Physiological Aspects in Relation with Obesity discusses various topics related to obesity including: - Meda dhatu, the physiological tissue responsible for fat storage and metabolism. - Hunger and appetite regulation controlled by the hypothalamus and various hormones. - An overview of energy metabolism including glycolysis, gluconeogenesis, and the citric acid cycle. - Components of energy expenditure including basal metabolic rate, the thermic effect of food, and physical activity.

2. Physiological
Aspects In
Relation With
Obesity
By;
Dr. Christy Jose Cherian
Assistant Professor
JSS AMC Mysore

3. CONTENTS
Meda dhatu
Hunger & regulation
Overview of energy metabolism
Energy expenditure
Storage of excess energy
Conclusion

4. MEDA DHATU
 मेदयति स्निह्यति अिेि इति मेदः ।
It is one among sapta dhatu and it smoothen the body by its Sneha Property
Utpatti:
Medodhatu is formed when the suksmabhaga of mamsa Dhatu, acted upon by
Medodhatvagni. The jaliya guna present in Medas facilitates increase in
sneha guṇa. Mamsa dhatu undergoes paka due to its agni and jala guna and
forms Medodhatu
 There are 2 types of Medodhatu.
 1. Poshaka Medodhatu 2. Poshya Medodhatu
Poshaka Medodhatu is gatiyukta, which is circulated in the whole body along
with Rasa, Rakta dhatu, to give the nourishment to Poshya Medodhatu.
Poshya Medodhatu is Gativivarjita, and its storage is done in Udara, Sphik,
Sthana etc . Medodhatu is a sneha dominant Drava dhatu which is Guru,
Snigdha guna yukta and has dominance of Pruthvi, Apa and Teja
Mahabootha

5.  Karma of Meda Dhatu
 मेढः स्नेहस्वेदौ दृढत्वं पुष्टिमस्थननं च |सु.सु.15/5
 निेहः (मेदसः श्रेष्ठं कमम ) | अ.हृ.सु.11/
The main functions of Meda dhatu are Snehana, Sweda, Drudhatva, Asthipusti and Netra, Gatra,
Snigdhata.
मेदसः स्ननयुसम्भव च.चच.15/17
Snayu is the Upadhatu of Meda
 स्वेदस्तु मेदसः मलः |च.चच.15/18
 Sweda is the Mala of Medo Dhatu
Medovaha Srotas:
 मेदोवहे वे ियोमममलं किी वृक्कौ च | सु.शा.9/12
 मेदोवहािां सोिसां वृक्को मूलं वपनपहनं च | च.वव.5/10
The channels, which give nutrition to the Medodhatu or the vessels carrying the nutritive material
up to the site of Medodhatu can be considered as Medovahasrotas. As an opinion of various
authors, it can be correlated with capillaries-of perinephric tissue or omentum etc

6. Medosara purusha lakshana:
 वर्मनवरिेत्रके शलोमिखदंिौष्ठममत्रपुरीषेषु ववशेषिः निेहो मेदःसारार्ाम् ।
सा सारिा ववत्तेच्र्यसुखोपभोगप्रदािान्यार्मवं सुकु मारोपचारिां चाचष्टे । च.वव. ८/१०६
 स्निग्धममत्रिेत्रनवरं बृहच्छरीरमायासासहहष्र्ुं मेदसा । सु.सम. ३५/१६
 Excess snehamsha in Varna, Svara, Netra, Kaksha, Loma, Nakha, Danta, Oshta,
Mutra and Purisha. The person will have Dhana, Aishvarya, Sukha, Upabhoga. He
will be Danashila, Sarala, Komala .
 Medodhatu Vridhi Lakshana:
 िदवन्मेदनिथा श्रमम अल्पेऽवप चेस्ष्टिे श्वासं स्निकनििोदरलम्बिम् |AH;SU 11
 (मांसं गण्डायुमदग्रस्न्थगण्डोरूदरवृस्ददिाः | कण्ठाचधष्वचधमांसं च |अ.हृ.सु.11/10)
Medodhatu vridhi causes snigdhata of shareera, udara, sthana, parshva vridhi, shwasa,
daurgandhata of shareera.

7. HUNGER AND SATIETY
Hunger and satiety are sensations.
Hunger is the painful sensation caused by lack of food that
initiates food-seeking behaviour
Satiety is the absence of hunger, satiation: is the feeling of
satisfaction and fullness that occurs during a meal and leads to
stop eating. Satiation determines how much food is consumed
during a meal. satisfaction that occurs after a meal and inhibits
eating until the next meal. Satiety determines how much time
passes between meals.
Appetite is another sensation experienced with eating , it is an
integrated response to the sight, smell, thought, or taste of
food that initiates or delays eating.

