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Obesity

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Obesity Obesity Presentation Transcript

  • We all know it’s a problem, but what does it do to our bodies?
    Obesity
  • WHAT IS FAT?
    On the inside fat cells are called Adipose tissue
    Droplets of fat in the blood are called lipids
    Fat seen through microscope
    Photo by: clcpages.clcillinois.edu
    Photo by: http://www.linkpublishing.com/video-cell.htm
  • FAT IS FAT…RIGHT?
    There are actually two different types of fat
    Brown fat is less plentiful in the body and serves mostly for heat production (2)
    White fat is more plentiful and is the cause of obesity (2)
    In the pictures, brown fat is on the left, white fat is on the right
    Photos provided by: http://arbl.cvmbs.colostate.edu/hbooks/pathphys/misc_topics/brownfat.html
  • WHAT DOES A WHITE FAT CELL DO?
    Provides 3 functions:
    Heat insulation- some fat is necessary in order to keep your body at an optimal temperature(2)
    Mechanical insulation- fat storage between your internal organs provides shock absorption(2)
    Energy storage- fat is a very efficient way to storeenergy, it can be accessed quickly when needed(2)
    Picture provided by Microsoft Clipart
  • WHEN DOES FAT BECOME UNHEALTHY?
    Experts refer to the BMI or body mass index to determine obesity
    BMI is a way of measuring your body fat based on your height and weight (3)
    There are limitations to the
    BMI index
    As indicated by the video,
    it does not take into account
    weight that is caused by
    muscle
    Video provided by: http://www.hhmi.org/biointeractive/obesity/bmi.html
    Underweight BMI: <18.5
    Normal BMI: 18.5-24.5
    Overweight BMI: 25-29.9
    Obese BMI: > 30 (2)
  • HOW DOES EXCESS FAT AFFECT THE BODY?
    Fat secretes a hormone called Leptin- once Leptin is released it is sent to the hypothalamus in the brain (1)
    The hypothalamus is responsible for interpreting the amount of Leptin secreted and regulating your appetite (13)
    Decreased fat in the body secretes less Leptin which causes your
    hypothalamus to increase your
    appetite
    Excess fat makes more Leptin
    which causes your hypothalamus
    to decrease your appetite
    Video provided by: http://www.hhmi.org/biointeractive/obesity/bmi.html
  • IF LEPTIN CONTROLS MY APPETITE HOW CAN I BECOME OVERWEIGHT?
    Remember, Leptin is secreted by molecules of fat, not by the amount of food you eat in a day
    Your stomach is mostly responsible for telling your brain when you are full, but it is easy to ignore this signal and eat more
    Fat storage does not occur overnight, so it is easy to consume thousands of extra calories before your Leptin levels have had a chance to tell you to stop!
    Over time you gain weight, and this can eventually lead to obesity
  • IF I AM OBESE WHY AM I STILL HUNGRY?
    Think back to two slides ago when we talked about the fact that fat tissue secretes the hormone Leptin
    The more fat tissue you have the more Leptin is produced, so theoretically your appetite should decrease
    But when you are obese the excess fat constantly secretes high levels of Leptin
    Over time, chronically high Leptin levels can create a condition called hyperleptinimia(14)
  • HYPERLEPTINIMIA?
    People with this condition actually become resistant to Leptin (14)
    The reason for hyperleptinimia appears to be similar to the cause of Type 2 diabetes in obese patients
    In Type 2 diabetes the pancreas secretes abnormally high levels of insulin to control the blood sugar level, over time the body becomes resistant causing your blood sugar levels to increase(4)
    Similarly, in hyperleptinimia the hypothalamus quits responding to the chronic output of Leptin by the fat tissue (14)
    It creates a vicious cycle- your hunger continues so you eat more, which creates more fat, which creates more Leptin, but the hypothalamus can’t recognize it so your appetite continues
  • ANOTHER MOLECULE SECRETED BY FAT
    Adiponectin is a protein released by fat tissue
    This protein hasanti-inflammatory properties and it helps maintain the body’s sensitivity to insulin (15)
    Unlike Leptin, as fat tissue grows it secretes less Adiponectin
    A drop in Adiponectin is thus thought to increase our chances of type 2 diabetes (16)
    A picture of Apidtonectin provided by yahoo images
  • WHAT ROLE DOES GENETICS PLAY?
    Some of the genetic factors for obesity are:
    Human Obesity Gene- There are a reported 22 genes which can contribute to obesity (12)
    Leptin Deficiencies- Leptin deficiencies occur when a person fails to produce a normal amount of Leptin
    One specific disease is called Congenital Leptin Deficiency in which a person is born without the ability to produce Leptin. This genetic malady causes severe early-onset obesity (6)
    Melanocortin-4 Receptor- this is a genetic receptor vital in the role of regulating appetite in the hypothalamus. Genetic mutations in this gene can be a significant factor in obesity (9)
    Proopiomelanocortin (POMC)- POMC is a protein pre-cursor with several functions. One of the functions is to regulate how and when our body burns fat. A genetic mutation in this protein could also contribute to obesity (11)
  • SO IT’S GENETICS, NOT ME
    While is would be convenient to blame our obesity problems on genetics, the fact is that obesity has only become a problem in the last 30 years
    So the more likely probability is that these genetic variations are quite rare and probably contribute to only a very small population of obese Americans
    "Despite obesity having strong genetic determinants, the genetic composition of the population does not change rapidly. Therefore, the large increase in . . . [obesity] must reflect major changes in non-genetic factors.“ (Hill, James O., and Trowbridge, Frederick L. Childhood obesity: future directions and research priorities. Pediatrics. 1998; Supplement: 571)
  • WHAT ABOUT MEDICAL PROBLEMS?
