Dual effect of the <i>GHRL</i> gene variant in the molecular pathogenesis of obesity

Becer, Eda; Ergoren, Mahmut Cerkez

doi:10.2478/bjmg-2021-0011

Cited by 7 publications

(3 citation statements)

References 38 publications

(54 reference statements)

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“…At present, it is generally recognized that genetic and environmental factors are the main causes of obesity 3 , 16 . Recent studies have shown that the intestinal microbiota, an environmental factor, is closely related to the occurrence and development of obesity 4 , 5 , 15 , 16 . Ilseung et al 18 generated a model of adiposity by administering subtherapeutic antibiotic therapy to young mice and evaluated changes in the composition and capabilities of the gut microbiome.…”

Section: Discussionmentioning

confidence: 99%

Establishment of a novel obesity mouse model: the induction of intestinal microbiota dysbiosis

Li,

Gao,

Jia

et al. 2024

Sci Rep

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To establish and evaluate an intestinal microbiota dysbiosis-induced obesity mouse model. 50 C57BL/6 J male healthy mice were randomly divided into an obesity model group and the control group. The body weight, body length, and Lee’s index of the two groups of mice at week 1 and week 10 were compared. Serum glucose (GLU), total cholesterol (TC) and triglyceride (TG) were measured by enzyme-labeled colorimetric methods. Illumina HiSeq 16S rDNA high-throughput sequencing technology was used to characterize intestinal microbiota in feces. The success rate of model establishment in obese mice was 52%. The body weight, body length, Lee’s index, and abdominal fat (wet weight) in the obese model group were all higher than those in the control group, and the differences were statistically significant (P < 0.01). Serum GLU and TC levels in the obesity model group were higher than those in the control group (P < 0.05), and there was no difference in TG levels between the two groups (P > 0.05). The control group contained more abundant intestinal microbiota phyla and genera than did the obesity model group; the differences between the two groups were significant (FDR ≤ 0.05, P ≤ 0.05). Intestinal microbiota dysbiosis can be used to generate an obesity model in mice.

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Section: Discussionmentioning

confidence: 99%

Establishment of a novel obesity mouse model: the induction of intestinal microbiota dysbiosis

Li,

Gao,

Jia

et al. 2024

Sci Rep

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“…This amino acid residue is outside of mature ghrelin. In a study of Becer and Ergoren (2021), it has been shown that the frequency of the minor allele rs696217 T (Met72) was significantly higher in obese individuals. At the same time, in the study of Yadegari et al (2022) individuals with the TT genotype at the locus had the lowest prevalence of obesity compared to other genotypes among individuals.…”

Section: Tablementioning

confidence: 99%

Effect of the GHRL gene (rs696217) polymorphism on the metabolic disorders in patients with obesity in the Ukrainian population

Prodan,

Dzubanovsky,

Kamyshnyi

et al. 2023

Endocrine Regulations

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Objective. Over the past four decades, the prevalence of obesity has tripled and limited genetic studies with specific SNPs have been conducted, but no investigations using ghrelin and obestatin prepropeptide (GHRL) gene have been reported in the Ukrainians population. The aim of this study was to evaluate changes in the level of metabolic hormones in the blood of obese patients in relation to the GHRL (rs696217) polymorphism. Methods. The study involved 53 obesity cases and 48 non-obesity subjects (controls). The GHRL (rs696217) polymorphism was genotyped using a TaqMan real-time polymerase chain reaction method. Blood hormones were determined with commercially available kits using a Multi-skan FC analyzer. Results. Carriers of the T allele of the GHRL (rs696217) polymorphism were statistically significantly more in patients diagnosed with obesity compared to controls indicating a genetically determined cause of obesity. We also established a significant effect of the presence of the T allele of the GHRL (rs696217) polymorphism on the decrease in the adiponectin level and the increase of resistin level in obese patients. The study of the effect of genotypes (TT, GT, GG) of the GHRL (rs696217) polymorphism on the metabolic hormone levels in the blood of obese patients did not show reliably significant differences. Conclusions. The presence of the T allele of the GHRL (rs696217) polymorphism in Ukrainian population indicates an increased risk of the obesity development regardless on the homozygous or heterozygous genotype.

