Why This Topic?

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OBESITY

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Why this topic? • Medical aspects - connected disorders - medical care - epidemic extent • Non – medical aspects

Why is obesity a problem? • Heart disease. • High blood pressure. • Arthritis. • Diabetes. • Indigestion. • Gallstones. • Some cancers (e.g. breast, prostate). • Snoring and sleep apnoea. • Stress, anxiety, and depression

BACK

COUNTSFacts about overweight and obesity

WHO’s latest projections indicate that globally in 2005: • approximately 1.6 billion adults (age 15+) were overweight; • at least 400 million adults were obese; • at least 20 million children under the age of 5 years are overweight. WHO further projects that by 2015, approximately 2.3 billion adults will be overweight and more than 700 million will be obese.

Introduction • Definition • Physiology • Treatment

What is the obesity? Abnormal or excessive fat accumulation that may impair health

Obesity according to WHO The World Health Organization (WHO) defines "overweight" as a BMI > 25 "obesity" as a BMI > 30

What is BMI? Body Mass Index

KG

BMI = M2

70kg, 1.75m, man BMI = 70/1.75 2 BMI=22.9

BMI CHART

BMI Overweight Adults (%) World

BMI Distribution – Poland, Most recent

BMI Gender Comparison PreObese - Poland

BMI Gender Comparison Overweight - Poland

Why do people develop obesity? 1. Lifestyle 2. Genes

Environmental factors • Reduced need for physical exertion to survive • Increased quality and quantity of avaible food • Nutrition during fetal development on body weight in later life • Stress • Sleep deprivation • Viral infections • Compositions of benign microbial communities within the body

Inborn factors Genes may help explain epidemic extent of obesity to scientists • FTO gene product • Ob.gene product • Adipokines (leptin, adiponectin, resistin,TNF, IL6) • Gut and pancreas hormones(insulin, ghrelin, CCK)

FTO gene • one its variationis linked to obesity • Its carriers are on average 3kg heavier than the rest of population • Double greater risk of obesity • Its role is unknown yet

Ob. gene Product: leptin (satiety hormone) Stimulates: angiogenesis, puberty Action on cell level: muscles, hepatocites, B cells – syntesis adipocites – fat breakdown

Ob.gene Action on system: aim: nucleus arcuatus hipothalami <–> adipocites

(leptin in fetus development)

Is there a Fat-o-Stat? physiology Control mechanisms of cell energy uptake and expenditure

How does it work?

INFORMATION STORED ENERGY STATUS • Circulating leptin indicates how much fat body contain

METABOLIC STATUS • Circulating glucose represents energy immediately available to cells • Various indicators of liver activity signal that ingested energy is being processed

FEEDING STATUS • Neural and chemical signals from the gut indicate whether digestive organs are full of food

BRAIN – COMMAND CENTER APPETITE CONTROL LOCATION: • nucleus arcuatus hypothalami • nucleus solitarius

NUCLEUS HIPOTHALAMI

LEPTIN

Mixed massages

Evolutionary trap Changes in diet and organism tricks to maintain stable weight when significantly alter energy intake • Sudden food restriction • Intentional overfeeding Observation of physiological and behavioral changes

Overriding obesity SIBUTRAMINE Raises available serotonin and norepinephrine, brain chemicals that affect appetite as well as mood and other functions

RIMONABANT Suppresses activity of CB1 receptors in brain and body tissues, which stimulate appetite and are involved in cellular fat processing(not approved in U.S.)

ORLISTAT Blocks fat absorption in intestines to reduce calorie intake

Overriding obesity BARIATRIC SURGERY Reduces and/or bypasses stomach pouch and part of intestine to decrease the amount of food taken in and digested. Also lowers appetite by changing intestine’s hormonal responses to food

Overriding obesity – new approaches APPETITE • Block activity of the appetite-stimulating neuropeptides MCH or NPY or gut peptide ghrelin • Boost appetite-suppressing activity of cellular MC4 receptors or certain serotonin receptor subtypes • Inhibit neural proteins SOC3 and PTP1B to couteract leptin resistance

Overriding obesity – new approaches ENERGY STORAGE • Reduce fat cells’ intake of energy and manufacture of trigliceride by inhibiting 11BHSD1 enzyme

STORED ENERGY USE Increase rate at which fat cells release trigliceride to bloodstream for use as fuel by stimulating PPAR and beta3-adrenrgic cellular receptors in body tissues Increase FGF21 protein, which causes liver cells to burn fat

MANY SUPPORT GROUPS

Opposite problem?

But this is another topic...

references • What fuels fat? Sci Am. 2007 Sep;297(3):72-81. • http://news.bbc.co.uk/2/hi/health/7230065.stm • http://www.who.int/mediacentre/factsheets/fs311/en/inde x.html • http://www.pulsmed.com.pl/document.php? id=106&pageNo=3&ctgSelect=7&module=menuTree