This document discusses pathophysiology of food intake and obesity. It covers neuroendocrine regulation of appetite, factors influencing food intake like hormones and metabolism. Obesity is defined using Body Mass Index and its complications are explained. Leptin's role in obesity is discussed along with theories on leptin resistance. Inflammation in adipose tissue of obese individuals and alterations in appetite-regulating gut hormones are also covered. The document concludes by discussing anorexia nervosa and potential biotechnological approaches for treating obesity and increasing omega-3 fatty acids.

1. Pathophysiology of food intake : Obesity.
& Biotechnological approaches in cure
GAURAV KUMAR PANDIT
SCHOOL OF LIFE SCIENCE
UNIVERSITY OF HYDERABAD
gauravbiologist@uohyd.ac.in

2. Pathophysiology
anorexia nervosa
Obesity
Cancer anorexia
neuroendocrine regulation of food intake
 central regulation of food intake –hypothalamus, neurohormones
 short- and long-term peripheral regulation of satiation and
energy balance
- GIT hormones (ghrelin)
- Adipose tissue hormones (leptin)
- Pancreatic hormones (insulin)

4. The physiological regulation of food intake
is a complex homeostatic process that is
regulated by many factor such as
 endocrine factor
 metabolic factors &
 combination with
 visual,
 olfactory,
 emotions,
 taste sensation,
 and the life conditions

6. Our prehistorical progenitors clearly did not have the
opportunity to suffer either from obesity or anorexia
nervosa

7. 2.5 milion of years 50 years
The progression of mankind development

8. Obesity is classified by
Body Mass Index (BMI)
Weight (kg)
Height (m2)
WHO, 1998
Classification BMI (kg/m2) Metabolic c.
Normal weight 18.524.9 average
Overweight 2529.9 increased
Obesity I 30.034.9 middle
Obesity II 35.039.9 high
Obesity III 40.0 Very high
BMI =

9. Complications of obesity
Mechanical
joint illness, dyspnoe, sleeping
apnoe, heart hypetrophy,…..
Metabolic
diabetes, hypertension,
hyperlipoproteinemia, ischemic heart
disease, ictus, tumours, sterility,
depression,…..
= Reaven metabolic syndrome

10. Leptin and obesity
 Leptin deficiency is not epidemiologically
significant cause of obesity (3 cases of leptin-
gene mutation in humans accompanied by morbid
obesity)
 Most of obese patients have hyperleptinemia i.e.
circulating leptin levels correlate with body fat
content
 Body weight loss induces decrease in circulating
leptin levels

11. Why hyperleptinemia does not
suppress food intake in patients
with obesity?
Resistance to leptin effects: either on the
levels of leptin transport across the blood-
brain barrier or on the postreceptor level
Primary leptin function is not to suppress
food intake, but to trigger complex
adaptive reaction of human body to
starvation.

12. Obesity is accompanied by local
inflammatory response in adipose
tissue

13. Obesity and GIT hormones
Decreased satiety perception
represents an important risk factor
for the development of obesity
Alterations in hormonal responses to
food intake contribute to decrease
satiety in obese .

14. Food fails to suppress ghrelin
in obese
English et al. 2002
Postprandial ghrelin response in obese is (in
contrast to healthy subjects) independent of
caloric content and macronutrient composition of
a meal
Contribution to resistance to weight loss in some
of obese patients.

15. People come in all weights and sizes. Some eat
but never gain a pound and others seem to gain
weight by looking at a piece of pizza. So what
causes some people to be overweight?

16.  Obesity is on the rise worldwide. Every year,
nearly 3 million people die of causes related to
being overweight, victims of the lengthy lists of
complications that can come with being obese—
heart disease, stroke, and diabetes among them.
Data on obesity from around the world are
worrisome, but a number of new treatments are
already helping patients control their weight..

17. Gene for Obesity
Two new papers in the journal Nature describe
the results of New genes identified in obesity.
Study identified four new Genetic marker
severe childhood obesity.
How much of weight is Genetics?

18.  The ideal anti-obesity drug would produce
sustained weight loss with minimal side effects.
The mechanisms that regulate energy balance
have substantial built-in redundancy, overlap
considerably with other physiological functions,
A Question about Leptin Researchers have found
that some obese individuals have high levels of
leptin, while some other obese individuals have low
levels of leptin. Based on what you know about this
protein, how do you think both of these situations
could result in obesity? An Internet or literature
search can help you find additional answers.

19. Biotechnological approach.
Bioengineering Healthier Food Fish are rich in
omega-3 fatty acids, which are increasingly
recognized as a “superfood” that appears to
boost everything from heart health to mood.
Unfortunately, many of the fish rich in omega-
3s are either quickly disappearing from the
oceans or contain worrisome levels of mercury,
or both.

20. .
C. elegans. The Caenorhabditis elegans
nematode worm is a soil-dwelling bisexual
organism. One of its enzymes can help
mammals produce healthful omega-3 fatty
acids.
insert a gene for an enzyme found in C.
elegans into mammalian cells that lack the
enzyme to convert omega-6 fatty acids
into omega-3 fatty acids
Biotechnological approach

21. More slim and more fit means more
success and beauty……..
……….. but sometimes this motto of
modern societies leads to death

22. Anorexia Nervosa (AN)
 Severe psychiatric disorder of unclear
etiology associated with significant
morbidity and mortality .
 Prevalence 0.3% of young girls, mortalty
of 6%/decade.
 Irrational fear of becoming fat even if
patient is of normal or usually
underweight.
 Phobic response to food, abnormal eating
behavior, hyperactivity, weakness,
muscle aches, sleep disturbances, GIT
complications, mood disturances,
alterations of wide variety of hormonal
and metabolic systems.
 Combination of cultural-social,
psychological, biological factors.

23. School of Life Sciences
University of Hyderabad