The Metabolic Mechanism of Satiety Signal and Adiposity Signal on

Food Intake Regulation

Bochen Li

The School of Food Science and Nutrition University of Leeds,

Leeds, U.K.

Keywords: Food Intake, Satiety Signals, Adiposity Signals, Neuron Pathways.

Abstract: Obesity rates rose sharply in past 40 years, owing to the availability of appetizing food and work-related

sedentary habits. Obesity is caused by a long-term positive energy balance, but by reducing food intake

significant weight loss can be achieved. Food intake is simultaneously regulated by biochemical signals

(homeostasis) and social factors (non-homeostasis). As two important homeostasis factors, satiety and

adiposity signals have been well studied, but it is relatively fragmented. Therefore, this study looks at satiety

and adiposity signals to understand the metabolic mechanism of human food related metabolic pathways from

the perspective of homeostasis factor. Satiety and adiposity signals are critical for reducing obesity, because

they play such a large role in appetite control to reduce food intake. This research analyses literature about

satiety and adiposity signals, such as references related to CCK, GLP-1, ghrelin, leptin and insulin, and

combines the research of exogenous injection satiety and adiposity signals for calorie restriction to better

illustrate the metabolic pathways of these hormones.Through the analysis of these factors, it is concluded

that satiety and adiposity signals are expressed on two neuron pathways via NTS and ARC to

synergeticly control food intake by regulating appetite, but it seems that the method of injecting exogenous

hormones to treat obesity is currently difficult to achieve.

1 INTRODUCTION

In the past 40 years, the global obesity level

exorbitantly rose by three times, according to WHO

report, the percentage of overweight and obesity for

18 years old and elder adults was 39% and 13% in

2016, respectively (Website:

https://www.who.int/news-room/fact-

sheets/detail/obesity-and-overweight). Obesity is

characterized as having a BMI of 30kg/m2 or above

and it has become one of the most important global

public health issues which affects human well-being

and lifetime. Thus, it is very important to find an

effective way to lose weight.

Increasing activities and dietary restriction are the

only two methods that have been proved effective in

improving obesity from the energy balance view.

Comparing these two methods, dietary restriction is a

more effective way for weight loss than moderate

energy expenditure without calorie restriction (Swift,

McGee, Earnest, Carlisle, Nygard, Johannsen 2018;

Varady 2011).

Food consumption is coordinately regulated by

homeostasis and non-homeostasis factors. Non-

homeostasis factors include all external social factors,

such as food availability, eating patterns, food

delectability and previous experience, so it is

unpredictable and hard to control for improving

obesity. However, homeostasis factors play an

important role in controlling food intake by

biochemical signals (hormones) and understanding

the fundamentals of food intake control is critical to

understanding the etiology of eating disorders and

obesity. Homeostasis factors have been extensively

explored in human physiology to assist people in

understanding the cause of obesity and develop

therapeutic targets to cure obesity.

Depending on energy requirements, the

physiological regulation of calorie intake is exerted

on the meal's conclusion through a subtle

modification of meal size and sensation of fullness.

Thus, satiety and adiposity signal as the homeostasis

factors are important in appetite regulation because

the amount of food consumed in each meal is mostly

determined by the gut secreted hormones (satiety

144

Li, B.

The Metabolic Mechanism of Satiety Signal and Adiposity Signal on Food Intake Regulation.

DOI: 10.5220/0011234400003438

In Proceedings of the 1st International Conference on Health Big Data and Intelligent Healthcare (ICHIH 2022), pages 144-150

ISBN: 978-989-758-596-8

signal) and adipose related hormones (adiposity

signal) (Brunerová, Anděl 2013), lots of exogenous

injection of satiety and adiposity signal has been put

forward to reinforce specific neurons by changing

hormone level for treating obesity. And it’s important

to combs out the metabolic mechanism of satiety and

adiposity signals to let more people know the

mechanism in a clearer way.