8. PHYSIOLOGY OF APPETITE AND HUNGER
REGULATION OF FOOD INTAKE
Physiological influences of hunger
Empty stomach, Gastric contractions, Absence of nutrients in small intestine GI, Hormones such
as Ghrelin, Leptin, Cholecystokinin, Endorphins, insulin, etc .
Sensory influences on appetite
Thought, sight,colour smell, sound, taste of food.
Cognitive influences on appetite
Presence of others, social stimulation, Favorite foods, foods with special meanings Time of day,
Abundance of available food

9. NEURAL CENTER FOR
REGULATION OF FOOD INTAKE
 Feeding center - lateral nucleus of the hypothalamic
 Satiety center - Ventromedial nucleus of the hypothalamus.
 Controlling center - Arcuate nucleus of the hypothalamus
 Limbic cortex
 Frontal cortex
Feeding center inhibited by satiety center and arcuate nucleus controls satiety
center by secreting stimulatory as well as inhibitory substance , are of
two type
1.Orexigenic(Neuropeptide Y ,Orexin A, B) increasing the food intake
2.Anorexigenic (MCH,CART,AGRP) decreasing food intake

10. CHEMICAL MEDIATORS WHICH
CONTROL FOOD INTAKE
INTRA HYPOTHALAMIC EXTRA HYPOTHALMIC
OREXIGENIC ANOREXIGENI
C
OREXIGENIC ANOREXIGENIC
NEUROPEPTIDEY
OREXIN A, B
AgRP,
MSH
CART
CRH
CCK
GHRELIN
(Stomach)
LEPTIN (Adipose )
ACTH (Ant .Pituitary)
CORTISOL,
CATACHOLMINES(Adrenal)
GRP CCK,MOTILIN (Gut)
Glucagon, GLP -1 (Pancreas)
They released in the blood and through median eminence (which
remain outside the blood brain barrier )reach Arcuate nucleus and
control the food intake

11. MECHANISM OF REGULATION OF
FOOD INTAKE
Glucostatic mechanism
 Lipostatic mechanism
Gut- Peptide & Hormonal mechanism
Thermostatic mechanism.

12. GLUCOSTATIC MECHANISM
Cells of satiety center function as glucostats or glucose
receptors, which are stimulated by increased blood
glucose level. While taking food, blood glucose level
increases. Slowly the glucostats are stimulated &satiety
center is activated & inhibits the feeding center and stops
the food intake.
However, glucostats do not give response to very high
level of glucose in blood (hyperglycemia).So the satiety
center does not inhibit the feeding center, so the frequency
of food intake increases (polyphagia).

13. LIPOSTATIC MECHANISM
Leptin is a peptide secreted by adipocytes .When the volume of adipose tissues
increases, adipocytes secrete and release a large quantity of leptin into the
blood. In hypothalamus, leptin inhibits the feeding center, resulting in loss of
appetite and stoppage of food intake.
 Mode of action of leptin
Leptin acts through some specific neuropeptides in hypothalamus, such as:
Neuropeptide Y: It is secreted in small intestine, medulla and hypothalamus.
Normally, this peptide stimulates the food intake. But, leptin inhibits
neuropeptide Y, leading to stoppage of food intake.
 Pro-opiomelanocortin (POMC): It is secreted from anterior pituitary. It is also
secreted from hypothalamus, lungs, GI tract and placenta. Normally, it inhibits
food intake. Leptin stimulates the secretion of POMC.
 Leptin receptor -Many leptin receptors are identified. However, leptin acts via
‘LepRb’, which is the only active receptor present in many nuclei of
hypothalamus.

14. GUT - PEPTIDE MECHANISM
Peptides regulate the food intake either by stimulating or
inhibiting the feeding center, directly or indirectly
Ghrelin is secreted in stomach during fasting. It directly stimulates
the feeding center and increases the appetite and food intake.
Besides ghrelin, several other peptides are involved in the
regulation of food intake.
Peptides, which increase the food intake:
a. Ghrelin b. Neuropeptide Y.
Peptides, which decrease the food intake:
a. Leptin b. Peptide YY.

15. HORMONAL MECHANISM
Endocrine hormones and GI hormones inhibit the food
intake by acting through hypothalamus.
Hormones which stimulate the food intake Ghrelin,
NeuropeptideY, galanin ,Dynomorphin, Norepinephrine,B-
endorphin
 Hormones which inhibit the food intake: Somatostatin,
Oxytocin ,Glucagon, Pancreatic polypeptide,
Cholecystokinin.

