HSN301 Diet and Disease Entire Note Summary
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1 Topic 1: Metabolic Syndrome Learning Objectives: 1. Define obesity 2. Factors causing obesity 3. Obesity as a risk factor for metabolic syndrome 4. The pathogenesis of metabolic syndrome 5. Treatment of metabolic syndrome LO 1. Define Obesity Abnormal or excessive fat accumulation that may impair health BMI is a simple index of weight-for-height that is commonly used to classify overweight and obesity! WHO BMI cut-offs for adults Underweight less than 18.5 Health Overweight 29.9 Obesity class Obesity class Obesity class 3 more than 40 BUT! There are other things to consider body fat mass, distribution of fat mass. LO2. Factors Causing Obesity This is a very complex process! It isn t just energy in vs energy out! Four main categories that contribute to obesity include: 1. Psychological 2. Food 3. Physical Activity 4. Physiology (e.g. genetics) We can also class factors into inside and outside! Inside the Person (genetic, medical and physical conditions, metabolic and physiological dysregulation) Genetics (FTO gene that codes for FTO protein. When there is a greater amount of FTO in the brain, it stimulates food intake) Medical conditions and metabolic dysregulation o Disordered eating (e.g. bulimia, binge eating) o Dementia and Alzheimer s Disease (e.g. they forget that they ate!) o Appetite dysregulation o Hypothyroidism o Age-related changes in metabolism: thermogenesis o Physical disabilities o Microbiota
2 Outside the Person (built environment, food environment) Energy expenditure sedentary lifestyle (e.g. occupation and built environment) Energy intake food environment o Foods: flavour, variety, portion size, energy density, food forms (e.g. fruit vs juice) o Feeding behaviours: eating frequently, food culture o Foods costs and marketing o Food convenience: 24 hr food outlets, vending machines etc. Obesity is a risk factor for metabolic disease! LO 3. Obesity and Risk Factors for Metabolic Diseases Metabolic Syndrome: The clustering of cardio metabolic factors (e.g. central obesity, hyperglycaemia, high BP, dyslipidaemia) that are likely to be linked to insulin resistance. There are many ways that MS has been defined or diagnosed. In this unit we are going to use the most recent diagnostic definition from the International Diabetes Foundation (IDF): In order for a person to be defined as having metabolic syndrome they must have central obesity plus any of the following 2: Raised triglycerides (1.7mmol/L +) Reduced HDL cholesterol (1.03 in males and 1.29mmol/L in females) Raised blood pressure (SBP 130+ or DBP 85mmHg+) Raised fasting plasma glucose (5.6mmol/L) NOTE: if BMI > 30, Central obesity is assumed NOTE: although there are these four additional risk factors that contribute to MS, there are other factors that are considered (in a non-clinical setting) such as insulin resistance, pro-inflammatory state, prothrombotic state, hormones NOTE: MS is an all or nothing diseases, but the risk is on a continuum! This means that as the number of risk factors increase, the chance of dying from CHD and being diagnosed with Diabetes increases! Central Obesity: Waist circumference with ethnicity specific values What does it mean by ethnic specific values for waist circumference? (see below!)
3 LO 4. The Pathogenesis of MS
4 LO 5. Treatment for MS Risk Factor Obesity Blood Glucose Blood pressure LDL-c/Triglycerides/HDLD-c Non-alcohol fatty liver disease PCOS Sleep Apnoea Cancer Current Therapy Lifestyle changes, bariatric surgery, orlistat, buproprion, liraglutide Lifestyle changes, insulin sensitizers, antidiabetic agents Lifestyle changes, anti-hypertensives Lifestyle changes, lipid lowering meds n-3 PUFAs, ezetimibe, insulin sensitizers OCPs or progestins, anti-androgens, topical creams PDE-inhibitors, testosterone, aromatase inhibitors Lifestyle changes, chemo, IGF-1 IGF-11 targeted receptors
5 Part 2 Learning Objectives: 1. What is chronic inflammation? 2. How is inflammation linked to obesity? 3. Importance of fat distribution on inflammation 4. Link between adipose-tissue-related secretions and the pathogenesis of MS 5. Underlying mechanism of the pathogenies of MS LO 1. What is Chronic Inflammation? A local response to cellular injury that is marked by increase blood flow, capillary dilatation, leucocyte infiltration, and the production of a host of chemical mediators, which serves to initiate the elimination of toxic agents and the repair of damaged tissue There are two types of inflammation: acute and chronic (chronic is the cause of MS) Process of Acute Inflammation: 1. Stimulus 2. Delivery of leukocytes and plasma components to the site of injury Initiated by tissue macrophages and mast cells 3. Production of inflammatory mediators (e.g. cytokines, chemokines, eicosanoids) to resolve stimulus 4. Extravasation of neutrophils and soluble components to the tissue 5. Activation and release of toxic agents and proteolytic enzymes 6. Elimination of injurious agent 7. Resolution and tissue repair a. Switching from pro to anti-inflammatory and pro-resolution mediators b. Apoptosis (death) of leukocytes and phagocytosis (engulf) and removal by macrophages If injurious agent is not eliminated, the inflammatory process persists and a state of chronic inflammation arises! Chronic inflammation associated with morbid obesity is characterised by a continuous activation of the acute inflammation! Stimulus Delivery of plasma componenets and leucocytes to site of insult (initiated by macrophages and mast cells) Production of different types of inflammatory mediators (e.g chemokines and eisconoids) Extravation of neutrophils to release proteolitic enzymes Injurious agent is eliminated and inflmmation resolved - tissue repair!
