 4 reasons why a wicked problem in general is difficult to solve?

A
  1. incomplete or contradictory knowledge
  2. the number of people and opinions involved
  3. Large economic burden
  4. the interconnected nature of these problems with other problems
    e.g. Poverty being linked with education, and nutrition being linked with poverty.
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7
Q

What are two of the main factors in relation to obesity being a wicked problem?

A
  • Double burden of malnutrition (drives of under and over nutrition are in women and children sharing common elements like poverty and food security)
  • Access to obesity prevention is inequitable (lots of children are at risk of failing to reach their full potential due to the impact of developmental risks on health., wellbeing and productivity throughout life.
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8
Q

Are obesity related behaviours established in early childhood and do they track through to adulthood?

A
  • YES and YES
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9
Q

What is the rough time period that is viewed as a crucial period for child obesity prevention?

A
  • First 2000 days (5 years)
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10
Q

Is obesity much harder to reverse than prevent?

A

Yes

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11
Q

True or false. A meta-analysis showed children with obesity have a five fold increase risk of having obesity in adulthood….

A

TRUE

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12
Q

Do we have any reliable tools to determine risk and protective profiles from infancy, to develop evidence-based interventions that will assist parents, educators, and health promotion practitioners to reduce the prevalence of excessive weight gain in the formative preschool years?

A
  • NO
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13
Q

Is there a link between higher weight status and cancers?

A
  • YES
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14
Q

What are three implications of childhood obesity beyond physical health?

A
  • Negatively impacting self esteem and mental health
  • Long term education
  • Quality of life
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15
Q

Are the causes of obesity simple or complex?

A
  • they are complex, extending from genetic to social-cultural factors.
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16
Q

What type of theory has been used to summarise the complex interplay between these multidimensional contributors to excess child weight development and inform childhood obesity research?

A
  • Ecological systems theory (quality and the context of a child’s environment)
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17
Q

What is Ecological systems theory?

A
  • It places the parent and child factors as the most PROXIMAL influences on the development of overweight and obesity during early childhood.
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18
Q

How is ecological systems theory integrated with the early obesity risk in the first 2000 days?

A
  • This involves the early mother/caregiver- child interactions: biological, behavioral, and psychosocial interactions.
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19
Q

What are three reasons why high quality parent-child interactions ‘matter’ to child development?

A
  1. responsive, sensitive parenting, helps to build trust in the relationship- child knows their parent can comfort/support them in times of stress
  2. High quality interactions impact on the neurophysiological structures (sleep, stress response, appetite), thus supporting optimal development of self-regulation
  3. Stress response, sleep and appetite are implicated in energy regulation and eating behavior (cortisol slows metabolism, stress eating etc)
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20
Q

What are examples of child-level factors?

A
  • Age
  • Gender
  • Temperament
  • Self-regulation
  • Eating behaviour
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21
Q

Do cross sectional studies give an idea of causation?

A
  • NO
  • Because the data is collected at one time point
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22
Q

What are the multi-level social-ecological interactions that shape parent/caregiver actions- in terms of childhood overweight/obesity?

A
  • Health equity
  • Political, economic and social drivers of inequities (including racism-related stressors, not soley race/ethnicity)
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23
Q

What are three integrating perspectives for addressing early childhood obesity prevention?

A
  • Childhood development (incorporates ages ad stages of child dev, quality of caregiver interactions)
  • Health equity (drivers of social determinants of health)
  • Critical race theory
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24
Q

What is critical race theory?

A
  • recognizes current and historical factors that drive widening inequities in obesity rates and disproportionate burden experienced by historically disadvantaged populations.
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25
Q

What is a BMI b/w 35 and 40 classified as?

A

Obese

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26
Q

What is a BMI>40 classified as?

A
  • Morbidly obese
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27
Q

What is the normal BMI range between?

A
  • 18.5 and 25
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28
Q

As of 2017-2018, what was the % of adult Australians with overweight and obesity?

A
  • 67% (compared to 38% in 1990)
  • This equates to 5, 844, 200 Australians
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29
Q

Is overweight/ obesity classed as an epidemic?

A
  • YES
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30
Q

What is overweight and obesity considered to be the leading cause of?

