33. Obesity Flashcards
How is BMI calculated? Why is this a crude measurement?
What is a better method?
Describe the prevalence of obesity in the world and the UK.
weight (Kg) / height (M2). Fat well correlated to BMI but limitations with v. muscular people. Not ethnic specific.
Waist circumference (waist:hip)
World: increased lots, most in US
UK: certain places where over 1/3 of people obese. Tower Hamlets: obese kids but not parents.
What factors contribute to the rise in obesity?
How does insulin induce obesity?
What is the effect of T2 diabetes drugs on insulin levels?
Cheap junk food, link between poverty, obesity and poor health. Increased food intake incl. sugar sweetened beverages. Less exercise. 10-15% weight issues related to medications e.g. mood stabilisers, diabetes meds, beta blockers.
Decreases lipolysis in adipose tissue and lowers plasma FA, stimulates lipogenesis in tissues, increases TGL uptake from blood -> adipose, decreases beta oxidation in muscle and liver. Lipohypertrophy if inject insulin in same place.
Increase: insulin, glitazones, sulfonylureas. Stable: metformin, DPP IV inhibitors. Decrease: SGLT-2 inhibitor, acarbose
What are heritability estimates for obesity?
What is the thrifty gene hypothesis?
What is syndromic monogenic obesity?
What is Bardet–Biedl & AlstrÖm syndrome?
V high (>0.70)
Genes that predispose to obesity would have a selective advantage in populations that frequently experience starvation. In today’s obesogenic env -> cause obesity. Polygenic situation.
V rare, characterised by mental retardation, dysmorphic features and organ specific abnormalities, in addition to obesity. Only 1 gene responsible.
Ciliopathy. 10 cilium has role in adipocyte differentiation, obesity partly caused by defect in adipogenesis. Cilia mediate leptin receptor signalling.
What is non-syndromic monogenic obesity?
What is polygenic obesity?
What 2 things play a key role in adipocyte differentiation?
Epigenetic variation also plays a role - what is it?
Single gene disorder leading to highly penetrant form of obesity. 12 genes ID’d so far that have roles in energy maintenance as part of the leptin-melanocortin pathway. Example: kid with no leptin production given leptin -> loses weight
Many diff genes with diff mutations combine to make person obese, associated with CNS, food sensing and digestion, adipocyte differentation, insulin signalling (leptin and insulin feed in together), muscle and liver biology (genetic fat handling), gut microbiota.
Cilopathies, mutations in PPAR gamma 2 (TF)
Environmental and nutritional influences during critial periods in developmennt can have permanent effects on person’s predisposition to obesity
What kind of organ is adipose tissue?
What is brown adipose tissue (BAT)? How is it different from white adipose tissue?
How are body shape and visceral fat linked?
Endocrine
Main site of adaptive thermogenesis, associated with protection against obesity and metabolic diseases like T2D and dyslipidaemia. Brown = heat loss. White = weight gain.
Apple = more visceral fat (higher risk of weight-related health problems), pear = less visceral fat (lower risk). Thus waistline measurement better than BMI
List some diseases that obesity is a major risk factor for.
Describe how adipocyte dysfunction leads to insulin resistance and T2D.
What is non-alcoholic fatty liver disease (NAFLD)?
CVD, pulmonary (e.g. sleep apnoea), metabolic (e.g. diabetes), osteoarticular, cancer, psychiatric illness. Childhood obesity - associated with early onset T2D
Rich fat diet -> chronic inflammation of adipocytes -> altered adipokine levels (high leptin) -> become leptin resistant -> breakdown of fat metabolism (accumulation of lipids in tissue) -> breakdown of regulation of glucose metabolism -> insulin resistance
Fat accumulation in liver, seen in overweight/obese. Associates with high chol/BP/T2D. Simple fat accumulation (steatosis) is reversible but if gets worse then irreversible due to cell death (from ROS from oxidative metabolism) and repleacement by fibroblasts (cirrhosis)
What are the 2 main options for obesity prevention?
How effective are diets and exercise?
What drug treatment is available in the UK for obesity? How does it work?
Why do monotherapies have limited efficacty?
Inform people about lifestyle, promote/develop non-obesogenic environment.
Diets: lose but then gain abit back afterwards, ghrelin increases and peptide YY reduced (satiety hormone). Exercise: health benefits but hard on body - carry lots of weight and heart has to work hard. LIFESTYLE CHANGES = FOUNDATION OF OBESITY TREATMENT
Orlistat - gastric and pancreatic lipase inhibitor; binds to lipase and prevents its absorption. Get steatorrhea. Vitamin supplements (fat sol ones: AKED)
Recruitment of alturnate and counter-regulatory pathways. Combination products in US
How easy is it for an obese pt to have surgery?
When and how is surgery performed?
What 3 types of surgery can be performed?
Need to first take weight management course.
Morbid obesity (BMI > 40), or BMI >35 AND obesity-related complications e.g T2D, and only after conventional medical treatments failed
1) Restrictive: restrict ability to eat e.g. adjustable gastric banding, vertical banded or sleeve gastroplasty
2) Malabsorptive: reduced ability to absorb nutrients e.g. biliopancreatic diversion and Roux-en-Y gastric bypass. Causes nutrient deficiencies, malnutirion, and ins ome cases, anastomotic leaks and the dumping syndrome
3) Restrictive + Malabsorptive: e.g. duodenal switch, intragastric balloon