6 LO 2. How is Inflammation Linked to Obesity? The homeostatic capacity of adipose tissue development (due to hypertrophic responding to fat accommodation needs) has its limits and may contribute to inflammatory response! In simple terms, hypertrophic obesity is associated with infiltration of macrophages into adipose tissue (which we know from above is linked to inflammation!!) The topography of adipocytes (fat cells) is very important! LO 3. Importance of Fat Distribution on Inflammation Adipose tissue pathogenicity differs according to adipose tissue localisation, visceral, or subcutaneous Before we look into this thought, let s look at the characteristics of adipose tissue! Characteristics of Adipose Tissue: Adipose tissue is an endocrine organ! They are highly vascularised and metabolically active! Hypertrophic vs hyperplastic Hypertrophy bigger cell size (hypertrophic is related to infiltration of macrophages into adipose tissue0 Hyperplasia increased number of adipocytes White vs Brown Adipose Tissues White adipose tissue (WAT): fat storage, endocrine organ, different location shave different implications Brown adipose tissue (BAT): site for lipid oxidation to produce heat (mitochondria) NOTE: lean people tend to have more brown fat than obese people this is what burns the calories. It s also more common in people in colder climates because of its ability to release heat! Distribution of Adipose Tissue: Locations of Different Fat: 1. Visceral (excess intra-abdominal fat deep fat) 2. Subcutaneous (fat directly under the skin) 3. Retroperitoneal (aka hepatic fat) 4. Local
7 Visceral Fat: Pro-inflammatory fat Waist adiposity is a proxy to predict visceral fat! Abdominal fat highly correlates with visceral fat! Visceral fat seems to be a predictor of conditions such as: Insulin sensitivity Impaired glucose tolerance Elevated BP Dylipidemia The relationship between FFA and Visceral Fat? Stimulated visceral fat has increased rates of lipolysis, thus increasing FFA release. Thus, visceral fat is BAD because FFAs and adipokines released from visceral fat communicate directly with the liver! NOTE: FFA spilt over from obese Ectopic Fat: include visceral and hepatic fat (aka retroperitoneal fat) LO 4. Link Between Adipose-Tissue-Related Secretions and the Pathogenesis of MS Adipose tissue secretes more than 50 hormones and signaling molecules, collectively called adipokines, which exert their biological roles in an autocrine, paracrine, or systemic manner and influence several physiological processes concerning energy, glucose metabolism, and immunity Terms: Cytokine: Proteins secreted by a certain cell for the purpose of altering either its own function (autocrine effect) or those of adjacent cells (paracrine effect) NOTE: In the adipocyte, there are several producers of cytokines (e.g. stromal cells, connective tissues, macrophages) NOTE: other tissues release cytokines as well! Adipokine: This guy is a type of cytokine! Bioactive mediators predominantly secreted from adipose tissues that can modulate metabolic, physiology and cell signally pathways. They can exhibit either pro or anti-inflammatory properties. Adipocytokines: Collective term used for both adipokines and cytokines released by adipose cells and adipose tissue. NOTE: this term is often used interchangeably with the term adipokine Adiposopathy: Adipose tissue that creates adverse paracrine, endocrine and immune responses which may promote CVD (either directly or indirectly) by stimulating major CVD risk factors such as type-2 diabetes, high BP or dyslipidaemia. It s basically just non-functioning fat cells!!!
8 Inflammatory Cytokines: See entire notes for the different types of inflammatory cytokines. We do not necessarily have to know the exact roles of every one of them! The 4 main roles of inflammatory cytokines are: 1. Promote inflammation 2. Promote prothrombin 3. Stimulate insulin resistance 4. Increase BP Pathogenesis of MS: 1. Weight Gain a. Release of TNF-alpha = release of MCP-1 AND damage to endothelial cells = release of macrophage b. Release of Leptin VEGF = angiotensin (growth of blood vessels) c. Release of FFA into blood stream = stress to endothelium 2. Chronic Weight Gain a. Continual macrophage release = continual MCP-1 release to promote more macrophage release b. Macrophage stimulates release of factors to adipocyte = insulin resistance In depth explanation: Adipocyte acting normal. During weight game the number of adipocyte does not change, but they are bigger (due to hypertrophy due to storage of fat function of adipotissue is to store fat). Adipocyte releases TNF alpha (when adipocyte is enlarged, the vascular system does not supply enough adipocyte, causing hypoxia and under that situation the cell feels suffocated and TNF alpha is released to tell the cells it is suffocating!). TNF alpha stimulates pre-adipocyte to release MCP-1. TNF alpha also causes injury to endothelia cells. MCP-
9 1 attracts macrophage to the site. Adipocytes also release Leptin VEGF which stimulates the growth of blood vessels (angiotensin). FFA are also released into blood vessels causing physical stress and damage to the endothelium When weight gain is temporary, this may resolve. However, if weight gain continues, there is an accumulation of macrophages (which also stimulates more MCP-1 being released to increase my macrophages), resulting in the release of other cytokines. These cytokines stimulate neighbouring cells (i.e paracrine) and insulin function is impaired (i.e. insulin resistance) LO.5 Underlying Mechanism of the Pathogenies of MS MS is largely due to the secretory activity of adipose tissue (particularly from visceral fat!) INSULIN RESISTANCE IS PRETTY MUCH THE START OF ALL MS! Insulin Resistance: Characterised by a high plasma insulin concentration that fails to suppress plasma glucose normally. How does insulin Resistance Occur? We know that stimulated visceral fat results in dysregulated adipokine secretion, resulting in increase in cytokine and FFAs. The release of these components has a whole-body effect, mainly to three organs I the body: 1. Brain a. Reduce energy expenditure b. Increase food intake c. Increase hepatic glucose production (i.e. liver increase glucose production) 2. Muscle a. Reduce glucose uptake b. Reduce FA oxidation 3. Liver a. Increase glycogenolysis (increase glucose in blood) b. Increase glucogensis (increase glucose in blood)
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