Inhibitory effect of alcohol on ghrelin secretion in normal man

Article (PDF Available)inEuropean Journal of Endocrinology 152(5):743-7 · June 2005with69 Reads
DOI: 10.1530/eje.1.01905 · Source: PubMed
Human appetite is stimulated by alcohol but the underlying mechanism is unknown. It is possible that hunger-stimulating hormones are mediators of this effect of alcohol. Ghrelin stimulates hunger, but how alcohol affects human ghrelin secretion has never been studied before. To investigate whether alcohol ingestion exerts an acute influence on serum ghrelin concentrations in healthy subjects. Eight healthy non-obese subjects participated in the study. All were investigated on two occasions (experiments A and B). Alcohol (0.55 g ethanol/kg body weight) was ingested in experiment A, and drinking-water in experiment B. Venous blood was collected before, and 30 and 60 min after consumption of the drinks. Serum concentrations of ghrelin, cortisol and ethanol were determined and neuropeptide Y (NPY) concentrations were determined in plasma. Alcohol lowered the ghrelin level by 13.9+/-5.0% at 30 min and by 17.5+/-2.6% at 60 min, in contrast to drinking-water which was without significant effect. Serum levels of cortisol and insulin were similar after alcohol and water as was plasma NPY. Alcohol has an acute inhibitory influence on human ghrelin secretion but no measurable effect on the secretion of NPY and cortisol. Hence, none of these hormones mediate the orexigenic effect of the drug.


Inhibitory effect of alcohol on ghrelin secretion in normal man
Jan Calissendorff, Olle Danielsson
, Kerstin Brismar and Sven Ro¨jdmark
Department of Endocrinology, Metabolism and Diabetology and
Department of Clinical Chemistry, Karolinska University Hospital, 17176 Stockholm,
Sweden and
Department of Medicine, Section of Endocrinology, Stockholm So¨der Hospital, Stockholm, Sweden
(Correspondence should be addressed to J Calissendorff; Email:
Background: Human appetite is stimulated by alcohol but the underlying mechanism is unknown. It is
possible that hunger-stimulating hormones are mediators of this effect of alcohol. Ghrelin stimulates
hunger, but how alcohol affects human ghrelin secretion has never been studied before.
Objective: To investigate whether alcohol ingestion exerts an acute influence on serum ghrelin concen-
trations in healthy subjects.
Subjects and design: Eight healthy non-obese subjects participated in the study. All were investigated on
two occasions (experiments A and B). Alcohol (0.55 g ethanol/kg body weight) was ingested in exper-
iment A, and drinking-water in experiment B. Venous blood was collected before, and 30 and 60 min
after consumption of the drinks. Serum concentrations of ghrelin, cortisol and ethanol were deter-
mined and neuropeptide Y (NPY) concentrations were determined in plasma.
Results: Alcohol lowered the ghrelin level by 13.9^5.0% at 30 min and by 17.5^2.6% at 60 min, in
contrast to drinking-water which was without significant effect. Serum levels of cortisol and insulin
were similar after alcohol and water as was plasma NPY.
Conclusion: Alcohol has an acute inhibitory influence on human ghrelin secretion but no measurable
effect on the secretion of NPY and cortisol. Hence, none of these hormones mediate the orexigenic
effect of the drug.
European Journal of Endocrinology 152 743–747
It is well known that alcohol ingestion may serve as an
appetizer causing increased food intake in both normal
weight (1, 2) and obese (2) individuals. The mechanism
underlying this effect is unclear, but it is known that
alcohol, besides suppressing fatty acid oxidation and
increasing short term thermogenesis, may also affect
neurochemical systems involved in the control of appe-
tite (3). Hormone systems may also be involved, since
both hunger and satiety are to a great extent regulated
by such systems within the central nervous system
(4, 5). Hypothalamic neuropeptide Y (NPY) plays a
key role in this context, since it has a strong stimu-
latory influence on hunger (6, 7). Leptin may also be
of importance. This adipocyte-derived hormone affects
hunger signals indirectly by inhibiting NPY (5, 8).
Other hormones may, in turn, influence leptin. This
applies to insulin and cortisol which increase leptin
secretion (9, 10), whereas testosterone and catechol-
amines have the opposite effect (11, 12). Considering
these previous findings it is reasonable to assume that
one or several of the above mentioned hormones,
acting alone or in concert, could mediate the appet-
ite-stimulating effect of alcohol.
