Etiology of obesity
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Transcript of Etiology of obesity
Etiology of Obesity Neural and Hormonal
By mahdi saleh
Introduction
Neural and Hormonal cause of obesity
Hormonal leptininsulin
PyyGhrelin
Neural Proopiomelanoc
ortinneuropeptide Yagouti-related
protein
Neural and Hormonal cause of obesity
-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
Leptin Leptin Fat cells Secreting cell
Hypothalamus Targetlong-term regulation
of energy balanceFunction
IL-6 type glycoprotein 130 cytokine receptor
Receptor
Leptin
Eat
Fat store
leptin
Hypothalamus
Stop eating
Leptin
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 missingEating MoreReduced Energy Expenditure
Leptin
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
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
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
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
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
Leptin Ghrelinendocrine cells in the
gastrointestinal mucosaSecreting cell
Hypothalamus Targetgrowth hormone release, feeding
behavior, glucose metabolism, memory,
and also antidepressant effects,
Function
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
Leptin PYY L-cells in the small
intestineSecreting cell
Hypothalamus Targetdecreased appetite and make people
feel full after eating
Function
receptors in the Brain
Receptor
For more informationChapter 9 : Environmental and Nutritional DiseasesP444-448
Chapter 72 Dietary Balances; Regulation of Feeding; Obesity and Starvation; Vitamins and MineralsP889-900
Chapter 17 Energy Balance and Temperature Regulation9621-624