A
  • Preventable death
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31
Q

What are examples of things that obesity is linked with?

A
  • high blood pressure
  • High blood sugar
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32
Q

What are 8 factors that may contribute to Obesity?

A
  • Genetics/epigenetics
  • Lifestyle eating/exercise patterns
  • Socioeconomic status
  • Psychological factors
  • Cultural background
  • Age
  • Hormonal, metabolic, and physiological factors
  • Sleep disturbances
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33
Q

Is the determination of body composition mono or polygenic?

A
  • Polygenic (>600 genes)
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34
Q

Is the heritability of BMI low or high?

A
  • Quite high (50-90%)
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35
Q

Has a genetic predisposition to Obesity been proven?

A
  • YES
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36
Q

Are monogenic forms of obesity common?

A
  • NO they are rare e.g. Ob-/Ob- gene
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37
Q

What is the most common syndromic cause of Obesity?

A
  • Prader-willi syndrome
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38
Q

What are the symptoms of prader-willi syndrome?

A
  • Hypotonia
  • Hypogonadism
  • Obesity (major one- excessive appetite- insatiable)
  • CNS and endocrine gland dysfunction
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39
Q

What is the genetic cause of Prader Willi syndrome associated with?

A
  • Lack of expression of paternal chromosome 15q11-q13 genes
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40
Q

What are 65-75% of cases of prader willi syndrome?

A
  • De novo microdeletion of the 15q11-q13 region of teh paternal chromosome
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41
Q

What are 20-30% of cases of Prader willi syndrome associated with?

A
  • maternal uniparental disomy (UPD)
    1. Two maternal chromosomes, none from father
    2. Associated with advanced maternal age
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42
Q

What are 2-5% of prader willi syndrome cases associated with?

A
  • Imprinting error- epigenetic transference
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43
Q

Which hormone is largely increased in children with prader willi syndrome?

A
  • ghrelin
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44
Q

Which gene is leptin encoded by?

A
  • The Ob gene
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45
Q

What is Leptin directly proportional to?

A
  • The amount of fat in the body
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46
Q

What is the basic role of Leptin?

A
  • To inform the brain how much fat there is in the body
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47
Q

What does a mutation in the ob gene result in?

A
  • Prevents Leptin from being secreted thus can’t reach the brain to let the body know when not to eat
  • Mice become “little balls of butter”
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48
Q

What are the symptoms of ob/ob deletion?

A
  • Profound obesity
    . Glucose intolerant/insulin resistant.
  • Cold intolerant
  • Immune dysfunction
  • No circulating leptin levels.
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49
Q

Is there a treatment for those that are deficient in leptin?

A
  • Yes you can have leptin replacement therapy. This allows the person to return to a relatively normal weight
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50
Q

Without leptin secretion, what does the body believe it is constantly in a state of, and what does this lead to?

A
  • In a constant state of starvation or there is an absence of fat stores.
  • This signals to the brain to increase food intake and reduce energy epxenditure
  • NO satiation (uncontrollable eating)
  • Leads to profound morbid obesity.
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51
Q

If individuals have a mutation in leptin receptor, do they respond to exogenous Leptin therapy?

A
  • NO
  • They have elevated circulating levels of Leptin and the brain can’t respond.
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52
Q

What is a potential treatment for the LepR mutation?

A
  • Growth Hormone treatment
  • Leads to lipolysis
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53
Q

Is idiopathic obesity monogenic?

A
  • NO it is polygenic (SNPs, epigenetics)
  • Many mutations and environmental factors at play
  • Increased adiposity= increased circulating levels of leptin
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54
Q

Do we all have a ‘set point’ weight?

A
  • YES
  • If you eat too much, the body undergoes compensatory changes in energy expenditure.
  • Body weight is thought to be predetermined by the genetic background ‘propensity genes’
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55
Q

Where is the ‘set point’ theory exemplified (experiment example)?

A
  • In hamsters
  • They lost body weight when food restricted but as soon as the restriction stopped, they returned to their normal body weight.
  • It is evident even with genetic manipulation (e.g. MC4-R KO)
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56
Q

When is set point thought to be established in terms of growth and development?

