Smoking Genes: A Case–Control Study of Dopamine Transporter Gene (SLC6A3) and Dopamine Receptor Genes (DRD1, DRD2 and DRD3) Polymorphisms and Smoking Behaviour in a Malay Male Cohort

Bakar, Ruzilawati Abu; Islam, Asiful; Muhamed, Siti Khariem Sophia; Ahmad, Imran

doi:10.3390/biom10121633

Cited by 8 publications

(12 citation statements)

References 66 publications

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“…In a study of rural China, the risk of early onset smoking for individuals with the rs27072-A allele was shown to be almost three times higher in smokers who were heavily dependent on nicotine than in total smokers (Ling et al, 2004) (Table 2). In Malay males, no association with smoking behavior was found at either the genotype or allele level (Ruzilawati et al, 2020). Gara et al (O'Gara et al, 2007) also studied polymorphisms in rs115, rs270, and rs296, with all three SNPs not associated with smoking cessation.…”

Section: Ddcmentioning

confidence: 99%

Advances in association of genetic polymorphisms within the dopaminergic system with nicotine dependence

Yang

Wang

Chen

et al. 2023

Preprint

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Nicotine is the main compound in cigarettes which leads to smoking addiction. Nicotine acts on the limbic dopamine reward loop in the midbrain through binding to nicotinic acetylcholine receptors, promoting the release of dopamine, resulting in a rewarding effect or satisfaction. This satisfaction is essential for continued and compulsive tobacco use, and therefore dopamine plays a crucial role in nicotine dependence (ND). Numerous studies have identified genetic polymorphisms of dopaminergic pathways which may influence nicotine susceptibility and the degree of addiction. Dopamine levels are greatly influenced by synthesis, storage, release, degradation, and reuptake related genes, including genes encoding tyrosine hydroxylase (TH), dopamine decarboxylase (DDC), dopamine transporter (DAT1/SLC6A3), dopamine receptor (DRD), dopamine 3-hydroxylase (DBH), catechol oxygen methyltransferase (COMT), and monoamine oxidase (MAO). In this paper, we review research progress on the effects of polymorphisms in the above genes on downstream smoking behavior and ND, to provide a theoretical basis for the elucidation of the genetic mechanism underlying ND and future personalized treatment for smoking cessation.

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Section: Ddcmentioning

confidence: 99%

Advances in association of genetic polymorphisms within the dopaminergic system with nicotine dependence

Yang

Wang

Chen

et al. 2023

Preprint

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“…The consumption of nicotine stimulates the production and utilization of DA in the brain [ 119 , 120 , 121 ], which would further encourage nicotine use in individuals with hypodopaminergic signaling. An individual with hypodopaminergic signaling (or RDS) may be more vulnerable to substance use, such as smoking [ 122 , 123 , 124 , 125 , 126 , 127 ], even during pregnancy [ 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 ], leading to potential obesity risks later on in offspring [ 65 , 66 , 91 , 103 , 113 , 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 ]. If this genetic risk is passed down as well, offspring may also then experience abnormal craving behaviors associated with both obesity and substance abuse.…”

Section: Genetic Factors Of Nicotine Use and Obesity Riskmentioning

confidence: 99%

Prenatal Effects of Nicotine on Obesity Risks: A Narrative Review

White

Roeder

Blum

et al. 2022

IJERPH

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Nicotine usage by mothers throughout pregnancy has been observed to relate to numerous deleterious effects in children, especially relating to obesity. Children who have prenatally been exposed to nicotine tend to have lower birth weights, with an elevated risk of becoming overweight throughout development and into their adolescent and adult life. There are numerous theories as to how this occurs: catch-up growth theory, thrifty phenotype theory, neurotransmitter or endocrine imbalances theory, and a more recent examination on the genetic factors relating to obesity risk. In addition to the negative effect on bodyweight and BMI, individuals with obesity may also suffer from numerous comorbidities involving metabolic disease. These may include type 1 and 2 diabetes, high cholesterol levels, and liver disease. Predisposition for obesity with nicotine usage may also be associated with genetic risk alleles for obesity, such as the DRD2 A1 variant. This is important for prenatally nicotine-exposed individuals as an opportunity to provide early prevention and intervention of obesity-related risks.

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“…(1) Receptor D1 . Whereas various investigations have failed to see any bipolar changes in the D1 receptor gene [ 71 , 72 ], a connection between polymorphism of the D1 receptor A48G and bipolar disease has been observed [ 73 , 74 ].…”

Section: Gpcrs and Mood Disordersmentioning

confidence: 99%

Insights into the Promising Prospect of G Protein and GPCR-Mediated Signaling in Neuropathophysiology and Its Therapeutic Regulation

Rahman

Islam

Mim

et al. 2022

Oxidative Medicine and Cellular Longevity

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G protein-coupled receptors (GPCRs) are intricately involved in the conversion of extracellular feedback to intracellular responses. These specialized receptors possess a crucial role in neurological and psychiatric disorders. Most nonsensory GPCRs are active in almost 90% of complex brain functions. At the time of receptor phosphorylation, a GPCR pathway is essentially activated through a G protein signaling mechanism via a G protein-coupled receptor kinase (GRK). Dopamine, an important neurotransmitter, is primarily involved in the pathophysiology of several CNS disorders; for instance, bipolar disorder, schizophrenia, Parkinson’s disease, and ADHD. Since dopamine, acetylcholine, and glutamate are potent neuropharmacological targets, dopamine itself has potential therapeutic effects in several CNS disorders. GPCRs essentially regulate brain functions by modulating downstream signaling pathways. GPR6, GPR52, and GPR8 are termed orphan GPCRs because they colocalize with dopamine D1 and D2 receptors in neurons of the basal ganglia, either alone or with both receptors. Among the orphan GPCRs, the GPR52 is recognized for being an effective psychiatric receptor. Various antipsychotics like aripiprazole and quetiapine mainly target GPCRs to exert their actions. One of the most important parts of signal transduction is the regulation of G protein signaling (RGS). These substances inhibit the activation of the G protein that initiates GPCR signaling. Developing a combination of RGS inhibitors with GPCR agonists may prove to have promising therapeutic potential. Indeed, several recent studies have suggested that GPCRs represent potentially valuable therapeutic targets for various psychiatric disorders. Molecular biology and genetically modified animal model studies recommend that these enriched GPCRs may also act as potential therapeutic psychoreceptors. Neurotransmitter and neuropeptide GPCR malfunction in the frontal cortex and limbic-related regions, including the hippocampus, hypothalamus, and brainstem, is likely responsible for the complex clinical picture that includes cognitive, perceptual, emotional, and motor symptoms. G protein and GPCR-mediated signaling play a critical role in developing new treatment options for mental health issues, and this study is aimed at offering a thorough picture of that involvement. For patients who are resistant to current therapies, the development of new drugs that target GPCR signaling cascades remains an interesting possibility. These discoveries might serve as a fresh foundation for the creation of creative methods for pharmacologically useful modulation of GPCR function.

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Smoking Genes: A Case–Control Study of Dopamine Transporter Gene (SLC6A3) and Dopamine Receptor Genes (DRD1, DRD2 and DRD3) Polymorphisms and Smoking Behaviour in a Malay Male Cohort

Cited by 8 publications

References 66 publications

Advances in association of genetic polymorphisms within the dopaminergic system with nicotine dependence

Advances in association of genetic polymorphisms within the dopaminergic system with nicotine dependence

Prenatal Effects of Nicotine on Obesity Risks: A Narrative Review

Insights into the Promising Prospect of G Protein and GPCR-Mediated Signaling in Neuropathophysiology and Its Therapeutic Regulation

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