Title: BV2 / BV2 - 2 / Modul 7 / Hunger & Satiety

Q: What type of disease is obesity considered to be?
A: Obesity is thought of as a lifestyle disease

Q: Why is obesity thought of as a life style disease?
A: - Because we move less, we eat more or richer foods
- An energy in - energy out kind of problem

Q: How can one reverse the disease (obesity)?
A: If u change your lifestyle u can reverse the disease, however it is not always true for all individuals

Q: How wide spread is the obesity problem?
A: It is
a worldwide problem, although
it does vary it's a problem that affects the whole world

Q: Which country has the highest number of obese females?
A: USA

Q: Which country has the highest number of obese males?
A: Argentina

Q: How many percent of males are considered overweight in Sweden?
A: 60.2%

Q: How many percent of males are considered obese in Sweden?
A: 19.9%

Q: How many percent of females are considered overweight in Sweden?
A: 46.6%

Q: How many percent of females are considered obese in Sweden?
A: 17.3%

Q: How does the distribution of overweight/obese people vary in Sweden?
A: Different distribution between countryside and city

Q: Can obesity be connected to epigenetics?
A: There may be a transgenerational effect/transmission, so not only what u do, but also what your parents and grandparents did which can make one more susceptible to become obese or susceptible to the metabolic syndrome

Q: What on ones DNA can determine how susceptible one is to obesity?
A: There are marks on the DNA that can condition how your DNA will be transcribed which can affect how susceptible one is - methylation

Q: What else can be attributed to obesity as a disease?
A: Obesity is now considered to be a disease, it carries medical complications and makes one more susceptible to other diseases
- Like depression
- Certain kind of cancers, 10-15 types of cancer

Q: What is unclear about obesity and its relation to other diseases?
A: Unclear what the reason is to why obesity leads to/causes other diseases

Q: What are some medical complications of obesity?
A: - Psychological
- Pulmonary
- Gastrointestinal
- Renal
- Musculoskeletal
- Neurological
- Cardiovascular
- Endocrine

Q: What does BMI measure?
A: Mass per surface area measurements

Q: What does BMI stand for?
A: Body Mass Index

Q: How is BMI calculated?
A: BMI=Mass(kg)/Height^2(m)

Q: What BMI is in accordance with underweight?
A: BMI<18.5

Q: What BMI is in accordance with normal weight?
A: BMI= 18.5-24.9

Q: What BMI is in accordance with overweight?
A: BMI = 25-29.9

Q: What BMI is in accordance with obesity?
A: BMI of 30 or greater

Q: What BMI is in accordance with morbidly obese?
A: BMI >36

Q: What doesn't BMI take into consideration?
A: It doesn't take into consideration your shape, only mass

Q: What is an example of when the BMI value doesn't work?
A: E.g. tall and muscular might be considered over weight with BMI

Q: What can be ussed to determine % of body fat?
A: MRI

Q: What is a more accurate measurement than BMI?
A: % of body fat

Q: Can adipocity differ?
A: Not all adipocity is the same

Q: What significance does where one stores ones fat in ones body have?
A: Where u carry your fat depends on how susceptible u are to diseases/metabolic syndrome

Q: Which 2 models are used to display 2 different types fat dirstribution?
A: - Apple shape
- Pear shape

Q: How can apple-shape obesity be described?
A: Visceral obesity

Q: Who is more prone to apple-shape obesity?
A: More common in men than women

Q: What is apple shape obesity associated with?
A: Is more associated with a bad prognosis connected to the metabolic syndrome, hypertension, diabetes

Q: What is pear-shape obesity characterized by?
A: More adipose tissue in subcutaneous depos, in legs and hips

Q: What is pear-shaped oesity associated with?
A: Less associated with metabolic syndrome

Q: How can one be more prone to the metabolic syndrome depending on where ones stores ones fat?
A: - It has to do with how well the adipose tissue is vascularized
- If u have adipose tissue around the visceral organs like liver, it can spill onto the liver

Q: What is another measurment of weight/obesity?
A: Waist-to-hip ratio (WHR)