We have focused on this issue in our recent investi-
gations and have noted that acute ingestion of moderate
amounts of alcohol inhibits leptin secretion significantly
(13), but leaves circulating glucose concentrations (13,
14) and the secretion of insulin (13, 14), cortisol (13),
catecholamines (15) and testosterone (13) unaffected.
Although the leptin decline after alcohol ingestion
suggests that leptin could be the appetite-stimulating
factor we are looking for, this cannot be taken for
granted, since leptin is known for long-term rather
than short-term effects on food consumption and caloric
homeostasis (16, 17). In order to find other plausible
mechanisms underlying the short-term appetite-stimu-
lating effect of alcohol, additional factors should be con-
sidered. One such factor is ghrelin. Ghrelin is
predominantly produced in the mucose membrane of
the upper gastrointestinal tract (18) and it stimulates
the production of NPY (19). How alcohol affects
human ghrelin secretion has not been studied before.
Therefore, the objective of the present investigation was
to study whether intake of a moderate amount of alcohol
exerts an acute influence on serum levels of ghrelin in
healthy subjects.
European Journal of Endocrinology (2005) 152 743–747 ISSN 0804-4643
q 2005 Society of the European Journal of Endocrinology DOI: 10.1530/eje.1.01905
Online version via
Subjects and methods
Eight healthy volunteers were included in the investi-
gation. Four were women aged 25^4 years and four
were men 21^2 years old. Their body mass indices
were 21^2 and 23^1 kg/m
respectively. All were
free of medication. They used moderate amounts of
alcohol at social events, but none was addicted to
liquor, and all refrained completely from using alcohol
in any form during the 3 days prior to the experiments.
They were informed of the purpose of the study and
gave their voluntary consent to participate. The investi-
gation was approved by the ethics committee at the
Karolinska University Hospital in Stockholm.
Each individual took part in two experiments (A and B),
which were performed in a metabolic ward, in random
order, and 1 2 weeks apart.
Experiment A At 0730 h a catheter was inserted into
one of the antecubital veins which was kept patent by a
slow drip of normal saline. After an equilibration period
of 30 min, basal blood samples were collected from the
catheter. Then, alcohol was given orally at a dose of
0.55 g ethanol/kg body weight (combustion of 1 g etha-
nol yields 6.9 kcal). Blood samples for determination of
serum ghrelin, cortisol and plasma NPY were taken
immediately before the alcohol ingestion (at 0800 h),
and subsequently at 0830 and 0900 h. Serum ethanol
concentrations were measured at 0800 and 0900 h.
Experiment B In this experiment drinking-water was
substituted for alcohol. In all other details experiments
A and B were identical.
After collection, serum and plasma samples were stored
deeply frozen (2 20 8C) until analysed 57 weeks later.
Means of duplicate determinations were used. All ana-
lyses in one single individual were included in the same
Total serum ghrelin concentrations were measured
by RIA (Ghrelin (total) RIA kit, Linco Research, St
Charles, MO, USA). The sensitivity of the assay was
100 pg/ml, and the intra- and interassay coefficients
of variation were 4.4% and 16.7% respectively at
serum ghrelin concentrations of approximately
3000 pg/ml.
Plasma NPY levels were also measured by use of an
RIA technique (20). The sensitivity of the assay was
1.9 pmol/l and the intra- and interassay coefficients of
variation were 7.2% and 9.3% respectively at plasma
concentrations of 43 pmol/l.
Serum cortisol levels were determined by fluor-
escence immunoassay (autoDELFIA, Wallac Oy,
Turku, Finland). Intra- and interassay coefficients of
variation were 4.9% and 6.4% respectively at serum
concentrations of 157 nmol/l.
An automated Hitachi 911 analyser from Roche
Diagnostics, Bromma, Sweden made it possible to
measure serum ethanol levels.
Statistical analysis
Difference over time with treatments, between treat-
ments, and interaction between time and treatment,
were analysed by two-way repeated measures ANOVA
and, if significant, followed by Newman-Keuls’ post-
hoc test. P values , 0.05 were considered significant.