16. THERMOSTATIC MECHANISM
Food intake is inversely proportional to body
temperature. So in fever, the food intake is decreased.
Exact mechanism of this fact is not known. It is suggested
that the preoptic thermoreceptors may act via feeding center.
The cytokines are also suggested to play a role in decreasing
the appetite during fever.
When we are fasting our temperature decreases slightly
this is sensed by posterior hypothalamus which stimulate
lateral hypothalamus & food intake increase

17. REGULATIONN OF BODY WEIGHT AND
OBESITY
LONG TERM REGULATION –LEPTIN
SHORT TERM REGULAION - MEAL SIZE
REGULATION (Glucostatic , Gut- Peptide )

18. OVERVIEW OF ENERGY METABOLISM
Stage 1
Break down of complex
molecule into simple ones
Stage 2
Formation of Acetyl coenzyme A
Stage 3
Acetyl coenzyme A enter into
kerb cycle undergo oxidation &
leads to the production of
energy along with co2 and H20

19. OVERVIEW OF WELL FED
STATE

20. OVERVIEW OF STARVING
STATE

21.  GLYCOLYSIS -the catabolism of carbohydrates, as glucose and glycogen, by
enzymes, with the release of energy and the production of lactic or pyruvic acid.
 GLYCOGENOLYSIS- process by which glycogen, the primary carbohydrate
stored in the liver and muscle cells , is broken down into glucose to provide
immediate energy and to maintain blood glucose levels during fasting.
 GLYCOGENISIS -the synthesis of glycogen from glucose that occurs chiefly in
the liver and skeletal muscle
 GLUCONEOGENESIS - is a metabolic pathway that results in the generation
of glucose From breakdown of proteins, Lipids such as triglycerides
,glycerol,& from other substrates like pyruvate etc.
 LINK REACTION -Pyruvate is decarboxylated: CO2 is removed It is added
to CoA to form Acetyl CoA, takes place only inside the mitochondrial matrix.

22. ELECTRON TRANSPORT CHAIN- The electron transport chain is a
series of electron transporters embedded in the inner mitochondrial
membrane that shuttles electrons from NADH and FADH2 to molecular
oxygen. In the process, protons are pumped from the mitochondrial
matrix to the inter membrane space, and oxygen is reduced to form water.
THE CITRIC ACID CYCLE /TCA CYCLE / KREBS CYCLE – is a
series of chemical reactions used by all aerobic organisms to release
stored energy through the oxidation of acetyl-CoA derived from
carbohydrates, fats, and proteins, into adenosine triphosphate and carbon
dioxide
 The Cori cycle in which lactate produced by anaerobic glycolysis in the
muscles moves to the liver and is converted to glucose.

23. ENERGY EXPENDITURE
Components Of Energy Expenditure
Basal Metabolic Rate (BMR):
The Thermic Effect Of Food (TEF)
 Physical Activity:

24. BASAL METABOLIC RATE (BMR)
 Basal or resting metabolic rate (BMR or RMR) is the amount of
energy per minute the body uses to maintain a quiet resting state.
 This is approximately 1 Cal per minute. Over the course of the day
(and night), a person will expend a substantial amount of calories
just to maintain the body (1440 minutes in a day x 1 Cal/min = 1440
Cal per day).
 Approximately 60% to 75% of the energy used every day is needed
to maintain the essential body functions that sustain life. These
functions include nervous system activity, breathing, heart
function, maintenance of body temperature (thermoregulation),
and hormone activity.

25. FACTORS THAT INFLUENCE
BASAL METABOLIC RATE
 Age: metabolism slows with age (2% to 3% per decade after 30 years of
age), primarily due to a loss in muscle tissue due to inactivity, but also
due to hormonal and neurological changes.
 Gender: generally, men have a faster metabolism than women because
they tend to be larger and have more muscle tissue.
 Body size: larger adult bodies have more metabolically active tissue,
which leads to a higher BMR/RMR.
 Body composition: muscle tissue uses more calories than fat, even at rest.
 Genetic predisposition: metabolic rate may be partly determined by genes.

26. (contd).
Growth: Infants and children have a higher BMR/RMR
related to the energy needs of growth and maintenance of
body temperature.
 Hormonal and nervous controls: Hormonal imbalances can
influence how quickly or how slowly the body burns calories.
 Environmental temperature: If temperature is very low or
very high, the body has to work harder to maintain a normal
temperature; this increases the BMR/RMR.
Infection or illness: BMR/RMR increases if the body has to
build new tissue or create an immune response to fight
infection.