    Hypothyroidism: Known as an underactive thyroid which fails to produce normal levels of certain hormones. Most common in women over the age of 50, obesity can be one of its affects (8)
    Hypothalamus abnormalities: Because we already know that the hypothalamus is a central figure in regulating our appetite, abnormalities within this brain structure might cause obesity
    Cushing’s Sydrome: Caused by abnormally high levels of cortisol.This syndrome is characterized by a fatty hump between the shoulders and a rounded face (5)
    Prader-Willi Syndrome: This is a rare syndrome is present at birth. Just one of the many problems associated with this syndrome is an uncontrollable hunger which does not go away (10)
  • SO MAYBE I HAVE A MEDICAL PROBLEM
    In such a short amount of time it is also unlikely that a majority of the population suffers from an obesity related disease
    Luckily, for those who do suffer from these diseases, many of them are easily treated
    The cause of obesity for most people is an over abundance of calories, and the only cure is to decrease the number of calories consumed
    However, if you do suspect that you might suffer from one of these diseases, either genetic or medical, it is extremely important to seek medical help right away
    Please remember to consult your doctor before starting any diet program
  • REFERENCES
    (1) Leptin. (n.d.). Retrieved October 18, 2010, from http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/bodyweight/leptin.html
    (2) Albright, A. L., & Stern, J. S. (n.d.). Adipose Tissue. Retrieved October 18, 2010, from Encyclopedia of Sports Medicine and Science: http://www.sportsci.org/encyc/adipose/adipose.html
    (3) Calculate Your Body Mass Index. (n.d.). Retrieved October 18, 2010, from National Heart Lunch and Blood Institute: http://www.nhlbisupport.com/bmi/
    (4) Causes of Type 2 Diabetes. (n.d.). Retrieved October 19, 2010, from WebMD: http://diabetes.webmd.com/guide/diabetes-causes
    (5) Cushing's Syndrome: Definition. (2010, September 11). Retrieved October 18, 2010, from MayoClinic.com: http://www.mayoclinic.com/health/cushings-syndrome/DS00470
    (6) Gibson, W. T., Farooqi, I. S., Moreau, M., DePaoli, A. M., Lawrence, E., O'Rahilly, S., et al. (2004). Congenital Leptin Deficiency Due to Homozygosity for the Delta133G Mutation: Report of Another Case and Evaluation of Response to Four Years of Leptin Therapy [Electronic Version]. The Journal of Clinical Endocrinology and Metabolism, 89 (10), 4821-4826.
    (7) Hill, James O., and Trowbridge, Frederick L. Childhood obesity: future directions and research priorities. Pediatrics. 1998; Supplement: 571
    (8) Hypothyroidism (underactive thyroid): Definition. (2010, June 12). Retrieved October 18, 2010, from MaycoClinic.com: http://www.mayoclinic.com/health/hypothyroidism/DS00353
  • REFERENCES (cont.)
    (9) Mohan, C., & Agarwal, A. K. (2009). Melanocrotin-4-Receptor Autoantibodies: A New Player in Obesity [Electronic Version]. The Journal of Clinical Endocrinology and Metabolism, 94 (3), 757-759.
    (10) Prader-WilliSyndrome: Definition. (2009, April 22). Retrieved October 18, 2010, from MayoClinic.com: http://www.mayoclinic.com/health/prader-willi-syndrome/DS00922
    (11) Raffin-Sanson, M., Keyzer, Y. d., & Bertagna, X. (2003). Proopiomelanocortin, a polypeptide precursor with multiple functions: from physiology to pathological conditions [Electronic Version]. European Journal of Endocrinology, 149(2), 79-90.
    (12) Rankinen, T., Zuberi, A., Chagnon, Y., Weisnagel, S., Argyropoulos, G., Walts, B., et al. (2006, April 14). The human obesity gene map: the 2005 update [Electronic Version]. Obesity (Silver Spring, MD), 529-644.
    (13) Sahu, A. (2003, December 24). Leptin Signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance [Electronic Version]. Frontiers in Nueroendocrinology, 225-253.
    (14) Sahu, A. (2004). Minireview: A Hypothalamic Role in Energy Balance with Special Emphasis on Leptin [Electronic Version]. Endocrinology, 145(6), 2613-2620.
    (15) Shanshan, L., Shin, H. J., Ding, E. L., & van Dam, R. M. (2009). Adiponectin Levels and Risk of Type 2 Diabetes [Electronic Version] . The Journal of the American Medical Association, 302 (2), 179-188.