A
  • Across the pubertal transition
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57
Q

Does the body try to defend/maintain the set point values?

A
  • YES e.g. if you eat less, the body will act to promote hunger and decrease energy expenditure, thus promoting food intake.
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58
Q

Can the body establish a new, lower setpoint?

A
  • NO
  • Can only establish a higher setpoint :((
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59
Q

What two factors is the set point determined by?

A
  • genes x environment
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60
Q

What is the process by which we identify susceptibility genes?

A
  • GWAS (genome wide association study)
  • This looks at a genome wide set of genetic variants (SNPs) in different individuals to see if any variant is associated with a trait.
  • It then relates the SNPs to obesity and tries to make an association
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61
Q

What is one common gene with the SNP study for Obesity?

A

-FTO (fat mass, and obesity associated gene-protein)
- mRNA demethylase

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62
Q

Which gene was identified as the first known to contribute to obesity and how was this identified?

A
  • FTO
  • Identified though GWAS
  • Individuals having 2 copies of variant FTO they were 1.67x more likely to be obese
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63
Q

What are the symptoms when FTO is overexpressed in mice?

A
  • Increase body weight
  • Drastically increased fat mass.
  • Increased food intake.
  • Increased preference for high calorie foods.
  • Reduced physical activity and energy expenditure.
  • Impaired Browning of white adipose tissue.
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64
Q

Is there only 1 FTO variant in humans?

A
  • NO there are multiple variants
  • 89 genetic variants within introns 1 and 2 of FTO have been associated with BMI
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65
Q

What is an issue with GWAS data and obesity related genes?

A
  • The GWAS data is present BUT difficult to interpret. This is because a lot of changes occur in non coding regions of the gene.
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66
Q

Does an increased BMI reduce longevity?

A
  • YES e.g. Life expectancy of a 20 year old morbidly obese male is 13 years shorter than a male of normal weight and the same age.
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67
Q

Do people who are considered as ‘healthy fat’ show any of the typical risk factors associated with obesity and the nasty diseases?

A
  • NO
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68
Q

What are the associated diseased with metabolic syndrome?

A
  • Neurological disorders
  • PCOS
  • Cancer
  • Cardiovascular disease
  • Type II diabetes
  • Stroke
  • NASH (Non Alcoholic Liver Disease)
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69
Q

What are some examples of risk factors associated with metabolic syndrome?

A
  • Inflammation
  • Oxidative stress
    -Abdominal adiposity
  • Blood glucose
  • Decrease in HDL-L
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70
Q

What type of fat is linked with many adverse events?

A
  • Visceral fat
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71
Q

What are the diagnostic criteria for metabolic syndrome?

A
  • Accumulation of visceral fat + two or more of the following criteria (Blood sugar hyperglycemic, BP >130/>85, Serum lipids either heaps of triglycerides or low HDL)
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72
Q

What is metabolic syndrome?

A
  • A cluster of conditions/risk factors that increase your susceptibility to certain diseases
73
Q

What role does insulin have in the liver?

A
  • Decreases hepatic glucose production via the inhibition of Gluconeogenesis
74
Q

What role does insulin have in the skeletal muscle?

A

-Increases glucose uptake via the translocation of the GLUT4 transporter (glycogen) and amino acids (protein).

75
Q

What role does insulin have in adipose tissue?

A
  • Increases glucose uptake, decreases lipolysis and the net action is triglyceride synthesis.
76
Q

What is the consequence of insulin resistance in the liver?

A
  • Increase in hepatic glucose production thus leading to hperglycemia
77
Q

What is the consequence of insulin resistance in the skeletal muscle?

A
  • Decrease in glucose uptake contributing to hyperglycemia
78
Q

What is the consequence of insulin resistance in the adipose tissue?

A
  • An increase in lipolysis to increase circulating FFA
79
Q

Does type 2 diabetes occur overnight?

A
  • NO
  • It occurs in a spectrum
  • You start to see deficits in glucose tolerance and insulin sensitivity ‘pre diabetes’
80
Q

What is pre diabetes defined as?

A
  • A massive increase in secretion of insulin to try and compensate for the decreased insulin sensitivity and an increase in plasma glucose level
81
Q

What is a blood glucose reading of 6.9 mmol/L classified as?