Values are shown as means^
S.E.M. Data processing
was performed using Statistica, Statsoft version 6.1
(Tulsa, OK, USA).
Serum ethanol
After ingestion of alcohol (experiment A) the ethanol con-
centration rose from zero to 19.0^0.6 mmol/l in 60 min
(P , 0.001). In experiment B the ethanol concentra-
tion remained at zero throughout the study (Fig. 1).
Serum ghrelin
In experiment A, the basal ghrelin level was
2662^165 pg/ml. It fell by 13.9^5.0% to
2274^172 pg/ml 30 min after ingestion of alcohol
(P , 0.02) and by 17.5^2.6% to 2178^110 pg/ml
after 60 min (P , 0.002). In experiment B, the basal
ghrelin concentration was 2611^194 pg/ml. This
was not significantly different from the corresponding
basal level in experiment A. It was 2649^188 pg/ml
30 min after ingestion of water, and 2606^166 pg/ml
after 60 min. These levels were not significantly differ-
ent from the basal level. When comparing the ghrelin
concentrations after the ingestion of alcohol or water
significant differencies were obtained (P , 0.02 at
30 min, and P , 0.01 at 60 min) (Fig. 1).
Plasma NPY
Basal plasma NPY levels were similar in experiments A
and B (18.6^2.0 and 16.1^1.9 pmol/l respectively
(not significantly different, NS)). The levels did not
change significantly after alcohol or water (Fig. 1).
Serum cortisol
Basal cortisol levels were 401^31 and 420^18 nmol/l
in experiments A and B respectively (NS). Cortisol levels
declined both significantly (P , 0.001 at both 30 and
J Calissendorff and others EUROPEAN JOURNAL OF ENDOCRINOLOGY (2005) 152
60 min) and similarly after alcohol and water as shown
in Fig. 1.
In this investigation alcohol inhibited ghrelin secretion
acutely in contrast to drinking-water which was with-
out significant influence. The ghrelin inhibition could
either be a direct effect of alcohol on ghrelin-producing
cells in the stomach, or an indirect influence mediated
by other factors. Leptin is one such factor. It is inhibited
by acute ingestion of alcohol (13). If leptin stimulates
the secretion of ghrelin an alcohol-induced ghrelin
decline would probably ensue. However, leptin has
not been found to stimulate human ghrelin secretion.
Instead, Chan et al. have shown that endogenous
serum levels of leptin and ghrelin are inversely corre-
lated (21). Furthermore, both physiological and phar-
macological doses of recombinant leptin fail to affect
human ghrelin secretion (21).
Cortisol may also be excluded from the list of possible
mediators of the alcohol effect. This is because we found
serum levels of cortisol in the current study which were
almost identical after ingestion of alcohol or drinking-
The dose of alcohol given to our participants
was 0.55 g/kg body weight. This dose is equivalent
to 10 cl whisky and yields 266 kcal in a 70 kg man.
It could be argued that it is this caloric provision,
rather than the ethanol solution per se, that inhibits
the secretion of ghrelin. However, if the recent findings
of Nedvidkova and colleagues are taken into account
this hypothesis also appears to be unlikely. They
found that the plasma ghrelin response to food
intake was independent of meal caloric value in healthy
subjects (22)
Although alcohol may affect ghrelin secretion via
changed NPY production, findings presented in this
study do not favour such a notion inasmuch as plasma
NPY levels remained unchanged after ingestion of both
alcohol and water. However, an unchanged NPY level
after alcohol does not unequivocally exclude NPY from
being a mediator of the alcohol effect on ghrelin. Small
changes in the production of NPY may be difficult to dis-
cern by measuring NPY concentrations in peripheral
blood, due to the fact that centrally produced NPY has
to traverse the blood brain barrier before being con-
siderably diluted in the systemic circulation.
Glucagon-like peptide 1 (GLP-1), gastrin-releasing
peptide (GRP), cholecystokinin (CCK) and peptide YY
(PYY) are hormones which are involved in the regu-
lation of food intake (23 28). Hence, all of them are
possible mediators of alcohol. They are all secreted by
endocrine cells in the gastrointestinal tract. GLP-1,
GRP and CCK inhibit gastric emptying partly by
Figure 1 Serum (S) ghrelin, NPY, cortisol
and ethanol levels in healthy subjects
after ingestion of alcohol (A; B) and water
(W; A). Values are means^
Alcohol and ghrelin 745EUROPEAN JOURNAL OF ENDOCRINOLOGY (2005) 152
conveying afferent vagal satiety signals to the brain
(25). It has been reported that the vagal system may
play an important role in the control of ghrelin
secretion (29, 30). If so, it is possible that alcohol
decreases ghrelin secretion via vaso-vagal reflexes.
