The interaction between MC4R gene variant (rs17782313) and dominant dietary patterns on depression in obese and overweight women: a cross sectional study

Hajmir, Mahya Mehri; Mirzababaei, Atieh; Clark, Cain C. T.; Ghaffarian-Ensaf, Rasool; Mirzaei, Khadijeh

doi:10.1186/s12902-023-01335-0

Cited by 4 publications

(2 citation statements)

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“…Specifically, the rs17782313 polymorphism of MC4R has been previously associated with higher BMI and higher appetite ( 30 ). Moreover, when C carriers are exposed to unhealthy eating patterns, the risk of developing depressive feelings increases ( 43 ). Our analysis revealed a tendency toward a correlation between the MC4R (rs17782313) CC + CT genotype and “Emotional overeating” mean value ( r = 0.211, p = 0.082) and as a categorical variable (Phi = 0.308, p = 0.010).…”

Section: Discussionmentioning

confidence: 99%

Relationship between energy balance and reward system gene polymorphisms and appetitive traits in young Mexican subjects

Rivera-Iñiguez,

Hunot-Alexander,

Sepúlveda-Villegas

et al. 2024

Front. Nutr.

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IntroductionAppetitive traits are influenced by the interplay between genetic and environmental factors. This study aimed to explore the relationship between gene polymorphisms involved in the regulation of energy balance and food reward and appetitive traits in young Mexican subjects.MethodsThis cross-sectional study involved 118 university freshman undergraduates who completed the Adult Eating Behaviour Questionnaire for Spanish speakers (AEBQ-Esp) to assess their appetitive traits. A real-time PCR system was employed to determine gene polymorphisms involved in energy balance (LEP rs7799039, MC4R rs17782313, FTO rs9939609, GHRL rs696217), and reward system (DRD2/ANKK1 Taq1A rs1800497 and COMT rs4680).ResultsThe mean age of participants was 20.14 ± 3.95 years, 71.2% were women and their mean BMI was 23.52 ± 4.05 kg/m2. COMT Met allele carriers presented a significantly higher “Emotional overeating” mean score than Val allele carriers (2.63 ± 0.70 vs. 2.23 ± 0.70, p = 0.028). The MC4R CC + CT genotype correlated positively with “Emotional overeating” (Phi = 0.308, p = 0.01). The COMT MetMet+MetVal genotype correlated with higher “Emotional overeating” (r = 0.257, p = 0.028; Phi = 0.249, p = 0.033). The protective genotype FTO TT correlated positively with “Emotional undereating” (Phi = 0.298, p = 0.012). Carriers of the risk genotype MC4R CC + CT presented a higher risk of “Emotional overeating” than TT carriers (OR = 2.4, 95% CI 1.3–4.8, p = 0.034). Carriers of the risk genotype COMT MetMet+MetVal (OR = 3.4, 95% CI 1.1–10.3, p = 0.033), were associated with a higher risk of “Emotional overeating” than ValVal carriers. The protective FTO genotype TT was associated with “Emotional undereating” (OR = 1.8, 95% CI 1.1–9.1, p = 0.014).DiscussionThe study found a relationship between the protective genotypes of FTO TT and “Emotional undereating” and risk genotypes of COMT Met/Met+Met/Val and MC4R CC + CT with “Emotional overeating.” These genetic factors may increase weight gain by enhancing hedonic food consumption and reducing satiety control. Future studies should focus on replication studies in ethnically diverse young adults and life stages to explore the relationship between polymorphisms and appetitive traits and weight. This will help tailor personalized nutrigenetic strategies to counteract disordered eating patterns leading to obesity and associated co-morbidities.

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Section: Discussionmentioning

confidence: 99%

Relationship between energy balance and reward system gene polymorphisms and appetitive traits in young Mexican subjects

Rivera-Iñiguez,

Hunot-Alexander,

Sepúlveda-Villegas

et al. 2024

Front. Nutr.

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“…The minor allele (C allele) for the MC4R rs17782313 variant has been associated with depressed mood. Previous studies have also investigated the interaction between the MC4R gene variant and dominant dietary patterns on depression in obese and overweight women (62).…”

Section: Mc4r Gene Polymorphism and Stress-induced Metabolic Dysfunctionmentioning

confidence: 99%

Genetic polymorphism and the link to stress-induced metabolic dysfunction

Mofolorunso,

Awobajo,

Okwute

2023

Babcock Univ. Med. J.

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Background: The impact of stress on health is well-established and it continues to influence modern life. While some individuals may manage stress well, others may experience detrimental impacts on their physical and emotional health. As stress has been related to several illnesses, including obesity, diabetes, cardiovascular diseases, and more, there is growing concern about stress-induced metabolic dysfunction. Main body: Here we review recent literature, elucidating the role of genetic polymorphisms in modulating an individual's reactivity to stress and susceptibility to stress-related metabolic disorders. This article discusses the genetic components, in particular the polymorphisms, that may predispose individuals toward metabolic dysregulation brought on by stress. Deoxyribonucleic acid (DNA) sequence differences that affect more than 1% of the population are known as genetic polymorphisms. Changes from genetic polymorphisms result in different gene expression, protein function, and other outcomes. Genetic polymorphisms in key stress-regulating genes can influence an individual's susceptibility to metabolic disturbances in response to chronic stress. Conclusion: The hypothalamic pituitary adrenal (HPA) axis and related molecular pathways play a pivotal role in mediating the effects of stress on metabolism. Understanding the genetic basis of stress-induced metabolic dysfunction has implications for personalized medicine and preventive strategies. By identifying individuals with genetic susceptibility to metabolic disturbances, targeted interventions can be designed to mitigate the adverse effects of stress on metabolic health. Furthermore, lifestyle modifications, stress management techniques, and tailored dietary interventions may be employed to promote overall well-being and prevent stress-induced metabolic disorders.

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Relative synonymous codon usage and codon pair analysis of depression associated genes

Khandia,

Gurjar,

Kamal

et al. 2024

Sci Rep

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Depression negatively impacts mood, behavior, and mental and physical health. It is the third leading cause of suicides worldwide and leads to decreased quality of life. We examined 18 genes available at the genetic testing registry (GTR) from the National Center for Biotechnological Information to investigate molecular patterns present in depression-associated genes. Different genotypes and differential expression of the genes are responsible for ensuing depression. The present study, investigated codon pattern analysis, which might play imperative roles in modulating gene expression of depression-associated genes. Of the 18 genes, seven and two genes tended to up- and down-regulate, respectively, and, for the remaining genes, different genotypes, an outcome of SNPs were responsible alone or in combination with differential expression for different conditions associated with depression. Codon context analysis revealed the abundance of identical GTG-GTG and CTG-CTG pairs, and the rarity of methionine-initiated codon pairs. Information based on codon usage, preferred codons, rare, and codon context might be used in constructing a deliverable synthetic construct to correct the gene expression level of the human body, which is altered in the depressive state. Other molecular signatures also revealed the role of evolutionary forces in shaping codon usage.

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The interaction between MC4R gene variant (rs17782313) and dominant dietary patterns on depression in obese and overweight women: a cross sectional study

Cited by 4 publications

References 70 publications

Relationship between energy balance and reward system gene polymorphisms and appetitive traits in young Mexican subjects

Relationship between energy balance and reward system gene polymorphisms and appetitive traits in young Mexican subjects

Genetic polymorphism and the link to stress-induced metabolic dysfunction

Relative synonymous codon usage and codon pair analysis of depression associated genes

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