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