Raben et al. recently observed that alcohol does not
influence the secretion of human GLP-1 (31). Whether
alcohol stimulates hunger by influencing the secretion
of GRP, CCK or PYY is unknown and has to be given
closer attention in future studies.
Multiple ulcers arise in rats when their gastric
mucosa is exposed to ethanol (32, 33). This makes it
reasonable to assume that alcohol may have a toxic
effect on ghrelin-secretory cells in the stomach, result-
ing in decreased hormone secretion. However, findings
in rats, recently presented by Konturek et al., are at var-
iance with such an assumption. These authors found
not only that the mucosal expression of ghrelin is
enhanced in rats after exposure to ethanol, but also
that ghrelin exhibits strong gastroprotection in these
animals (33). Why ghrelin responsiveness to ethanol
appears to differ between humans and rats is not
readily apparent, but species differences, different alco-
hol doses, or differences in the length of alcohol
exposure are plausible explanations which merit
additional investigation.
In conclusion, alcohol has an acute inhibitory influ-
ence on ghrelin secretion but has no significant effect
on NPY and cortisol. When it is taken into account
that alcohol both stimulates appetite and inhibits appe-
tite-stimulating ghrelin secretion, it may be concluded
that ghrelin is not a hormone which mediates the
orexigenic effect of alcohol.
This study has been supported by funds from Capio’s
Research Foundation and by a scholarship from the
Eva and Oscar Ahre
n’s Foundation. We appreciate the
skilful experimental assistance of Eva-Lena Forsberg,
Agneta Reinholdsson and Alice Skogholm at the Clini-
cal Research Unit, Karolinska University Hospital.
Agneta Hilding is gratefully acknowledged for provid-
ing the statistical evaluation of the results.
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Received 16 November 2004
Accepted 10 February 2005
Alcohol and ghrelin 747EUROPEAN JOURNAL OF ENDOCRINOLOGY (2005) 152
    • "The ghrelin system was originally considered a promising target for development of medications to treat obesity (Dhillo & Bloom, 2001; Muccioli et al., 2002). More recently, it came to the attention of alcohol researchers following numerous reports of relationships between ghrelin levels, alcohol craving, and alcohol consumption in humans (Addolorato et al., 2006; Calissendorff, Danielsson, Brismar, & Rojdmark, 2005; Leggio et al., 2012 ). The effectiveness of ghrelin antagonists to decrease alcohol consumption was demonstrated in rats and mice ( Jerlhag et al., 2009; Kaur & Ryabinin, 2010 ). "
    [Show abstract] [Hide abstract] ABSTRACT: Most preclinical studies of medications to treat addictions are performed in mice and rats. These two rodent species belong to one phylogenetic subfamily, which narrows the likelihood of identifying potential mechanisms regulating addictions in other species, ie, humans. Expanding the genetic diversity of organisms modeling alcohol and drug abuse enhances our ability to screen for medications to treat addiction. Recently, research laboratories adapted the prairie vole model to study mechanisms of alcohol and drugs of abuse. This development not only expanded the diversity of genotypes used to screen medications, but also enhanced capabilities of such screens. Prairie voles belong to 3-5% of mammalian species exhibiting social monogamy. This unusual trait is reflected in their ability to form lasting long-term affiliations between adult individuals. The prairie vole animal model has high predictive validity for mechanisms regulating human social behaviors. In addition, these animals exhibit high alcohol intake and preference. In laboratory settings, prairie voles are used to model social influences on drug reward and alcohol consumption as well as effects of addictive substances on social bonding. As a result, this species can be adapted to screen medications whose effectiveness could be (a) resistant to social influences promoting excessive drug taking, (b) dependent on the presence of social support, and (c) medications affecting harmful social consequences of alcohol and drug abuse. This report reviews the literature on studies of alcohol and psychostimulants in prairie voles and discusses capabilities of this animal model as a screen for novel medications to treat alcoholism and addictions.