Q: What does abdominal obesity count as according to WHR?
A: Men > 0.9
Women > 0.85

Q: What does WHR stand for?
A: Waist-to-hip ratio

Q: What does WHR allow one to see?
A: Allows one to see the distribution of fat

Q: Which people do people have the least empathy with?
A: People have the least empathy with obese people

Q: What part of the brain induces hunger or satiety?
A: Hypothalamus induces hunger or satiety

Q: From where does hypothalamus get signals about nutrient-levels in our body which it can use to induce hunger or satiety?
A: - Circulating hormones
- Gut signals

Q: Where is the hunger center in the brain?
A: Lateral hypothalamus

Q: Where is the satiety center in the brain?
A: Ventromedial hypothalamus

Q: What does the lateral side of the hypothalamus do?
A: Lateral induces hunger if stimulated

Q: What does the ventromedial side of the hypothalamus do?
A: Ventromedial induces satiety if stimulated

Q: What happens if the hunger center in the hypothalamus is destroyed?
A: If hunger centre is destroyed - anorexia

Q: What happens if the satiety center in the hypothalamus is destroyed?
A: If satiety centre is destroyed - obesity

Q: What is the glucostat theory?
A: Low blood sugar stimulates food intake

Q: What is the lipostat theory?
A: Free fatty acids in the plasma inhibit food intake

Q: What are the traditional views on control of food intake?
A: - Glucostat theory
- Lipostat theory
- Negative feedback from the gastrointestinal tract

Q: Vad does the lipostat theory induce?
A: Induces satiety

Q: What does the glucostat theory induce?
A: Induces Hunger

Q: What is food intake not only controlled by?
A: It's not just a question of will - obesity/food intake

Q: What is hypothalamus integrated to?
A: Hypothalamus is integrated to cortex

Q: Concerning the hypothalamus being integrated with the cortex, which other component is involved in food intake?
A: There is an individual component on what one thinks of food, experience, preference

Q: What other part of the brain can influence hunger/satiety in the hypothalamus?
A: The amygdala with fear also influences if we eat or not

Q: What can be said about the many of mechanisms involving food, what can they also be connected to?
A: Many mechanisms involving food are involved in our defence mechanisms, the 2 can be conneted (from the time when we had to protect/defend out food coz it was scarce)

Q: What do some populations of neurons in the brain contain?
A: There are populations of neurons in the hunger/satiety centre containing OGT

Q: What is OGT?
A: - OGT is a substance, to be built in the body it needs different parts from the building blocks
  - It integrates components of all fuels presents in the body

Q: What happens to synthesized OGT?
A: It will be transferred onto proteins and influence neurons

Q: What do OGT-expressing neurons act as?
A: As nutrient receptors in the hypothalamus and the brainstem, which can influence the outcome

Q: What does the paraventricular nucleus (PVN) do?
A: Controls feeding and satiety

Q: What does the arcuate nucleus (ARC) do?
A: Controls adipose metabolism

Q: What is UDP-GlcNAc?
A: UDP-GlcNAc is the donor for O-GlcNAc transferase (OGT) and an ideal sensor of the metabolic status of the cell

Q: What is UDP-GlcNAc built up by?
A: - Nucleotide metabolism (UD)
- Overall energy (P)
- Glucose metabolism (Glc)
- Nitrogen metabolism (N)
- Fatty acid metabolism (Ac)

Q: What do pre-absorptive signals that regulate food intake include?
A: Pre-absorptive
- Is the food to ones please?
- Before foods are absorbed into circulation
- Personal experience

Q: What do absorptive signals that regulate food intake include?
A: Absorptive
- Nerves
- Hormones

Q: What do post-absorptive signals that regulate food intake include?
A: Postabsorptive signals
- The nutrients themselves that are circulating in one's body
- The release of insulin
- Leptin - adipocytes
- Adiponectin -released from adipocytes
  - These will signal to the brain if we need to eat more or less

Q: What is the purpose of adiponectin?
A: It will be released from adipocytes and signal to the brain if we need to eat more or less