A
  • A pre diabetic
82
Q

Who is an oral glucose tolerance test (OGTT) recommended for?

A
  • People with a fasting blood plasma glucose level of 5.5-7.7 mmol/L or a randoma plasma glucose level of 7.8-11.0 mmol/L
83
Q

After an OGTT, what does a plasma glucose level of >11.1 mmol/L indicate?

A
  • That the person has diabetes, anything below that and above 7.8 is classified as impaired glucose tolerance
84
Q

What are two factors that are associated with diabetes?

A
  • Age and obesity
85
Q

As of 2007-08, was diabetes at an equal proportion in M/F?

A
  • NO
  • Males was greater than females
86
Q

Is type 2 diabetes heritable?

A
  • Partly
  • the person may have a genetic predisposition to the disease, as well as an environmental trigger setting it off.
  • having a parent with the disease increases the risk of it 2-fold with both parents being 6-fold increase
87
Q

What is fat mass inversely correlated with?

A
  • Insulin sensitivity
  • so the higher the fat, the lower the insulin sensitivty, thus insulin resistance
88
Q

there is a dose response relationship between plasma insulin concentration and _______.

A

There is a dose-response relationship between plasma insulin concentration and insulin-mediated glucose uptake (reduced insulin sensitivity with obesity).

89
Q

Is there a dose-response relationship between the plasma insulin concentration and insulin mediated suppression of Hepatic glucose production (HGP) ?

90
Q

When is a clinical diagnosis of type 2 diabetes made?

A
  • When the pancreas stops producing insulin
91
Q

Which two things is type 2 diabetes characterised by?

A
  1. Insulin resistance
  2. Beta cell dysfunction (loss of compensation by insulin secreting beta-cells to systemic insulin resistance)
92
Q

What are the 3 basic stages of how type 2 diabetes manifests?

A
  • Insulin resistance
  • Beta cell compensation (increase in insulin secretion)
  • Beta cell failure (decrease in insulin secretion) - type 2 diabetes then manifests
93
Q

Which type of tissue is a major player in insulin resistnace?

A
  • Skeletal muscle
94
Q

What is insulin resistance manifested by?

A
  • An increase in lipolysis in adipose tissue
95
Q

Does insulin resistance manifest in multiple tissues?

96
Q

What are 4 theories in obesity causing insulin resistance?

A
  1. Lipotoxicity
  2. Inflammation
  3. Altered endocrine signals
  4. Mitochondrial dysfunction (decreased capacity to ‘clear’ lipids. Also production of ROS)
97
Q

What is the theory of Lipid toxicity in obese people?

A
  • Adipocytes get to a size where they become hypoxic and can’t store lipids anymore. Lipids then spill over and are taken up into other organs e.g. Liver and Skeletal Muscle
  • This is ‘ectopic’ insulin deposition and can lead to insulin resistance
98
Q

What are the specifics of Lipid toxicity in skeletal muscle?

A
  • Free FA in blood are broken down by lipases and capillaries in muscle BUT once they enter the muscle, they can be RE ESTERIFIED to form lipids. Large lipid drops then start to accumulate in muscles
99
Q

What are the specifics of Lipid toxicity in the liver?

A
  • Lipid can take up excess glucose and de novo lipogenesis can occur to produce the lipid
100
Q

Why is the build up of fats in the muscle bad?

A
  • Because free FAs can go on to form long chain FAs in muscle
  • These long chain FAs can then block insulin signaling
101
Q

What role does Ceramide have in the inhibitor of insulin action in skeletal muscle ?

A
  • blocks the phosphorylation of Akt, thus preventing the translocation of GLUT4 receptors to the surface of the cell for glucose uptake.
  • Ceramide is derived from the long chain fatty acids
102
Q

What are the molecular mechanisms occurring with long chain FAs blocking insulin signaling in skeletal muscle?

A
  • the FAs enter the skeletal muscle cell
  • they are oxidised by the mitochondria BUT with an excess of these, the mito can’t deal with it
  • Because the mito can’t oxidise all the extra FAs in cell, Long chain Fatty Acids form: DAG and Ceramides ,which directly inhibit insulin action
103
Q

How do the LCFA DAGs prevent insulin action in the skeletal muscle cells?

