Title: BV2 / BV2 - 2 / Modul 7 / Nutrition & Metabolic Syndrome

Q: Which 5 health aspects are included in the metabolic syndrome?
A: - Viceral obesity
- Low HDL-cholesterol
- High TAG
- Hypertension
- Insulin resistance

Q: What is an indicator that one is more prone to be affected to the metabolic syndrome?
A: If u have 3 of these aspects u are more prone to be affected by the metabolic syndrome
- Viceral obesity
- Low HDL-cholesterol
- High TAG
- Hypertension
- Insulin resistance

Q: What is included in the metabolic syndrome?
A: - Heart disease
- Lipid problems
- Hypertension
- Type-2 diabetes
- Dementia
- Cancer
- Polycystic ovarian syndrome
- Non-alcoholic fatty liver disease

Q: What is the first line treatment of the metabolic syndrome?
A: Lifestyle intervention:
- Reduce and/or modify caloric intake
- Increase physical activity

Q: What are additional therapeutics of the metabolic syndrome?
A: - Diuretics and ACE inhibitors for hypertension
- Statins to lower cholesterol
- Address insulin resistance (metformin, thiazolidinediones)
- Surgery (gastric bypass)

Q: How much can one expect to correct metabolic syndrome from caloric intake vs exercise?
A: - In obesity diet is more effective
- However, exercise can have good benefits

Q: What can be used to address the metabolic syndrome immediately?
A: Medications can be used to address immediately
- E.g. for hypertension, cholesterol
Surgery can also be performed

Q: Which are the "best" diets?
A: Flexitarian and Mediterranean are the most sustainable, best, long term diets

Q: What is the mediterranean diet?
A: Increase amount of veggies, more fish than meat, more exercise

Q: What is as good as the mediterranean diet?
A: - Flexitarian
- Nordic diet

Q: What is a dietary approach to combat hypertension?
A: Reduce salt

Q: What is the diet called that reduces salt intake to reduce hypertension?
A: DASH diet

Q: What happens when u remove a nutrient form your diet?
A: - It's as if u take a letter from the alphabet, the conversation won't be the same
- It can change the functionality of tissues

Q: What ought one to have in mind when going on a low-carb or low-fat diet?
A: What is the long-term effect

Q: Which are the top 3 diets overall?
A: 1. Mediterranean
2. DASH diet
3. Flexitarian

Q: What can rapid weightloss result in?
A: People that participated in biggest loser attempted to lose weight fast, which resulted in a lower metabolism which made them regain the fat again once they show ended

Q: Why does diabetes make one more prone to get other diseases?
A: - Every person has a max capacity of storing fat in adipocytes, once that is crossed the fat starts spilling over
- After that point, if one consumes more than one uses one can obtain ectopic fat deposition, which can lead to low-grade inflammation
- This can lead to insulin resistance, dyslipidemia, and hypertension

Q: What is ectopic fat accumulation?
A: Fat accumulation in other tissues/organs than adipose tissue

Q: What does ectopic fat accumulation result in?
A: Low-grade inflammation

Q: What is non-alcoholic fatty liver determined by?
A: Fat > 5% hepatocytes

Q: How many in the population have fatty liver disease?
A: 30-33% of the population has fatty liver disease

Q: What are stages in the spectrum of non-alcoholic fatty liver disease (NAFLD)?
A: - Healthy liver
- Fatty liver
- NASH (non-alcoholic steatohepatitis)
- Cirrhosis (Scar tissue)

Q: What is fatty liver characterized by?
A: Simple fat accumulation

Q: Which stages in the spectrum of NAFLD are revserible?
A: - Fatty liver
- NASH

Q: How can some stages in NAFLD be reversed?
A: Can be reversed with diet and exercise

Q: ALthough NASH can be reversed, what is a complication that remains?
A: At the NASH stage there will be fibrosis which is difficult to reverse

Q: Can fatty liver be measured via tests?
A: There are no
good measures for fatty liver

Q: What is the standard method for checking for NAFLD?
A: Biopsy is the standard method of checking for NAFLD

Q: What does NAFLD result in?
A: - Dyslipidemia
- Increased fasting glucose
- Insulin resistance

Q: What happens if there is less tryptophan?
A: Less tryptophan -> less serotonin -> less melatonin

Q: WHat can be said regarding receptors for aa and FA?
A: Many AA and FA have specific receptors

Q: How does a metabolite signal via a GPCR?
A: 1. Binds to GCR
2. G-protein activates Adenylyl cyclase
3. Adenylyl cyclase activates cAMP
4. cAMP activates PKA
5. PKA phosphorylates a transcription factor

Q: How does a metabolite signal via an ion channel?
A: 1. Enters the cell via the ion channel
2. Activates Ca2+/calmodium kinase 4
3. Ca2+/calmodium kinase 4 affects a transcription factor

Q: What can be said about GPCRs?
A: One of the larges classes of membrane receptors
- There are many varieties
- They have different specificizes