Q: What is meant by hedonic aspects of feeding behaviour?
A: Pleasure aspects

Q: Which signals does the vagus nerve relay?
A: Signals from the periphery - vagus - from GI or peptides that have orexigenic or anorexigenic effects

Q: What does cholecystokinin do?
A: CCK inhibits food intake and has a direct effect on CNS via the blood as well as an effect on the afferent vagus nerve

Q: What does peptide YY (PYY) do?
A: PYY is released from the small intestine and colon after a meal and inhibits food intake

Q: What does glucagon like peptide-1 (GLP-1) do?
A: Inhibits food intake and delays gastric emptying as well as has a direct effect on the CNS

Q: What does Ghrelin do?
A: Released between meals from the GIT and stimulates food intake and has a direct effect on the CNS

Q: Which types of neurons does insulin stimulate?
A: Orexigenic and anorexigenic

Q: How does insulin stimulate orexigenic neurons?
A: Inhibits orexigenic neurons

Q: How does insulin stimulate anorexigenic neurons?
A: It activates/stimulates them

Q: What are orexigenic neurons?
A: Appetite-increasing neurons

Q: What are anorexigenic neurons?
A: Appetite-supressing neurons

Q: Where are orexigenic and anorexigenic neurons found?
A: In the Arcuate Nucleus of the hypothalamus

Q: What does CCK do (hunger/satiety)?
A: Inhibits food intake

Q: What does CCK have an effect on?
A: - Direct effect on CNS via the blood
- Effect on the afferent vagus nerve

Q: From where is Peptide YY released?
A: Released from the small instetine and colon after a meal

Q: When is peptide YY released?
A: After a meal

Q: What does PYY do?
A: Inhibits food intake

Q: What does glucagon-like peptide 1 do?
A: GLP-1 inhibits food intake

Q: What does GLP-1 have an effect on?
A: - Direct effect on the CNS

Q: What effect does GLP-1 give rise to?
A: Delays gastric emptying

Q: When is ghrelin released?
A: Released between meals

Q: From where is ghrelin released?
A: Gastrointestinal tract

Q: What does ghrelin stimulate?
A: Stimulates food intake

Q: What does ghrelin have an effect on?
A: Direct effect on the CNS

Q: WHich gastrointestinal hormone can artifical analogues be made to imitate?
A: GLP-1 analogues

Q: What happens if there is dysfunction in the tissue due to it accumulating too much fuel?
A: If there is dysfunction in the tissue there will be sterile inflammation, tissue accumulates too much fuel, releases cytokines

Q: WHat does the release of cytokines from a tissue result in?
A: Immune cells will enter to tissues to help

Q: WHat will excesive fuel accumulation in tissues result in?
A: Low grade chronic inflammation

Q: What is low grade chronic inflammation?
A: Low state of constant inflammation over long time which damages them

Q: WHat can low grade chronic inflammation lead to?
A: Depression

Q: From where is leptin released?
A: Adipose tissue

Q: WHat is leptin?
A: A hormone released by adipose tissue controlling food intake

Q: What does leptin do?
A: Induces satiety

Q: What does adiponectin stimulate?
A: Is hunger-suppressing

Q: WHat are adipokines?
A: Cytokines from fat

Q: What are ex of an adipokine?
A: - Leptin
- Adiponectin

Q: How does the amount of fat and leptin correlate?
A: The more fat the more leptin will be released

Q: What is ob/ob?
A: Deficiency in leptin production

Q: What is db/db?
A: Deficiency in leptin receptors

Q: WHich one can be treated, ob/ob or db/db?
A: ob/ob can be treated via addition of leptin

Q: What can be a cause of childhood obesity?
A: Congenital leptin deficiency - can't produce leptin

Q: What happens to patients with congenital leptin deficiency when they start taking leptin?
A: Their weight decreases

Q: What does leptin supplementation only work with?
A: Only works with a leptin deficiency, not where the receptors are broken

Q: How does leptin signalling work?
A: The brain signals to the adipose tissue to stimulate lipolysis where there is a decrease in food intake, however, when there is an increase in body weight, the adipose tissue will signal to the brain, using leptin, to reduce appetite