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    • "Severe alcohol consumers (≥50.0 g/d) had an increased risk of central obesity in middle-aged and elderly Chinese [43] , especially in men [50,51] and in beer or liquor drinkers [50] because beer or liquor provides more energy than other types of alcoholic beverages and severe drinkers may lead to obesity because of excessive energy intake, lipid oxidation and fat accumulation [52]. A recent study demonstrated that alcohol also inhibits ghrelin secretion, resulting in appetite stimulation among men [53]. Moreover, type of alcoholic beverage may play an impotent role in association with MS components. "
    [Show abstract] [Hide abstract] ABSTRACT: Accumulative evidence in the literature suggests alcohol consumption is a protective factor of the metabolic syndrome (MS). However, few studies investigated the relationship between alcohol consumption and components of MS. We examined association of several types of alcoholic beverage with components of MS among people in rural China. In the Nantong Metabolic Syndrome Study (NMSS), a cross-sectional study, a total of 20,502 participants, including 13,505 women and 6,997 men aged 18-74 years, were recruited between 2007 and 2008 in Nantong, China. Socio-economic status, dietary intake, physical exercise, alcoholic beverage consumption, and smoking status information were obtained, and triglycerides (TG), high-density lipoprtein cholesterol (HDL-c), blood pressure (BP) and blood glucose level were examined for all participants. Logistic regression model and the restricted cubic spline approach were used to analyze the associations between alcoholic beverage consumption and MS components. The MS prevalence was 21.1% in the whole population, which was significantly low among drinkers (20.6%), compared with non-drinkers (23.6%) in women, and was comparable in men (16.4% versus 17.1%). High HDL-c level was observed among drinkers, compared with non-drinkers in both men and women. Low TG level and Systolic BP (SBP) were found only among rice wine drinkers in women, and high waist circumference, high TG and BP were found among beer and liquor drinkers in men. Furthermore, we found that the highest quartile of rice wine drink in women may decrease 24% risk of high TG, 30% risk of low HDL-c and 43% risk of high glucose among MS components cases respectively, compared with non-drinkers (p for trend <0.01 for those three components). While compared non-drinkers among men, the highest quartile of liquor drink may increase 32% risk of high SBP, 55% risk of high Diastolic BP (DBP) and 34% risk of abdominal obesity among MS components cases respectively, but decrease 45% risk of low HDL-c (p for trend <0.05 for those four components). Our data suggested that all alcoholic beverages increased HDL-c level. Rice wine decreased both TG level and blood glucose in women only and it could be one of healthy alcoholic beverages in MS prevention in Chinese women. While excessive liquor consumption increased BP and waist circumference level and it may lead to hypertension and central obesity in Chinese men.
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    • "To date, the evidence suggests that alcohol does not appear to increase appetite through the action of peptide YY (PYY), ghrelin, gastric inhibitory peptide (GIP), or cholecystokinin (CCK)5758596061. Calissendorf et al. [58] found that alcohol did not increase plasma levels of neuropeptide Y (NPY); however, animal models have shown that central NPY levels are increased following alcohol consumption [62]. Alcohol can also influence hunger via several central mechanisms. "
    [Show abstract] [Hide abstract] ABSTRACT: Recreational alcohol intake is a widespread activity globally and alcohol energy (7 kcal/g) can be a contributing factor to weight gain if not compensated for. Given that both excessive alcohol intake and obesity are of public health interest, the present paper provides an update on the association between alcohol consumption and body weight. In general, recent prospective studies show that light-to-moderate alcohol intake is not associated with adiposity gain while heavy drinking is more consistently related to weight gain. Experimental evidence is also mixed and suggests that moderate intake of alcohol does not lead to weight gain over short follow-up periods. However, many factors can explain the conflicting findings and a better characterization of individuals more likely to gain weight as a result of alcohol consumption is needed. In particular, individuals who frequently drink moderate amounts of alcohol may enjoy a healthier lifestyle in general that may protect them from weight gain. In conclusion, despite the important limitations of current studies, it is reasonable to say that alcohol intake may be a risk factor for obesity in some individuals, likely based on a multitude of factors, some of which are discussed herein.
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