This document discusses obesity and excess body fat. It defines different types of fat, such as white and brown fat, and explains their functions. White fat provides insulation and energy storage. Excess white fat can become unhealthy and lead to obesity. Obesity is linked to many health issues and is defined using BMI scores. The document explores how hormones like leptin and adiponectin regulate appetite and insulin sensitivity. Genetics and medical conditions can also play a role in obesity for some individuals. Overall, the leading cause of obesity for most people is consuming more calories than are burned through physical activity.

1. W E A L L K N O W I T ’ S A P R O B L E M , B U T W H A T
D O E S I T D O T O O U R B O D I E S ?
Obesity

2. 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: http://www.linkpublishing.com/video-cell.htm
Photo by: clcpages.clcillinois.edu

3. 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

4. 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 store energy, it can
be accessed quickly when needed(2)
Picture provided by Microsoft
Clipart

5. 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
 It does not take into account weight that is caused by muscle so
weight lifters might appear to overweight when they are not
 To figure out your BMI you can go to
www.nhlbisupport.com/bmi/
Underweight BMI: <18.5
Normal BMI: 18.5-24.5
Overweight BMI: 25-29.9
Obese BMI: > 30 (2)

6. 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
 So theoretically your body should be helping to regulate
your appetite

7. 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

8. 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)

9. 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

10. ANOTHER MOLECULE SECRETED BY FAT
 Adiponectin is a protein released by fat tissue
 This protein has anti-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

11. 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)

12. 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)

13. 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)

14. 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

15. 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

16. 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-Willi Syndrome: 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.