Effects of ethanol on plasma ghrelin levels in the rat during early and late adolescence

Healey, Kati L.; Landin, Justine D.; Dubester, Kira; Kibble, Sandra; Marquardt, Kristin; Brutman, Julianna N.; Davis, Jon F.; Swartzwelder, H. Scott; Chandler, L. Judson

doi:10.1016/j.alcohol.2019.12.006

Cited by 15 publications

(8 citation statements)

References 45 publications

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“…Results from clinical observations support data showing that active drinking in alcohol-dependent individuals may suppress both ghrelin levels and its production [50][51][52], observed in our previous study on highalcohol preferring rats as well [47]. Active form of ghrelin (acyl-ghrelin) elevation by EtOH during early adolescence was observed [48]. Experiments in model animals (two-bottle choice protocol) indicate that the key role of the ghrelin signaling pathway in lowering of alcohol voluntary intake appears to be equal for both sexes [49].…”

Section: Introductionsupporting

confidence: 86%

“…Interesting observations were made in the course of the analysis of changes in the peripheral concentration of ghrelin, both in rodents [47][48][49] and in clinical trials [50][51][52][53] under conditions of significant ethanol consumption. Results from clinical observations support data showing that active drinking in alcohol-dependent individuals may suppress both ghrelin levels and its production [50][51][52], observed in our previous study on highalcohol preferring rats as well [47].…”

Section: Introductionmentioning

confidence: 99%

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Differential Influence of Pueraria lobata Root Extract and Its Main Isoflavones on Ghrelin Levels in Alcohol-Treated Rats

et al. 2021

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The study was carried out on alcohol-preferring male Wistar rats. The following drugs were repeatedly (28×) administered: acamprosate (500 mg/kg, p.o.), naltrexone (0.1 mg/kg, i.p), and Pueraria lobata (kudzu) root extract (KU) (500 mg/kg, p.o.) and its isoflavones: daidzin (40 mg/kg, p.o.) and puerarin (150 mg/kg, p.o.). Their effects on a voluntary alcohol intake were assessed. KU and alcohol were also given for 9 days in an experiment on alcohol tolerance development. Finally, total and active ghrelin levels in peripheral blood serum were measured by ELISA method. Acamprosate, naltrexone, daidzin, and puerarin, reducing the alcohol intake, caused an increase in both forms of ghrelin levels. On the contrary, though KU inhibited the alcohol intake and alcohol tolerance development, it reduced ghrelin levels in alcohol-preferring rats. The changes of ghrelin concentration could play a role as an indicator of the currently used drugs. The other effect on the KU-induced shift in ghrelin levels in the presence of alcohol requires further detailed study.

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Section: Introductionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Differential Influence of Pueraria lobata Root Extract and Its Main Isoflavones on Ghrelin Levels in Alcohol-Treated Rats

et al. 2021

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“…A dosage of 5.0 g/ kg ethanol (35% EtOH v/v in water at 18.12 ml/kg; VWR, Suwanee, GA) or isovolumetric water was administered by intragastric gavage (i.g.). EtOH doses were selected to produce blood EtOH concentrations consistent with our previous studies and with human adolescent binge drinking episodes (199.7 ± 19.9 to 172.8 ± 13.3 mg/ dl, measured 60 min after dose 2, 4, 6, 8, and 10, (Healey, Landin, et al, 2020;Risher, Sexton, et al, 2015;Swartzwelder et al, 2015Swartzwelder et al, , 2019. Groups were assigned by cage numbers selected from a random number generator.…”

Section: Significancementioning

confidence: 99%

Effects of adolescent intermittent ethanol on hippocampal expression of glutamate homeostasis and astrocyte‐neuronal tethering proteins in male and female rats

Healey

Kibble

Bell

et al. 2020

J of Neuroscience Research

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Adolescent alcohol drinking is widely recognized as a significant public health problem, and evidence is accumulating that sufficient levels of consumption during this critical period of brain development have an enduring impact on neural and behavioral function. Recent studies have indicated that adolescent intermittent ethanol (AIE) exposure alters astrocyte function, astrocyte-neuronal interactions, and related synaptic regulation and activity. However, few of those studies have included female animals, and a broader assessment of AIE effects on the proteins mediating astrocyte-mediated glutamate dynamics and synaptic function is needed. We measured synaptic membrane expression of several such proteins in the dorsal and ventral regions of the hippocampal formation (DH, VH) from male and female rats exposed to AIE or adolescent intermittent water. In the DH, AIE caused elevated expression of glutamate transporter 1 (GLT-1) in both males and females, elevated postsynaptic density 95 expression in females only, and diminished NMDA receptor subunit 2A expression in males only. AIE and sex interactively altered ephrin receptor A4 (EphA4) expression in the DH. In the VH, AIE elevated expression of the cystine/glutamate antiporter and the glutamate aspartate transporter 1 (GLAST) in males only.Compared to males, female animals expressed lower levels of GLT-1 in the DH and greater levels of ephrin receptor B6 (EphB6) in the VH, in the absence of AIE effects.These results support the growing literature indicating that adolescent alcohol exposure produces long-lasting effects on astrocyte function and astrocyte-neuronal interactions. The sex and subregion specificity of these effects have mechanistic implications for our understanding of AIE effects generally.

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“…Following the removal of these Vapor Chronic intermittent alcohol vapor was used to show that neurons in the central nucleus of the amygdala that are activated during alcohol withdrawal contain corticotropin-releasing factor neurons that play a role in the escalation of alcohol drinking and somatic signs of withdrawal. (Healey et al, 2020) Vapor Acute exposure to alcohol vapor was used to show that acyl-ghrelin (a gut-brain signaling hormone) is elevated in male rats following exposure to alcohol in early adolescence. (Finegersh & Homanics, 2014) Vapor and 2BC Chronic intermittent alcohol vapor was used to show that paternal alcohol exposure can cause epigenetic modifications within male offspring.…”

Section: Understanding Resultsmentioning

confidence: 99%

Experimental Models of Alcohol Use Disorder and Their Application for Pathophysiological Investigations

2023

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Alcohol use disorder (AUD) is a complex disorder characterized by compulsive alcohol use and a lack of control over alcohol intake. Several experimental methods using mouse models have been developed to improve research regarding this disorder. Mouse behavioral paradigms are advantageous in inducing alcohol dependence and evaluating alcohol intake, circumventing ethical issues, and increasing experimental control over human-based experiments. These behavioral methods typically fall under one of two categories: forced exposure and voluntary consumption. This paper highlights two common paradigms used to study AUD in rodent models: one forced exposure method (use of a vapor inhalation system for alcohol exposure) and one voluntary consumption method (the two-bottle choice procedure). The effectiveness and experimental validity of these behavioral paradigms for pathophysiological investigations of AUD and how they can be combined are also discussed, along with their individual strengths and weaknesses.

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Effects of ethanol on plasma ghrelin levels in the rat during early and late adolescence

Cited by 15 publications

References 45 publications

Differential Influence of Pueraria lobata Root Extract and Its Main Isoflavones on Ghrelin Levels in Alcohol-Treated Rats

Differential Influence of Pueraria lobata Root Extract and Its Main Isoflavones on Ghrelin Levels in Alcohol-Treated Rats

Effects of adolescent intermittent ethanol on hippocampal expression of glutamate homeostasis and astrocyte‐neuronal tethering proteins in male and female rats

Experimental Models of Alcohol Use Disorder and Their Application for Pathophysiological Investigations

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