Hormonal leptin insulin Pyy Ghrelin Neural Proopiomelanocortin neuropeptide Y agouti-related protein

1. Etiology of Obesity
Neural and Hormonal
By mahdi saleh

2. Introduction

3. Neural and Hormonal cause of obesity
Hormonal
leptin
insulin
Pyy
Ghrelin
Neural
Proopiomelanoc
ortin
neuropeptide Y
agouti-related
protein

5. Neural and Hormonal cause of obesity

6. -a 16-kD hormone
-synthesized by fat cells, is the product of the
ob gene.
-The leptin receptor (OB-R) belongs to the type
I cytokine receptor
-deficient in leptin or leptin receptors fail to
sense the adequacy of fat stores, overeat,
and gain weight, behaving as if they are
undernourished.
Leptin

7. LeptinLeptin
Fat cellsSecreting cell
HypothalamusTarget
long-term regulation
of energy balance
Function
IL-6 type
glycoprotein 130
cytokine receptor
Receptor

8. Leptin
Eat
Fat store
leptin
Hypothalamus
Stop eating

9. Leptin

11. When the brain doesn’t receive the leptin
signal, it erroneously thinks that the body is
starving, even though it has more than
enough energy stored.
This makes the brain change our physiology
and behavior in order to regain the fat that
the brain thinks we’re missing
Eating More
Reduced Energy Expenditure
Leptin

12. Eating More: The brain thinks
that we MUST eat so that
we don’t starve to death.
Reduced Energy Expenditure:
The brain thinks we need to
conserve energy, so it makes us
feel lazier and makes us burn
fewer calories at rest.
Leptin

13. In this way… eating more and exercising less is not the cause of
weight gain, it is the consequence of leptin resistance, a hormonal
defect .
For the great majority of people, trying to exert cognitive inhibition
(willpower) over the leptin-driven starvation signal is next to
impossible.
Leptin

14. Ghrelin is produced in the stomach and in the arcuate
nucleus of the hypothalamus. It is the only known gut
hormone that increases food intake (orexigenic effect).
Ghrelin

15. Its injection in rodents elicits voracious feeding, even after
repeated administration.
Long-term injections cause weight gain, by increasing
caloric intake and reducing energy utilization.
Ghrelin

16. Ghrelin acts by binding the growth hormone secretagogue
receptor, which is abundant in the hypothalamus and
the pituitary. Although the precise mechanisms of
ghrelin action have not been identified, it most likely
stimulates NPY/AgRP neurons to increase food intake.
Ghrelin levels rise before meals and fall between 1 and 2
hours after eating.
In obese individuals the postprandial suppression of
ghrelin is attenuated and may contribute to overeating.
Ghrelin

17. LeptinGhrelin
endocrine cells in the
gastrointestinal mucosa
Secreting cell
HypothalamusTarget
growth hormone
release, feeding
behavior, glucose
metabolism, memory,
and also antidepressant
effects,
Function

19. PYY is secreted from endocrine cells in the ileum and
colon. Plasma levels of PYY are low during fasting and
increase shortly after food intake.
Intravenous administration of PYY reduces energy intake,
and its levels generally increase after gastric bypass
surgery.
By contrast, levels of PYY generally decrease in
individuals with the Prader-Willi syndrome (caused by
loss of imprinted genes on chromosome), a disorder
marked by hyperphagia and obesity.
These observations have led to ongoing work to produce
PYYs for the treatment of obesity.
PYY

20. LeptinPYY
L-cells in the small
intestine
Secreting cell
HypothalamusTarget
decreased appetite
and make people
feel full after eating
Function
receptors in the
Brain
Receptor

22. For more information
Chapter 9 : Environmental and Nutritional Diseases
P444-448
Chapter 72 Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitamins and Minerals
P889-900
Chapter 17 Energy Balance and Temperature Regulation
9621-624