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Related Concept Videos

Chronic Pancreatitis II: Pathophysiology01:21

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...
Chronic Pancreatitis I: Introduction01:25

Chronic Pancreatitis I: Introduction

Chronic pancreatitis is a long-standing, relapsing inflammation of the pancreas, characterized by irreversible damage to the gland. It results in progressive destruction of the pancreatic parenchyma, fibrosis, and eventual loss of both exocrine and endocrine function. The disease may evolve gradually after multiple episodes of acute pancreatitis or develop independently.EtiologyChronic pancreatitis can arise from a variety of causes:Alcohol use is the leading cause, accounting for 70–80% of...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
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Cushing Syndrome II: Pathophysiology01:19

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Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance01:23

Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance

The elimination half-life and drug clearance of drugs following nonlinear kinetics can vary with dosage. The Michaelis-Menten parameters and drug concentration influence these factors. As the dose increases, the elimination half-life tends to lengthen, resulting in a reduction in clearance and a disproportionately larger area under the curve. The total clearance can be derived from the Michaelis-Menten equation for drugs following a one-compartment model.
A study on guinea pigs examined the...
CNS Depressants: Alcohol and Nicotine01:27

CNS Depressants: Alcohol and Nicotine

Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...

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Related Experiment Video

Updated: Jun 11, 2026

Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder
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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder

Published on: June 23, 2023

Hyperprolactinemia following chronic alcohol administration.

Dipak K Sarkar1

  • 1Endocrine Program, Biomedical Division of the Center of Alcohol Studies and Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, N.J., USA.

Frontiers of Hormone Research
|July 10, 2010
PubMed
Summary

Ethanol consumption, or alcohol intake, is a risk factor for elevated prolactin (PRL) levels, a condition known as hyperprolactinemia. Chronic alcohol use in animal models increases pituitary lactotrope proliferation via complex signaling pathways.

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Construction of Vapor Chambers Used to Expose Mice to Alcohol During the Equivalent of all Three Trimesters of Human Development
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Assessment of Glutamine as a Fuel Source for Alveolar Macrophages Exposed to Chronic Ethanol Using an Extracellular Flux Bioanalyzer
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Published on: July 13, 2014

Area of Science:

  • Endocrinology
  • Neuroscience
  • Toxicology

Background:

  • Elevated prolactin (PRL) levels, or hyperprolactinemia, are reported in individuals with alcohol use disorders.
  • Alcohol-induced hyperprolactinemia has been observed in both human and animal studies, suggesting ethanol as a risk factor.

Purpose of the Study:

  • To investigate the mechanisms by which ethanol consumption influences prolactin (PRL) production and pituitary lactotrope proliferation.
  • To elucidate the molecular signaling pathways involved in ethanol's effects on lactotropes.

Main Methods:

  • Animal studies involving chronic ethanol administration.
  • Analysis of pituitary lactotrope proliferation and plasma PRL levels.
  • Investigation of signaling pathways including dopamine D2 receptors, TGF-beta, and b-FGF.

Main Results:

  • Chronic ethanol administration elevated plasma PRL levels and increased pituitary lactotrope proliferation in animal models.
  • Ethanol's effects involve modulation of dopamine D2 receptor signaling, TGF-beta pathway, and b-FGF production.
  • MAP kinase p44/42 pathway activation is implicated in b-FGF production and secretion.

Conclusions:

  • Ethanol consumption is a significant risk factor for hyperprolactinemia.
  • Ethanol disrupts normal lactotrope function through complex molecular signaling, impacting PRL production and cell proliferation.
  • Targeting these pathways may offer therapeutic strategies for alcohol-related endocrine disturbances.