A
  • They prevent phosphorylation at the IRS (insulin response signal) thus GLUT4 can’t translocate
    (the Ceramides prevent this by inhibiting P of Akt)
104
Q

What are two types of LCFAs? -

A
  • DAGs and Ceramide
105
Q

What occurs to the adipocytes in terms of insulin resistance in obese people?

A
  • Adipocytes become necrotic (due to hypoxia)
  • They then die and thus M1 macrophages come along and release pro inflammatory cytokines (TNF-a, IL-6, IL-1, Leptin, IL-8 and IL-12)
  • TNFa and IL-6 are highly linked to insulin resistance
106
Q

Which two cytokines are highly linked to insulin resistance?

A
  • TNFa and Macrophages
107
Q

How does TNF-a lead to impairment of insulin signalling?

A
  • Allows for signalling via the Janus Kinas pathway (JKK) which both inhibits IRS-1 phosphorylation AND alllows for AP-1 to be produced (TF)
  • The inhibition of IRS-1 means GLUT4 can’t be translocated and thus no glucose uptake
  • Also INCREASES hepatic glucose production
108
Q

What are adipokines?

A
  • These are cytokines secreted by adipose tissue, thus allowing an impact on insulin sensitivity from inflammation.
109
Q

What are examples of adipokines?

A
  • Leptin
  • Adiponectin
  • Resistin
  • Visfatin
110
Q

Is the adipokine ‘Resistin’ increased or decreased in obesity?

A
  • increased and it is ofset by adiponectin
111
Q

Which adipokines are anti inflammatory?

A
  • Adiponectin (also IL-10, SFRP5)
112
Q

What are the pro inflammatory adipokines?

A
  • Leptin
  • Resistin
113
Q

What are the levels of Adiponectin, and resistin with enlarged adipose tissue?

A
  • Adiponectin is reduced and Resistin is increased
  • Leads to inflammation, insulin resistance, dyslipidemia, NAFLD and other characteristics of metabolic syndrome
114
Q

What are the specifics of mitochondrial dysfunction in type 2 diabetes?

A
  • Reduced mitochondrial number and reduced FA oxidation proteins
  • FAs are only partially oxidised
  • IRS-1 is inhibited from being P’d
115
Q

What does mitochondrial dysfunction lead to increased production of?

A
  • ROS –> this can go on to inhibit insulin signaling
116
Q

What is a hormone that is an appetite stimulator?

117
Q

What are some hormones that are appetite inhibitors?

A
  • Leptin
  • Insulin
  • GLP-1
  • CCK
  • PYY
  • These signal to the brain
118
Q

What types of metabolites control food intake?

A
  • Glucose and FFAs
119
Q

What is the most potent orexigen?

120
Q

Is the brain desensitized to NPY like it is for other peptides?

A
  • NO the brain is NOT desensitized therefore it is always sensitive to NPY to allow for a continuous increase in appetite
121
Q

Which receptors does NPY/AgRP neurons increase food intake via?

A
  • The Y1 and Y5 receptors
122
Q

Does NPY promote or decrease food intake?

A
  • Promotes food intake
123
Q

Which receptor does POMC reduce food intake via?

A

MC4R in the Paraventricular Nucleus (PVN)

124
Q

Does POMC increase or reduce food intake?

A
  • Decreases food intake–> it is an inhibitor and indicates satiety
125
Q

What type of hormone does POMC produce?

A
  • Melanocortins (melanocyte stimulating hormone)
126
Q

Where is the location of the NPY/AgRP/GABA and POMC neurons in the brain?

A
  • Base of the third ventricle (hypothalamus)
127
Q

In which neuron cell type is AgRP co-produced in over 90% of?

A
  • AgRP is co-produced in over 90% of NPY cells
128
Q

What is the rough mechanism by which AgRP INCREASES food intake?

A
  • By antagonising the effect of alphaMSH
129
Q

Which pathway is AgRP the endogenous antagonist of?

A
  • Melanocortin pathway
130
Q

Is the melanocortin pathway a satiety mechanism or the opposite?