27. Factors that influence basal
metabolic rate contd....
Crash dieting, Starving, or Fasting: Eating too few calories
encourages the body to conserve through a potentially significant
decrease in BMR/RMR. There can also be a loss of lean muscle
tissue, which further contributes to reducing BMR/RMR.
Physical activity: Hard-working muscles require extra energy
during activity. Regular exercise increases muscle mass, which
increases energy consumption, even at rest.
 Stimulants: Use of stimulants (e.g., caffeine) increases energy
expenditure at rest. However, this is not a healthy way to lose
weight.

28. THE THERMIC EFFECT OF FOOD
(TEF)
Thermic effect of food (TEF) is the energy required to
process the food we eat.
Approximately 10% of the calories in a meal are used to
digest, metabolize, and store the food just eaten.
 The energy expenditure is directly related to the size of the
meal and the food composition (i.e., the amount of protein,
fat, and carbohydrate).
Carbohydrates: 5 to 15% of the energy consumed
Protein: 20 to 35%
Fats: at most 5 to 15%

29. PHYSICAL ACTIVITY:
Physical activity is defined as any bodily movement produced by
skeletal muscles that results in energy expenditure.
 The US Dept of Health and Human Services and guidelines which
include:
 1) 30 minutes of moderately intense daily physical activity may be
effective in cardiovascular risk reduction,
 2) 60 minutes of moderate to vigorous daily physical activity may be
effective in the prevention of weight gain,
 3) 60-90 minutes of moderate daily physical activity may be effective
in sustaining weight loss

30. High intensity exercise reduces ghrelin levels and transient rises in
GLP-1 blood levels in both obese and normal weight individuals reduce
energy intake in obese and normal weight subjects.
 High intensity exercise increase gut peptide hormones (cholecystokinin,
amylin,) exert their anorexigenic effects in hypothalamus.
 The body likewise uses carbohydrate and glycogen stores as its primary fuel
source during the initial 20 minutes. After 20 minutes of constant movement,
the body starts to burn body fat to power the muscles and body. This is known
as "aerobic fat-burning."
 Aerobic exercise increases your endurance and cardiac health
 Anaerobic exercise will not only help you burn fat but also help you gain lean
muscle mass and that increase ur RMR there by prevent regaining of weight .

31. CLASSIFICATION OF LIPIDS
 Dietary fats are classified into two types:
1. Saturated fats 2. Unsaturated fats
 SATURATED FATS- The fatty acids having maximum amount of hydrogen
ions without any double bonds between carbon atoms are called saturated
fatty acids.
 Unsaturated fats are classified into three types:
1. Monounsaturated fats -
2. Polyunsaturated fats
3. Trans fats.
 MONOUNSATURATED FATS- Unsaturated fats which contain one
double bond between the carbon atoms are called monounsaturated fats

32.  Polyunsaturated Fats Unsaturated fats with more than one double bond
between the carbon atoms are called polyunsaturated fats. Polyunsaturated fats
belong to the family of essential fatty acids (fatty acids required in diet).
 Polyunsaturated fats are of two types:
 1. Omega-3 fats or omega3 fatty acids having double bond in the third space
from the end of the carbon chain
 2. Omega-6 fats or omega6 fatty acids having double bond in the sixth space
from the end of the carbon chain
 Trans fat is a fat (lipid) molecule that contains one or more double bonds
in trans geometric configuration. ... In trans configuration, the carbon chain
extends from opposite sides of the double bond

33. ROLE OF ADIPOSE IN OBESITY
Adipose, or fat, tissue is loose connective tissue composed
of fat cells known as adipocytes.
Adipocytes contain lipid droplets of stored triglycerides.
These cells swell as they store fat and shrink when the fat
is used for energy.
There are three types of adipose tissue: white, brown, and
beige adipose.
White adipose stores energy and helps to insulate the
body.
Brown and beige adipose tissue burn energy and generate
heat. Their colour is derived from the abundance of blood
vessels and mitochondria in the tissue.

34. Role of adipose adipose tissue in obesity (contd)
 Adipocytes form an extensive amount of peptide hormones known
as adipokines (or adipocytokines).
 In general, they mainly regulate the energy metabolism and their
effect on appetite and feeding behaviour influences a long-term
regulation of the body weight.
 Leptin-which inhibit appetite, reduce the mass of the adipose tissue
and increase the amount of energy expenditure which results in the
loss of body mass. It inhibition of lipogenesis, stimulation of lipose,
and an increase of oxidation of fatty acids

35. CONTD …..
Adiponectin increases insulin sensitivity of tissues. Secretion of
the hormone increases with reduction of body mass and decreases in
the case of obesity.
 Resistin - reduce insulin sensitivity of tissues activates insulin
resistance, and acts as a proinflammatory factor by increasing
production of TNF, IL 1, IL 6, and IL 12 & leads to obesity
 Visfatin - stimulates insulin secretion and increases insulin
sensitivity and glucose uptake by muscle cells and adipocytes &
produce obesity