Q: How does signaling with norepinephrine via GPCR work?
A: 1. Binds to GPCR
2. Gs-alfa-subunit activates adenylyl cyclase
3. Adenylyl cyclase activates cAMP
4. cAMP activates PKA
5. PKA increases protein phosphorylation

Q: How does signaling with glutamate via GPCR work?
A: 1. Binds to GPCR
2. Gq-alfa-subunit activates phospholipase C
3. Phospholipase C activates DAG and IP3
4. DAG activates protein kinase C
4. IP3 stimulates Ca2+ release
5. Both PKC and Ca2+ release result in an increase in protein phosphorylation and activates Ca2+ binding proteins

Q: How does signaling with dopamine via GPCR work?
A: 1. Binds to GPCR
2. G1-alfa-subunit activates adenylyl cyclase
3. Adenylyl cyclase activates cAMP
4. cAMP activates PKA
5. PKA increases protein phosphorylation

Q: Where are GPCRs expressed?
A: They are expressed in a variety of cells

Q: For what are GPCRs important?
A: Important how different tissues sense the availability of different nutrients

Q: How do GPCRs work as sensors in beta-cells?
A: In beta cells 2-MAG, LCFAs, beta-hydroxybutyrate, acetate, and aromatic amino acids can bind to GPCR and result in the secretion of insulin

Q: How do GPCRs work as sensors in the adipocyte?
A: beta-hydroxyocatnoate, beta-hydroxybutyrate, succinate, acetate, lactate, LCFAs, and NEFAs can bind to GPCRs and stimulate processes in the adipocyte, eg. lipolysis

Q: What is GPR120?
A: A medium/long chain fatty acid sensor

Q: Where can GPR120 be found?
A: - Tongue
- Adipose tissue
- Intestine
- Macrophages
- Hypothalamus
- Pancreas

Q: What stimulates GPR120?
A: MCFAs and LCFAs

Q: What does activation of GPR120 lead to in the tongue?
A: Taste perception

Q: What does activation of GPR120 lead to in the adipose tissue?
A: - Adipocyte differentiation
- Lipid accumulation

Q: What does activation of GPR120 lead to in the intestine?
A: GLP-1 and CCK secretion

Q: What does activation of GPR120 lead to in macrophages?
A: Macrophage inactivation

Q: What does activation of GPR120 lead to in the hypothalamus?
A: Anti-inflammation

Q: What does activation of GPR120 lead to in the pancreas?
A: Somatostatin secretion

Q: What does activation of GPR120 lead to in all the tissues/organs it affects?
A: Regulation of glucose and lipid metabolism -> energy homeostasis

Q: What can the nutrients do if they enter the cell?
A: If the nutrients can get into the cell they can affect transcription

Q: What is DBD?
A: DNA binding domain

Q: What does DBD do?
A: Recognized sequences on the DNA close to those it has to regulate

Q: What is LBD?
A: Ligand binding domain

Q: What does LBD do?
A: Has a pocket that can accept an amino acid or something else, when in the pocket active, pocket empty-inactive

Q: What does endocrine receptors get their names from?
A: They get their names from their ligands

Q: What are orphan receptors?
A: Ligands not identified

Q: What are Adopted
orphan receptors?
A: Orphan receptors where the ligand was later identified

Q: What do nuclear receptors sense?
A: - They link sensing environmental cues, such as food, pollution
- Therapy (treatment, drugs)
- Disease
- Physiology
- Development

Q: What do nuclear receptors affect?
A: - Physiology
- Development
- Disease
- Therapy (treatment, drugs)

Q: What is FXR?
A: FXR - bile acid receptor

Q: What is LXR?
A: LXR - receptor that binds cholesterol/allosterol

Q: What does FXR stand for?
A: Farnesoid X receptor

Q: What does LXR stand for?
A: Liver X Receptor

Q: What does activation of LXR promote?
A: Activation of LXR promotes
- Cholesterol transport and modulation
- Fatty acid synthesis and regulation (increased lipogenesis)
- Bila acid synthesis (increased conversion of cholesterol to bile acids)

Q: WHat activates FXR?
A: Increase in bile acid levels

Q: What is FXR important for?
A: Important for nutrient availability

Q: What does activation of FXR promote?
A: - Bile acid metabolism (decreased bile acid synthesis, decreased bile acid hepatic uptake, increased bile acid modification and secretion)
- Lipid metabolism (decreased lipogenesis)
- Glucose metabolism (decreased gluconeogenesis)

Q: What can be said about microbiota and out body?
A: Microbiota is part of our body

Q: Is the microbiota the same in everyone?
A: They vary from person to person

Q: What can the microbiota do?
A: They can convert food into things that can affects to certain receptors, which can affect our metabolism, thus, in a way obesity

Q: What can be done with the microbiota to affect obesity?
A: Faecal transplantation

Q: For who e.g. is faecal transplantation an option?
A: E.g. for IBS patients