Inhibitory effect of alcohol on ghrelin secretion in normal man.
ABSTRACT 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.
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ABSTRACT: The reward systems are important for rewards, natural and artificial. An important part of these systems is the mesolimbic dopamine system, consisting of a dopamine projection from the ventral tegmental area to nucleus accumbens. There is an underlying disruption in the reward systems in individuals with alcohol dependence. Elucidation of the neurochemical mechanisms involved in the ability of alcohol to activate the mesolimbic dopamine system could identify novel targets for the treatment of alcohol dependence. The role of dopamine, for example, by using the dopamine stabilizer (-)-OSU6162, in alcohol dependence will be revised. Data showing that local perfusion of alcohol into reward nodes activates the mesolimbic dopamine system will be reviewed. The effects of alcohol on ligand-gated ion channels will be introduced. Finally, the findings demonstrating that gut-brain peptides, such as ghrelin and glucagon-like peptide-1, are important for alcohol-mediated will be presented.Progress in brain research 01/2014; 211:201-33. · 5.10 Impact Factor
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ABSTRACT: Psychiatric disorders are often associated with metabolic and hormonal alterations, including obesity, diabetes, metabolic syndrome as well as modifications in several biological rhythms including appetite, stress, sleep-wake cycles, and secretion of their corresponding endocrine regulators. Among the gastrointestinal hormones that regulate appetite and adapt the metabolism in response to nutritional, hedonic, and emotional dysfunctions, at the interface between endocrine, metabolic, and psychiatric disorders, ghrelin plays a unique role as the only one increasing appetite. The secretion of ghrelin is altered in several psychiatric disorders (anorexia, schizophrenia) as well as in metabolic disorders (obesity) and in animal models in response to emotional triggers (psychological stress …) but the relationship between these modifications and the physiopathology of psychiatric disorders remains unclear. Recently, a large literature showed that this key metabolic/endocrine regulator is involved in stress and reward-oriented behaviors and regulates anxiety and mood. In addition, preproghrelin is a complex prohormone but the roles of the other ghrelin-derived peptides, thought to act as functional ghrelin antagonists, are largely unknown. Altered ghrelin secretion and/or signaling in psychiatric diseases are thought to participate in altered appetite, hedonic response and reward. Whether this can contribute to the mechanism responsible for the development of the disease or can help to minimize some symptoms associated with these psychiatric disorders is discussed in the present review. We will thus describe (1) the biological actions of ghrelin and ghrelin-derived peptides on food and drugs reward, anxiety and depression, and the physiological consequences of ghrelin invalidation on these parameters, (2) how ghrelin and ghrelin-derived peptides are regulated in animal models of psychiatric diseases and in human psychiatric disorders in relation with the GH axis.Frontiers in Endocrinology 10/2014; 5:163.
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ABSTRACT: Peptides synthesized in endocrine cells in the gastrointestinal tract and neurons are traditionally considered regulators of metabolism, energy intake, and appetite. However, recent work has demonstrated that many of these peptides act on corticostriatal-limbic circuitry and, in turn, regulate addictive behaviors. Given that alcohol is a source of energy and an addictive substance, it is not surprising that increasing evidence supports a role for gut-brain peptides specifically in alcohol use disorders (AUD). In this review, we discuss the effects of several gut-brain peptides on alcohol-related behaviors and the potential mechanisms by which these gut-brain peptides may interfere with alcohol-induced changes in corticostriatal-limbic circuitry. This review provides a summary of current knowledge on gut-brain peptides focusing on five peptides: neurotensin, glucagon-like peptide 1, ghrelin, substance P, and neuropeptide Y. Our review will be helpful to develop novel therapeutic targets for AUD.Frontiers in Neuroscience 09/2014; 8:288.
Inhibitory effect of alcohol on ghrelin secretion in normal man
Jan Calissendorff, Olle Danielsson1, Kerstin Brismar and Sven Ro ¨jdmark2
Department of Endocrinology, Metabolism and Diabetology and1Department of Clinical Chemistry, Karolinska University Hospital, 17176 Stockholm,
Sweden and2Department of Medicine, Section of Endocrinology, Stockholm So ¨der Hospital, Stockholm, Sweden
(Correspondence should be addressed to J Calissendorff; Email: email@example.com)
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 (0.55g ethanol/kg body weight) was ingested in exper-
iment A, and drinking-water in experiment B. Venous blood was collected before, and 30 and 60min
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 30min and by 17.5^2.6% at 60min, 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
thanshort-termeffects onfood consumptionand 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
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
exerts an acute influence on serum levels of ghrelin in
is ghrelin. Ghrelin is
European Journal of Endocrinology (2005) 152 743–747 ISSN 0804-4643
q 2005 Society of the European Journal of EndocrinologyDOI: 10.1530/eje.1.01905
Online version via www.eje-online.org
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 23^1kg/m2respectively. 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 0730h 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 30min, basal blood samples were collected from the
catheter. Then, alcohol was given orally at a dose of
0.55g ethanol/kg body weight (combustion of 1g etha-
nol yields 6.9kcal). Blood samples for determination of
serum ghrelin, cortisol and plasma NPY were taken
immediately before the alcohol ingestion (at 0800h),
and subsequently at 0830 and 0900h. Serum ethanol
concentrations were measured at 0800 and 0900h.
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 (2208C) until analysed 5–7 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
100pg/ml, and the intra- and interassay coefficients
of variation were 4.4% and 16.7% respectively at
Plasma NPY levels were also measured by use of an
RIA technique (20). The sensitivity of the assay was
1.9pmol/l and the intra- and interassay coefficients of
variation were 7.2% and 9.3% respectively at plasma
concentrations of 43pmol/l.
Serum cortisol levels were determined by fluor-
escence immunoassay (autoDELFIA,
Turku, Finland). Intra- and interassay coefficients of
variation were 4.9% and 6.4% respectively at serum
concentrations of 157nmol/l.
An automated Hitachi 911 analyser from Roche
Diagnostics, Bromma, Sweden made it possible to
measure serum ethanol levels.
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).
centration rosefromzero to19.0^0.6mmol/lin60min
(P , 0.001). In experiment B the ethanol concentra-
tion remained at zero throughout the study (Fig. 1).
2274^172pg/ml 30min after ingestion of alcohol
(P , 0.02) and by 17.5^2.6% to 2178^110pg/ml
after 60min (P , 0.002). In experiment B, the basal
ghrelin concentration was 2611^194pg/ml. This
was not significantly different from the corresponding
basal level in experiment A. It was 2649^188pg/ml
30min after ingestion of water, and 2606^166pg/ml
after 60min. 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
30min, and P , 0.01 at 60min) (Fig. 1).
Basal plasma NPY levels were similar in experiments A
and B (18.6^2.0 and 16.1^1.9pmol/l respectively
(not significantly different, NS)). The levels did not
change significantly after alcohol or water (Fig. 1).
Basal cortisol levels were 401^31 and 420^18nmol/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
60min) 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 0.55g/kg body weight. This dose is equivalent
to 10 cl whisky and yields 266kcal in a 70kg 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
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^S.E.M.
Alcohol and ghrelin
EUROPEAN 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
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
EUROPEAN JOURNAL OF ENDOCRINOLOGY (2005) 152