However, there is relatively few article that combs

out these two signals and their effect in human’s

brain, thus, this study aims to evaluate the impacts of

two key hormonal signals (adiposity signal and

obesity signal) in the metabolic pathways on food

intake and discuss the feasibility for administration of

the exogenous key hormonal signals for weight loss.

Through this paper, relevant researchers can get a

clear idea of the internal mechanisms of obesity. And

for those who are relatively fat, knowing the related

concepts and mechanism about dietary restriction will

also help them lose weight and find a healthier life

style in a more scientific way.

2 FOOD IN TAKE RELATED

METABOLIC PATHWAY

As homeostasis regulation, key hormone signals

control dietary calorie intake via meal size, satiety,

and feeding interval, these controlling are based on

the action of these hormones to the brain to regulate

food intake, such as cephalic insulin (Ahrén, Holst

2001). To understand the effect of these hormones, it

is essential to understand their metabolic pathways.

As two important food intake related hormones,

satiety and adiposity signals regulate appetite through

reaching the signal integration site, the arcuate

nucleus of the hypothalamus (ARC) and the nucleus

tractus solitarius (NTS).

Hypothalamus as the body's most important brain

tissue to regulate of food intake has several regions,

as shown in Fig.1, the lateral hypothalamus and

ventromedial nucleus are associated with hunger and

satiety, which has been proved in animal experiments.

As the main region for integrating food intake related

signals to controlling food intake in hypothalamus,

ARC is close to the third ventricle. ARC is engaged

in two well-studied interconnected neural pathways

that are crucial for controlling food intake. The effects

of the two neuronal groups on food intake are

diametrically opposed, where the synergy of pro-

opiomelanocortin (POMC) and cocaine- and

amphetamine-regulated transcript (CART) are

responsible for satiety to reduce

Figure 1: The metabolic pathways of food related signals in

hypothalamus.

food intake and the coordinated expression of

neuropeptide Y (NPY) and agouti related peptide

(AgRP) is related with inhibiting of satiety by

releasing AgRP neuron on melanocortin 4 receptor

(MC4R) to antagonize with POMC pathway neuron

(αMSH) (Zhan 2018). Notably, some signal

hormones like ghrelin govern hunger by stimulating

one of the two neuron routes, whereas some specific

signaling hormones like leptin and insulin can control

food intake by simultaneously affecting both neuron

pathways.

Like the hypothalamus, NTS, as shown in Fig.2,

is the integration site in the hindbrain for taste-

relative information and vagal and circulating signals,

NTS offer physicochemical property information and

quantity about food to the POMC and AgRP neurons

to rapidly promote satiety after meal digestion (Sohn

2015). Additionally, the NTS also express taste-

relative information which is non-homeostasis factor

to the ARC to control feeding behavior (Valassi,

Scacchi, Cavagnini 2007).

Figure 2: The metabolic pathways of food related signals in

nucleus tractus so-litarius (hindbrain).

Although satiety and adiposity signals share the

same neuron pathway, their biochemistry and

duration of action are different. Satiety signals are

short-term signals of negative feedback of the body's

The Metabolic Mechanism of Satiety Signal and Adiposity Signal on Food Intake Regulation

145

rapid response, satiety signals control hunger

sensation, satiety and feeding interval, it changes

constantly with the start of eating (ghrelin excepted),

while the adiposity signal is a long-term signal

targeted at maintaining the body's energy balance, it

does not change dramatically due to the beginning of

eating behaviors ,but they constantly control the

appetite through negative feedback of the amount of

adipose tissue. The satiety signal that is transmitted to

the NTS via the vagal and spinal nerves, is eventually

transmitted to the neuron routes in the hypothalamus,

while the adiposity signal, which express to the ARC

via the median eminence or by crossing the blood-

brain barrier (BBB) to enter the two specific neuron

pathways (Abdalla 2017).