A
  • It is a satiety mechanism
  • AgRP inhibits this pathway via competitive blocking of the MC4R with AgRP peptide released from the AgRP neurons
  • It therefore blocks the ability for alpha-MSH to bind to the MC4R and signal, thus promoting hunger “inhibits the inhibition”
131
Q

What do NPY cells talk to POMC cells via?

A
  • They talk to POMC cells via GABA
  • GABA INHBITIS the POMC cell
132
Q

Do NPY and GABA neurons present in the acruate nucleus, act to increase or decrease food intake, and what types of neurons in the PVN do they act on?
Additionally, are these slow or rapid signals?

A
  • they act to INCREASE food intake, thus acting on the orexigenic neurons in the PVN and inhibiting the satiety signals via GABA
  • These are rapid sighnals
133
Q

Does Glutamate producing neurons in the Arcuate nucleus act to increase or decrease food intake, and what type of neuron does it act on in the PVN?

A
  • glutamate producing neurons act to DECREASE food intake, thus acting on the Satiety neurons in the PVN
  • These are rapid signals
134
Q

What are the slow signals controlling food intake?

A
  • alpha-MSH acting to promote satiety signals in the PVN via the MC4R
  • AgRP acting to antagonise this effect (block them) to promote food intake
135
Q

Are AgRP neurons essential for survival, and if so, what proves this?

A
  • YES they ARE
  • This is because the brain doesn’t receive any signals regarding food hunger.
  • No trigger to eat so the animals die of starvation if these neurons are destroyed (it affects both the NPY and AgRP neurons)
136
Q

What occurs if POMC cells are genetically ablated?

A
  • Animals go onto develop obesity and type II diabetes.
  • Food intake increases thus glucose intolerance
137
Q

Does the Acruate Nucleus have a tight or leaky blood brain barrier?

A
  • It has a leaky blood brain barrier
138
Q

What is the access of blood-borne factors determined by?

A
  • Fenestrated capillaries (median eminence) and tancytes (glial cells)
139
Q

What are examples of first order neurons and where are they located?

A
  • POMC/CART and AgRP/NPY neurons in the Arcuate nucleus
  • These are known as first order neurons because circulating factors can easily come to those neurons e.g. Leptin and Ghrelin and Insulin
140
Q

Where are second order neurons located in the context of the POMC AgRP/NPY first order neuron projections?

141
Q

What do orexigenic neurons express?

A
  • AgRP and NPY
142
Q

What do anorexigenic neurons produce?

143
Q

Are Leptin and Insulin receptors found on both the AgRP/NPY AND POMC neurons, or only one or the other?
How do they work?

A
  • They are found on BOTH!!
  • They act to regulate food intake by INHIBITING the AgRP/NPY cell and ACTIVATING the POMC cell.
  • this leads to a reduced release of NPY, AgRP, increased secretion of alpha-MSH that drives a REDUCTION IN FOOD INTAKE
144
Q

What are the 4 main functions of Ghrelin?

A
  1. Increases food intake
  2. Increases adipodisity
  3. Increases blood glucose
  4. Increases growth hormone
145
Q

When are levels of Ghrelin increased in plasma?

A
  • during negative energy balance (fasting)
146
Q

When are levels of Ghrelin decreased in plasma?

A
  • During positive energy balance (obesity)
147
Q

Which hormone drives feeding and the activation of NPY/AgRP neurons to protect against starvation?

148
Q

Which types of neurons does Ghrelin DIRECTLY activate?

A
  • AgRP/NPY neurons
149
Q

Which type of neuron does Grhelin INDIRECTLY inhibit?

A
  • POMC neurons via GABA
150
Q

What is the dual centre hypothesis?

A
  • Indicaes that the Ventro medial hypothalamus (VMH) is considered the satiety centre
151
Q

What happened when the LH (Lateral hypothalamus) as destroyed in animals?

A
  • Reduction in food intake and weight loss
152
Q

What is the dual centre hyothesis?

A
  • The combination of the VMH and LH
  • So eat, increase in blood glucose, activation of the VMH, Satiety signal, Eating STOPS, Decrease in blood glucose, Activation of the LH, hunger signal, eating (cycle repeats)
153
Q

Which types of neurons project to the VMH?