36. LIPO PROTEINS
A lipoprotein is a biochemical assembly that contains both proteins and
lipids , bound to the proteins , which allow fats to move through the
water inside and outside cells
TYPES AND FUNCTIONS
VLDL- Transports triglycerides from liver to adipose tissue
LDL- are the principal cholesterol and fat transporter in human blood
that carries cholesterol from the liver to the body tissues and cells.
 IDL-Transports triglycerides, cholesterol and phospholipids from liver
to peripheral tissues
HDL- Transports cholesterol and phospholipids from tissues and organs
like heart back to liver

37. ROLE OF ENOCRINE SYSTEM IN
OBESITY
ACTIONS OF INSULIN
Facilitating transport and uptake of glucose by the cells,
 Increasing the peripheral utilization of glucose,
 Increasing the storage of glucose by converting it into glycogen in
liver and muscle,
Inhibiting glycogenolysis, Inhibiting gluconeogenesis
Preventing conversion of proteins into glucose,
 Synthesis of fatty acids and triglycerides,
Transport of fatty acids into adipose

38. ACTIONS OF GLUCAGON
Facilitating glucose transport into liver cells
 Increasing glycogenolysis
 Increasing gluconeogenesis
Increases utilization of amino acids for ENERGY
Increases lipolysis

39. ACTIONS OF THYROID
HORMONES
 It increases BMR by increasing the oxygen consumption of the tissues. The
action that increases the BMR is called calorigenic action
 Increases the absorption of glucose from GI tract ,Enhances the glucose
uptake by the cells, by accelerating the transport of glucose through the cell
membrane, increases the breakdown of glycogen into glucose Accelerates
gluconeogenesis.
 Thyroxine decreases the fat storage by mobilizing it from adipose tissues and
fat depots. The mobilized fat is converted into free fatty acid and transported
by blood.
 Thyroxine increases synthesis of protein but it also causes catabolism of
proteins.

40. ACTIONS OF GROWTH
HORMONE
growth hormone stimulates protein anabolism in many tissues.
This effect reflects increased amino acid uptake, increased
protein synthesis and decreased oxidation of proteins.
Fat metabolism: Growth hormone enhances the utilization of
fat by stimulating triglyceride breakdown and oxidation in
adipocytes.
Carbohydrate metabolism: it supresses the abilities of
insulin to stimulate uptake of glucose in peripheral tissues and
enhance glucose synthesis in the liver.

41. ACTIONS OF GLUCOCORTICOIDS
By promoting gluconeogenesis in liver from amino acids:
Glucocorticoids enhance the breakdown of proteins in
extrahepatic cells, particularly the muscle. It is followed by
release of amino acids into circulation. From blood, amino acids
enter the liver and get converted into glucose (gluconeogenesis)
 Glucocorticoids cause mobilization of proteins from tissues other
than liver. Mobilization of fatty acids from adipose tissue
Increasing the concentration of fatty acids in blood , Increasing
the utilization of fat for energy.
It stimulate Calorigenic effect of glucagon ii. Lipolytic effect of
catecholamines

42. ACTIONS OF CATECHOLAMINE'S
Adrenaline increases the blood glucose level by increasing
the glycogenolysis in liver and muscle. So, a large quantity
of glucose enters the circulation
 Adrenaline causes mobilization of free fatty acids from
adipose tissues.

43. ACTIONS OF SEX HORMONES
Estrogen induces anabolism of proteins, by which it
increases the total body protein.
On fat metabolism Estrogen causes deposition of fat in the
subcutaneous tissues, breasts, buttocks and thighs.
progesterone favour the storage of tfat in adipose and
breast tissue
Testosterone it increase the anabolism of protein ,it
increase basl metabolic rate , it increase the mobilisation
of fat

44. HORMONE - FAT DISRIBUTION
Back of the hips - elevated insulin levels.
Thighs - elevated estrogen level
Back of arms - Low testosterone levels and elevated insulin
level
Stomach- elevated oestrogen, insulin and cortisol
Upper back fat- high level of insulin & low level of
thyroxine
Cankles - high level of insulin & low level of growth
hormone

45. CONCLUSION
Overconsumption of calorie-dense foods is one significant
causal factor in obesity, which may provoke the food
addiction mechanism.
 Obesity may result from a combination of dysfunction of
brain circuits and neuroendocrine hormones.
It leads to pathological overeating, physical inactivity and
other patho-physiological conditions which leads to obesity.