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“…[ 31 ] A dual effect of GHRL gene variants (i.e., rs34911341‐c.152C > T and rs696217‐c.214G > T) was reported in obesity and cholesterol metabolism in obese and non‐obese Turkish‐Cypriot subjects employing a case‐control study. [ 32 ] The rs696217 variant (c.214G > T) was found to be significantly higher in obese patients and in those with lower serum high‐density lipoprotein cholesterol than with the wild‐type genotype; hence, this susceptibility variant may be considered as a risk allele and a crucial marker for both obesity and cholesterol metabolism in this population and could potentially be implicated in clinical diagnosis and care.…”

Section: Introductionmentioning

confidence: 99%

Syndromic and Nonsyndromic Obesity: Underlying Genetic Causes in Humans

Duis

Butler

2022

Advanced Biology

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cardiovascular disease, hypertension, cancers, orthopedic problems, and reduced fertility.Genetic factors can be classified as monogenic or caused by variants of single genes, polygenic involving several interacting genes, or syndromes accompanying obesity and recognized phenotypes. Neurological dysfunction or abnormal regulation of energy utilization, expenditure or storage via hormone production, transport or receptors impact overall energy homeostasis. [1,2] Furthermore, heritability estimates indicate that genetic factors may contribute to up to 70% of obesity, primarily affecting genetic pathways common in lipid metabolism, fat deposition or lipid transport, eating behavior, food selection and hormones, physical activity or energy expenditure based on studies from monozygotic twins reared apart and living in a different environment. [3] Heritability estimates do increase from infancy through adolescence. Over 10 000 references in the medical literature were identified when searching for obesity genes and syndromes with approximately 80 recorded obesityrelated syndromes. [1][2][3][4][5] The prevalence estimates for monogenic obesity syndromes range from about one in 550 to aprroximately one in 1 million. [5] Clinical findings identified in genetic obesity syndromes often overlap, as found in at least 52 related obesity syndromes displaying some form of intellectual disability while seven syndromes present with macrocephaly and seven syndromes with microcephaly. [5] Obesity syndromes may exhibit complex patterns of inheritance including autosomal dominant (e.g., Alstrom), autosomal recessive (e.g., Carpenter), X-linked (e.g., Borjeson-Forssman-Lehmann), errors in genomic imprinting (e.g., Prader-Willi), triallelic inheritance (e.g., Bardet-Biedel) or chromosome anomalies (e.g., 16p11.2 deletion). Hormonal Pathways and Genetic RegulationHormones and their role in appetite control and weight regulation are now an active area of research with clinical trials often focusing on hyperphagia and overeating, common in rare obesity-related disorders such as Prader-Willi syndrome. [6] Eating hormones are becoming increasingly recognized as playing a role in the central nervous system (CNS), particularly regions Growing evidence supports syndromic and nonsyndromic causes of obesity, including genome-wide association studies, candidate gene analysis, advanced genetic technology using next-generation sequencing (NGS), and identification of copy number variants. Identification of susceptibility genes impacts mechanistic understanding and informs precision medicine. The cause of obesity is heterogeneous with complex biological processes playing a role by controlling peptides involved in regulating appetite and food intake, cellular energy, and metabolism. Evidence for heritability shows genetic components contributing to 40%-70% of obesity. Monogenic causes and obesity-related syndromes are discussed and illustrated as well as biological pathways, gene interactions, and factors contributing to the obesity phenotype. Over 550...

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Dual effect of the GHRL gene variant in the molecular pathogenesis of obesity

Cited by 7 publications

References 38 publications

Establishment of a novel obesity mouse model: the induction of intestinal microbiota dysbiosis

Establishment of a novel obesity mouse model: the induction of intestinal microbiota dysbiosis

Effect of the GHRL gene (rs696217) polymorphism on the metabolic disorders in patients with obesity in the Ukrainian population

Syndromic and Nonsyndromic Obesity: Underlying Genetic Causes in Humans

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