A
  • Arcuate nucleus neurons
154
Q

Can leptin act in the VMH?

A
  • Yes, it alters the BDNF (brain derived neurotrophic factor) within the VMH to reduce food intake
155
Q

Which types of neurons can NPY/AgRP neurons inhibit food intake via?

A
  • They can inhibit food intake by inhibiting the Orexin and MCH neurons
156
Q

Which types of neurons in the LHA (Lateral Hypothalmic area) increase food intake?

A
  • Orexin and melanin concentrating hormone (MCH)
157
Q

Which types of peptides (from POMC) (1) inhibit neurons in the LHA to decrease food intake?

A
  • Melanocortins inhibit Orexin and MCH neurons in the LHA to decrease food intake
158
Q

Which gut hormone can ONLY signal via the vagal afferents (only the brainstem) ?

159
Q

Where can Ghrelin act to decrease food intake?

A
  • Can act at the brainstem via vagal afferents AND at the hypothalamus from the circulation
160
Q

How do PYY and GLP-1 reduce food intake?

A
  • via the actions at the brain stem AND at the area postrema at the brain stem, also at the hypothalamus
161
Q

How is the Area postrema similar to the arcuate nucleus?

A
  • Has a leaky BBB and allows hormones to readily signal at neurons within the region)
162
Q

Which type of neuron does GLP-1 act directly on?

A

Acts directly on POMC neurons

163
Q

When GLP-1 is secreted by the intestines, and signals via the vagus nerve, what does it signal via?

A
  • NTS (nucleus tractus solaris) to the brain stem
164
Q

Is GLP-1 an endocrine factor?

A
  • YES (can act at area postrema of brainstem + hypothalamus)
165
Q

Within the hypothalamus, where are GLP-1Rs located?

A
  • On the POMC cells
166
Q

What does GLP-1 act to decrease food intake via?

A
  • DIRECT action on the POMC neuron
167
Q

What are the indirect effects that GLP-1 can have?

A
  • NPY cells via GABA neurons (GLP-1 Rs are present) to INDIRECTLY inhbiti the AgRP/NPY neuron
168
Q

Does PYY have the opposite effect to GLP-1?

A
  • YES
  • Inhibits food intake via the Y2 receptors (NPY/AgRP) to reduce food intake
169
Q

Which neurons are the Y2 receptors located on?

A
  • NPY/AgRP neurons only
170
Q

Does the Y2 receptor (what PYY binds to) inhibit food intake?

A
  • YES and it does this by blocking the AgRP neurons via a DIRECT action at Y2 receptors (NOT the POMC neurons)
171
Q

What receptor does PYY bind to?

172
Q

What is the decrease in Ghrelin after meals due to?

A
  • The release of glucose
173
Q

As well as Ghrelin, what does the release of glucose stimulate the secretion of?

A
  • Insulin and amylin
  • insulin to signal satiety and post prandial metabolic response to increase the uptake of glucose into tissues
174
Q

Does GLP-1 triggers insulin secretion?

A
  • YES
  • An additive effect on regulation of blood glucose
175
Q

Is CKK for short term or longer term satiety?

A
  • Longer term satiety (similar with PYY)
176
Q

What happens after weight loss/fasted state?

A
  • Inhibition of satiety peptides, increase in Ghrelin and a reduction in Leptin levels. Signals to the brain to activate the AgRP and NPY neurons and to inhibit the POMC neurons to cause a hunger response.
    These are LONG TERM effects. With weight loss, there is this chronic form of hunger, and this is why most diets fail. They also link in with reward pathways and increase our cravings.
177
Q

What happens in the fed state in terms of gut peptides?

A
  • Increased release of gut peptides PYY, GLP-1, CCK). Increased secretion of leptin, and also inhibition of Ghrelin. Acts together to signal to the hypothalamus to lead to a REDUCTION in AgRP, NPY and an increase in POMC cells to thus trigger SATIETY.
178
Q

Cause of obesity - Assumption

A

Energy in > energy out
overeating
physical activity

BMS3052_ (12 decks)

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