In this article, we will learn about appetite -concerned with human physiology.
Introduction: The desire to eat is the appetite for food. Appetite is mainly due to hunger; however, it may be due to appealing foods without hunger.
Appetite is related to every individual choice, socioeconomic background, and emotion. For example, stress reduces appetite.
Table of content:
| 1. | Introduction |
| 2. | Physiological Basis of Insomnia |
| 3. | Causes of Insomnia |
| 4. | Prevention Strategies for Insomnia |
| 5. | Conclusion |
| 6. | References |
Appetite controls energy intake and maintains the demand of the body. Therefore, appetite or approach behavior is responsible for food intake-energy intake, whereas the rest are associated with energy expenditure.
Theories to Explain the Origin of Appetite
There are many theories to explain the origin of appetite and how it subsides.
We know that GIT is the largest endocrine organ of the body. The gastrointestinal tract secrets many hormones. Different hormones and neuronal communication from other parts of the GIT influence hunger. The GIT has its nervous system (Enteric nervous system) with rich contact with ANS CNS).
Food intake-(Bray2000) and energy homeostasis are -( Murphy and Bloom 2006) controlled by gut-brain energy with GIT in the center.
Anorexia-Decreased desire to eat is known as anorexia, whereas polyphagia or Hyperphagia is an increased desire to eat.
Anorexiogenic agents cause decreased appetite. Orexigenic agents cause an increased appetite.
Abnormal appetite is abnormal eating habits leading to malnutrition, obesity, and other metabolic problems.
Regulation of appetite:-
Two main factors regulate appetite-
1) Genetic factors and
2) Environmental factors
Any abnormalities in either may cause abnormal appetite.
Anorexia may be due to the following:-
1) Physical causes like-
a) Infectious diseases.
b) Malignant diseases.
c) Autoimmune diseases.
2) Psychological causes-
a) Mental disorders
b) Stress and depression
Hyperphagia may be due to the following:-
1) Physical causes like increased body demand -exercise, physical work. Appetite increases after exercise and physical activity.
2) Dyspepsia, dysgensia(bad taste) effect appetite to a great extent.
Abnormal appetite may be due to genetic factors- Chromosomal abnormalities -e.g., Anorexia nervosa, Bulimic nervosa, Prader- willy syndrome, etc.
The hypothalamus of the brain controls appetite. It plays a vital role in appetite control.
Appetite centers:-
1. Ventromedial nucleus of the hypothalamus is the satiety center.
2. Lateral area of the hypothalamus is the feeding center.
Lateral area of the hypothalamus:-
It receives neuronal hormonal or nutritional signals. Neurons of the lateral area of the hypothalamus are secondary neurons.
Ventromedial nucleus:
Neurons of this area are primary neurons. They are responsible for the modulation and coordination of inputs received from the secondary center. This ventromedial nucleus is the satiety center and inhibits the feeding center.
Primary neurons
Secondary neurons
Higher center + + – –
–
Food intake Energy balance
Many sensory input control appetite and food intake and the hypothalamus integrates and modulates this information.
In the hypothalamus, the ventromedial nuclei of the hypothalamus are the satiety center, while the lateral hypothalamic area is the feeding center. The Satiety center controls feeding by inhibiting the ‘feeding center.’
The Satiety center is the primary center that regulates food intake. Therefore, when bilateral centers are, damaged feeding centers will increase food intake, causing obesity -hypothalamic obesity.
The feeding center is in the lateral hypothalamic area, which is located caudolateral to the mammillary bodies and is always active, causing eating.
The satiety center regulates the feeding center.
The neurons of the satiety center are glucose receptors (that is, receptors for glucose in the blood)- a glucostat.
These neurons need insulin for glucose utilization; therefore, the glucose receptors are unique in the brain.
If glucose receptors receive less glucose, they become less active, so the inhibitory effect on the feeding center decreases – promoting and increasing food intake.
And vice versa, when glucose receptors receive adequate glucose, they inhibit the feeding center and reduce food intake. As a result, the man will feel satisfied.
The feeding center is permanently active if inhibitory signals from the satiety center are absent.
Lateral area of the hypothalamus – Excitatory hormones
Neuropeptide Y (NPY) and Agouti-related peptides (Ag RP) Ghrelin
Inhibitory hormones:- Suppress the feeding center.
CART
α-MSH
β-endorphin
Ghrelin hormone -is a peptide hormone produced by the pancreas and released from the gastric wall when the stomach is empty. The ghrelin release is inhibited in a full stomach. As a result, the Ghrelin level is high in anorexia.
Peptide Tyrosine Tyrosine (PPY) is a peptide hormone secreted from the ileum and colon cells in response to feeding. It inhibits appetite.
Insulin:– secreted from beta cells of the islet of Langerhans of pancreas suppress appetite.
Leptin:– Adipocytes (fat cells) secrete leptin- a peptide hormone. Leptin is a polypeptide hormone secreted mainly, if not exclusively, in the adipose tissue.
Leptin stimulates neurons of the ventromedial neurons of the satiety center. This will increase the inhibition of the feeding center. Feeding will stop.
Leptin receptors are distributed widely in various body tissues but mainly in brown adipose tissues and microvessels of the brain. Therefore, any defect in the leptin receptors gene will lead to obesity.
Leptin decreases the release of neuropeptide Y from the hypothalamus, reducing food intake.
Leptin controls body fat deposits.
The amount of body fat deposits initiates neuronal and hormonal signals to the hypothalamus and controls food intake.
Leptin level decrease in fasting and is associated with :
Decreased thyroid activity and delayed puberty onset.
- Ghrelin reactive IgG affects Orexigenic response.
–
Feeding center Satiety center
+ +
Ghrelin (stomach) leptin (Adipose tissue)
Any disturbance in the production of ghrelin and leptin can lead to obesity. When body fat accumulates, leptin production rises, and if its level persists for a period, the hypothalamus becomes resistant to leptin.
Now hypothalamus will not respond to leptin. Ghrelin function is not suppressed. The feeding center will continue feeding, causing obesity.
(Leptin is from the Greek word meaning lean.)
Obesity may be hereditary. Defect hypothalamic signaling receptors. Me- 4 receptors will reduce response to the satiety center and promote development.
The glycemic index of the food affects the satiety center. High glycemic food, e.g., potato, reduces appetite more than low glycemic food.
Clinical:-
Binge eating disorder (BED) is characterized by excessively eating between periodic time intervals. The person suffering from this disorder cannot resist excessive eating. It is a hereditary disease.
Body dysmorphic disorder involves food restriction and is usually associated with depression.
Anorecties – appetite suppressants are used to suppress appetite. It is used to weigh less. For example- Phentermine.
When the leptin gene is absent, leptin is reduced, causing hyperphagia and severe obesity.
In Lipodystrophy, there is Latin deficiency which can be heated by exogenous leptin.
Quotations:
“Those who let their appetites take hold of them.
Suffer torture and affliction like an enemy-held prisoner”.
John of the Cross, The ascent of Mount Carmel, Book 1, chapter 7, sector 2. Now good digestion waits on appetite and health on both.
William Shakespeare, Macbeth 1605 act III, scene 4, line 38.
Ascent of Mt. Carmel | EWTN. https://www.ewtn.com/catholicism/library/ascent-of-mt-carmel-12494
Ascent of Mt. Carmel | EWTN. https://www.ewtn.com/catholicism/library/ascent-of-mt-carmel-12494
Introduction
Origin of appetite
Regulation of appetite
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| 1. | origin of appetite |
| 2. | regulation of appetite |
| 3. | clinical |
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