3 THE SATIETY

SIGNAL- SHORT-TERM

Satiety signals are produced in the GI tract from one

hour before the start of the meal to the completion of

the meal as a signal to regulate food intake. Satiety

signal production is linked to eating anticipation, such

as the usual eating surroundings, daily habitual eating

time and the aroma and beauty of food. The brain

receives sensory stimulus or biological clock

regulation, the external stimulus and internal

regulation instruct the GI tract to create satiety signals

and transmits them down the vagal and spinal nerves

to the NTS (except ghrelin), then they express onto

neuron pathways and causing hunger or satiety.

Cholecystokinin (CCK), glucagon, glucagon-like

peptide-1 (GLP-1), ghrelin (hunger signal), and

peptide YY (PYY) are the most prominent satiety

signals which have been studied. To improve obesity,

significant pharmaceutical research has been

conducted based on this information.

Interestingly, a national survey has found that fast

eaters eat significantly more (for the same weight)

than slow eaters (Zeng, Cai, Ma, et al 2018), owing to

the fact that the slow eaters' satiety signal hasn't yet

reached the POMC pathway to increase satiety and

stop eating, whereas heavy eaters feel fuller after

meals due to more satiety signals reaching MC4R

receptors and increasing satiety. On the flip side of the

capacity to regulate food intake quickly, most satiety

signals have short half-lives, which will be discussed

further in the particular satiety signals section.

3.1 Cholecystokinin (CCK)

CCK as the first satiety signal to be identified and

investigated has been widely studied. CCK is

produced in the duodenum and jejunum and acts on

the CCK 1 receptor via the vagal afferent nerve to

inhibit food intake by activating the POMC pathway.

In a human trial of exogenous CCK injection, it was

discovered that exogenous CCK decreased food

intake in a dose-dependent manner. Furthermore,

food intake in mice treated with a CCK 1 receptor

antagonist was significantly greater (when compared

to the placebo group), demonstrating the satiety-

enhancing impact of endogenous CCK(Beglinger,

Degen, Matzinger, D'Amato, Drewe Loxiglumide

2001).

Exogenous CCK injection, on the other hand, has

been shown to have some limitations in rat

experiments. The administration of exogenous CCK

more than 15 minutes before feeding seemed to have

no effect on the amount of food consumed by mice,

whereas the treatment of CCK immediately before

feeding significantly reduced the amount consumed

by mice(Begg, Woods 2013). This also proved that

CCK has a short half-life in human metabolism and

that the injection time must be carefully regulated to

get the desired effect of lowering consumption.

Additionally, when mice were continuously

injected with CCK over a long period of time, the

drop in food intake was shown to vanish after a very

short amount of time. According to the findings of

E.A. Duncan et al., rat consumption was significantly

reduced in the first three days after receiving

consecutive CCK injections compared to the saline

group (control group), but there was no significant

difference in consumption between the two groups

from day 4 to the end of the experiment (day 11). On

the other hand, from day one until the completion of

the experiment (day 28), the intermittent group

(exogenous CCK injections every three days)

consumed significantly less sucrose than the control

group (saline).

On the test of final day sucrose intake level, the

consecutive CCK group (110.0 ± 6.2% of baseline)

consumed significantly more sucrose than the

intermittent CCK group (98.6 ± 2.5% of baseline), t

(16) = 1.72, p≤0.05, and the saline group (97.4 ±

3.5% baseline), t (17) = 1.83, p<0.05 (Duncan,

Davita, Woods 2005). This state (consecutive CCK no

effect) could be caused by behavioral tolerance or

extinction of the learned respond (for endogenous

CCK) of CCK receptors. Accordingly, the results of

these rat trials are helpful in determining the

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administration time and interval for exogenous CCK

injection in clinical practice.

3.2 GLP-1

GLP-1, another key intestinal hormone, stimulates

insulin synthesis and secretion triggered by glucose

while inhibits glucagon secretion. The injection of

exogenous GLP-1 was linked to a reduction in food

intake (which was dose-dependent) and weight loss in

mice, but it was shown that after a long-term infusion,

the obese group's post-meal GLP-1 release gradually

declined, providing a reference for clinical use

(Kanoski, Hayes, Skibicka 2016). GLP-1's clinical

application is additionally hampered by its short half-

life, as GLP-1 can be rapidly inactivated in the body

by an enzyme called Dipeptidyl Peptidase IV

(DPPIV) (Maselli, Camilleri 2020).

