III.5.D. Stimulation of food intake

a) Neuropeptide Y (NPY)

This is produced by the hypothalamic nucleus arcuatus and the peripheral nervous system.

The AGRP accounts for 90% of the expressed products of these neurons.

The NPY neurons have leptin receptors too.  

Leptin inhibits the release of NPY. In the lack of NPY, the symptoms are similar to those of fasting.  

Its effects: It stimulates the carbohydrate and food intake (it has the strongest effects on the stimulation of food intake). The desire for carbohydrates is increased in the morning. 

It acts on the brown adipose tissue and the thyroid and thereby inhibits energy consumption.

Its production is stimulated by fasting, lactation, physical activity, glucocorticoids, a low leptin level, decreased by blood Glu level and a low insulin level.

It is inhibited by leptin.

b) Agouti-related peptide (AGRP)

It is found in the nucleus arcuatus.

Its level is high in obese people. It has an appetite-stimulating effect.

It is inhibited by leptin.

It is stimulated by OXA and opioids.

c) Ghrelin

This is secreted from various organs:

            in the central nervous system: the hypothalamus (nucleus arcuatus), brain cortex, limbic system and pituitary,

            peripherally: the stomach, lungs, placenta, pancreas, kidneys, intestines and testis.

Its main effects:        

GH secretion ↑,

food intake ↑,

BP ↓,

Long-term memory ↑,

GH receptor-like effects (agonist),

GH ↑,

neuron activation ↑ in the nucleus arcuatus,

NPY and  GRP mRNA expression ↑,

weight gain ↑,

fat mass ↑ (antagonist effect to leptin and GH) ,

respiration ↑, and hence the energy consumption is driven to glycolysis.

It acts on ACTH, prolactin secretion, the Glu and lipid metabolism, the heart function and sleep regulation. 

It inhibits POMC neurons.

In the event of obesity and physical inactivity, its level is decreased.

d) Melanin-concentrating hormone (MCH)

This is synthesized by the lateral hypothalamus.

It increases food intake by inhibiting CART.  

e) Orexins (OXAs)

These are produced by the lateral hypothalamus.

Two peptides are known (A and B); the former is the more effective.  It stimulates NPY, and hence increases food intake. This effect prevails in the daytime. Peripheral OXA treatment does not influence eating in humans, but decreases the leptin level and gastric emptying.

f) Gamma-aminobutyric acid (GABA)

This is produced in the hypothalamus: the nucleus paraventricularis band of the nerve cells.

It increases the carbohydrate uptake.

g) Norepinephrine (N)

This is produced in the hypothalamus: the nucleus paraventricularis band of the nerve cells.

It increases the carbohydrate uptake and the

          alpha 2 receptor effect.

h) Galanin

This is produced in the hypothalamus.

Its effect: It increases fat uptake in the rat, but not in humans.

            This effect is influenced by estrogen.

a) Opioid peptides

These increase fat uptake and therefore protein uptake.

The need for fat intake occurs predominantly in the late afternoon.

Table 5 presents an overview of the hormones.

Table 5. An overview of food intake-stimulating hormones
(E = epinephrine, Ach = acetylcholine, ACTH = adrenocorticotropic hormone, AA = amino acid, Arg = arginine, CCK = cholecystokinin, CRH = corticotropin-releasing hormone, G = gastrin, GH = growth hormone,
GIP = glucose-dependent insulinotropic polypeptide, gastrin inhibitory peptide, gastric inhibitory polypeptide,
GLP = glucagon-like peptide, Glu = glucose, GHRH = GH releasing hormone, Leu = leucine, Lys = lysine, , MCH = melanin-concentrating hormone , AGC = adrenal gland cortex, AGM = adrenal gland medulla, N = norepinephrine, NPY = neuropeptide Y, OXA = orexin, OXM = enteroglucagon, glicentin, oxyntomodulin, PP = pancreas polypeptide, T₄ = thyroxine, TSH = thyroid-stimulating hormone, VIP = vasoactive intestinal polypeptide, glycogenolysis = glycogen breakdown, lypolysis = fat breakdown, glycolysis = glucose breakdown, gluconeogenesis = glucose production)