Q: In what else does adiponectin have a role?
A: Also has a role in inflammation - antiinflammatory effect

Q: What does adiponectin signalling result in in the liver?
A: - Decreased glucose output
- Decreased fat accumulation
- Decreased inflammation

Q: What does adiponectin signalling result in in the muscles?
A: - Increased glucose uptake
- Decreased fat accumulation
- Increased energi expenditure

Q: What does adiponectin signalling result in in the heart?
A: - Decreased inflammation
- Decreased endothelial adhesion
- Decreased foam cell formation

Q: What effects does insulin have on special neurons?
A: - Positive effect on anorexigenic neurons
- Negative effect on orexigenic neurons

Q: What effects does leptin have on anorexigenic vs orexigenic neurons?
A: - Positive effect on anorexigenic neurons
- Negative effect on orexigenic neurons

Q: Can bones regulate food intake?
A: Bones release a substance that talks directly to the brain to control food intake

Q: What in the bone is it that enables it to have a hunch of whether we should eat more or less?
A: Bones feel the weight

Q: Which mechanism regulating food intake still works in ob/ob mice?
A: Bones - body weight homeostat

Q: How does communication with arcuate nucleus work?
A: - Anorexigenic and orexigenic neurons in the arcuate nucleus receive appetite-suppressing and -stimulating signals respectively
- The ARC then signals to the Paraventricular nucleus, the satiety center
- Signals also go to the lateral hypothalamic area, the hunger centre
- The PVN and the LHA then directly induce satiety or hunger

Q: What does the PVN signal to?
A: Cortex, Pituitary gland and brainstem

Q: How does the cerebral cortex induce hunger/satiety?
A: Via LHA and PVN

Q: What does PVN stand for?
A: Paraventricular nucleus

Q: WHat does LHA stand for?
A: Lateral hypothalamic area

Q: How does the pituitary gland induce hunger/satiety?
A: - Via TRH, CRH
- Via PVN

Q: How does the SNS induce hunger/satiety?
A: Directly or indirectly via adrenal medualla

Q: How does the brainstem induce hunger/satiety?
A: From the solitary tract and "short-acting food-stimulated satiety centre" it signals directly as well as via the PVN and LHA

Q: WHat do anorexigenic agents do?
A: Reduce food intake

Q: WHat do orexigenic agents do?
A: Increase food intake

Q: What are examples of anorexigenic agents?
A: - Leptin
- CRH
- Insulin
- CCK
- GLP
- CART
- PYY
- alfa-MSH

Q: What are examples of orexigenic agents?
A: - Ghrelin
- Cortisol
- Endorfins
- Orexin A & B
- NPY
- AgRP
- MCH
- Endocanaboids

Q: What can be said about nutrients themselves within signalling?
A: Nutrients are signals in themselves

Q: What is a normal energy balance?
A: Balance between energy intake and energy expenditure

Q: What is negative energy balance?
A: When the energy expenditure>energy intake

Q: What is positive energy balance?
A: When the energy expenditure<energy intake

Q: Which is the largest family of integral membrane proteins?
A: G-protein-coupled receptores (GPCR)

Q: What does 50% of all modern drugs and 25% of the top 25% best selling drugs esitmated to target?
A: GPCR

Q: What do GPCRs do?
A: Transduce the signals mediated by diverse signaling molecules, such as ions, peptides, lipids and photons, to induce different intracellular functions

Q: What does the G-proteins (beta- and gamma-subunits) stimulate?
A: - Ion channels
- PI3K
- Phospholipases
- Adenylylacylases
- Receptor kinases

Q: What does the G-protein Gi-alfa stimulate?
A: - Ion channels
- Inhibition cAMP
- Phospholipases

Q: What does the G-protein Gs-alfa stimulate?
A: Increase cAMP

Q: What does the G-protein Gq-alfa stimulate?
A: - Increase DAG
- IP3

Q: What does the G-protein G_12,13-alfa stimulate?
A: - Activates Rho

Q: What else can GPCR work as?
A: Extracellular sensors

Q: What can GPCRs sense?
A: They sense the presence of each of the nutrients