GlP-1 levels typically peak approximately an hour

before a meal, perhaps to promote insulin production

by islet B cells to digest incoming nutrients (glucose).

This is because insulin, as a long-term adiposity

signal, needs to take a long time to reach ARC and

induce satiety.

Long-acting GLP-1 agonists and DPPIV

inhibitors based on GLP-1 mechanisms have been

demonstrated to lower food intake in mice trials,

although most of these medications (for humans) are

still in development.

3.3 Ghrelin

Ghrelin, as the only hormone produced by GI tract

that promotes appetite among satiety signals,

expresses on ARC. Ghrelin stimulates the NPY and

AgRP pathways to boost appetite, and the NPY

pathway's activation also inhibits the POMC pathway

to be further hunger(Abizaid, Liu 2006). Ghrelin

levels spiked in the hour leading up to feeding and

then plummeted back to baseline once feeding began

(Begg, Woods 2013). This wide range of ghrelin

levels also suggests that ghrelin, as a satiety signal,

has a rapid and short-term potential to control eating

behavior.

Ghrelin has also been linked to body weight self-

control. According to the experimental outcomes,

ghrelin levels are higher in anorexia patients and

lower in obese patients (Begg, Woods 2013),

implying that ghrelin is engaged in the negative

feedback regulation of body weight change. The

findings may also shed light on why people who lose

weight struggle to manage their appetites. But chronic

ghrelin administration for anorexia patients will limit

fat utilization as a source of energy, it may be an

unhealthy method for gaining weight. In addition,

ghrelin has been linked to reproduction, glucose and

lipid metabolism, gastric motility, acid secretion,

sleep, and antiproliferative activity.

4 THE ADIPOSITY

SIGNAL- LONG-TERM

Adiposity signal is a long-term hormone that informs

the brain about the state of the body (the number of

fat cells) and aids the body in changing its diet to

maintain health. With the exception of insulin, other

obesity signals are produced by adipose tissue as the

signals to feedback information to the brain. The

adiposity signals are named because these hormones

are proportionate to body fat content. The two most

well-studied adiposity signals, insulin and leptin, are

proportional to the degree of obesity(Bagdade ,

Bierman, Porte 1967; Lönnqvist, Arner, Nordfors,

Schalling 1995), and insulin and leptin promote

catabolism while blocking anabolism and they

activate or inhibit the appropriate neuron pathways to

lower food intake by expressing on their respective

receptors on the ARC via active transport to the

blood-brain barrier (BBB).

4.1 Leptin

Leptin, the first adipocytokine that is identified, is the

primary regulator of the "brain gut axis," with the

bulk of leptin generated by white adipose tissue. To

lower meal size and extend time intervals, leptin

enters particular neuron pathways via activating

leptin receptors on the ARC, stimulating the POMC

pathway and inhibiting the NPY route. Leptin also

has a long-term control on obesity through regulating

energy metabolism by altering the energy utilization

ratio of glucose and fat.

Both congenital leptin and leptin receptor

deficiency contribute to obesity (which is very rare in

humans), and it has been demonstrated that leptin and

leptin receptor deficiency obesity patients treated

with recombinant human leptin and leptin

dramatically lowered their weight and food intake

(Valassi, Scacchi, Cavagnini 2007).

However, the experiment discovered that persons

with obesity who did not have a congenital deficit had

much greater blood leptin levels, indicating that

obesity is linked to leptin resistance. The molecular

mechanism behind resistance is unclear now.

The Metabolic Mechanism of Satiety Signal and Adiposity Signal on Food Intake Regulation

147

4.2 Insulin

Obesity can disrupt the body's energy metabolism and

is the major cause of Type 2 Diabetes (T2D), it is

mostly caused by insulin resistance induced by a lipid

metabolism disorder. Insulin and leptin function in

various ways. Insulin enters the ARC and activates

the POMC Neuron, but it does not inhibit the AgRP

and NPY pathways. Interestingly, insulin stimulated

AgRP production while inhibiting NPY (Vettor,

Fabris, Pagano, Federspil 2002). According to a

randomized crossover trial for oral insulin in healthy

male subject, as shown in Figure 3 and Figure 4, it

can be seen that the total exposure [AUCIns338,0-∞]

and maximum concentration [Cmax,Ins338] of

insulin 338 were both significantly lower for 0 versus

360 minutes post-dose fasting (ratio [95 percent

confidence interval (CI)]: 0.36 [0.26-0.49], p ＜

0.001, and 0.35 [0.25-0.49], p < 0.001, respectively)

(Halberg et al 2019). This trial suggests insulin can

reduce food intake by increasing satiation and so

control body weight in terms of results.

Figure 3:Post-dose fasting period (Halberg et al 2019).

Figure 4: Post-dose fasting period (Halberg et al 2019).

The study of H.A. Halem et al. have shown that

central insulin injections can significantly reduce

intake in animal models (Halem, Taylor, Dong, Shen,

Datta, Abizaid, Diano, Horvath, Culler 2005), but the

major effect of insulin is to lower blood glucose

through glycogen synthesis and accelerate glucose

absorption in cells, which will let patients consume

more food due to hypoglycemia, that is why it is

impossible to use significant amounts of insulin to

treat obesity in clinical treatment.

5 SIGNALS INTERACTION AND

SENSITIVITY

As previously stated, adiposity and satiety signals are

expressed in the same weight-control neuron

pathways. Surprisingly, these hormones can alter the

sensitivity of each other's receptors, for enhancing the

appetite-controlling effect and this can be interpreted

as a mechanism for the body to maintain weight

effectively. For example, obese persons will have

higher amounts of leptin which boosts insulin

receptor sensitivity to improve production and lower

blood sugar to preserve health. However, insulin and

leptin, as long-term adiposity signals, can also

influence the sensitivity of satiety signal represented

by CCK (Begg, Woods 2013). For instance, patients

who were losing weight had lower levels of insulin

and leptin which affected a reduction in CCK 1

receptor sensitivity to prevent satiety, it is thought to

be the body's regulation to maintain weight stability.

These studies also suggest another reason why

exogenous insulin and leptin injections might help

people lose weight: increasing insulin and leptin can

help people lose weight by modifying CCK and GLP-

1 sensitivity.

6 CONCLUSIONS

In sum, satiety signal and adiposity signal are

expressed via different integration centers (NTS and

ARC) to the POMC and AgRP neurons that

coordinate regulate food intake to keep the body

weight, these biochemical pathways are essential for

researchers to understand the underlying processes of

obesity, such as changes in associated hormone levels

and neuron pathway reinforcement, calorie restriction

therapy also requires a deep understanding of the

fundamental mechanism of obesity. A clinically

significant weight loss benefit is not easy to occur

without side effects from recognized satiety and

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adiposity signals and pathways. Food intake

homeostasis is a complicated system governed by

numerous hormones, and the precise mechanism by

which insulin and leptin influence satiety signal

sensitivity need to be investigated further, the

regulation of satiety signal sensitivity is a potential

target for improving obesity clinically. This paper

only discusses some important satiety and adiposity

signal, but not include some novel studied signals

such as GLP-2 and adiponectin. However, the future

clinical treatment of obesity should also be focused

on dietary control (mild case) and bariatric surgery

(severe case), because of the complexity of human

metabolic pathways and the side effects (resistance)

caused by exogenous hormones injection.

ACKNOWLEDGEMENTS

Some basic biochemical knowledge was provided by

the School of Food science and nutrition- University

of Leeds. Thanks for inspiration from Xiaoying Wang

in King’s College London. This work was supervised

by Professor Andrew Murray in University of

Cambridge.

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