Associations between the &lt;b&gt;&lt;i&gt;LEP&lt;/i&gt;&lt;/b&gt; -2548G/A Promoter and Baseline Weight and between &lt;b&gt;&lt;i&gt;LEPR&lt;/i&gt;&lt;/b&gt; Gln223Arg and Lys656Asn Variants and Change in BMI &lt;b&gt;&lt;i&gt;z&lt;/i&gt;&lt;/b&gt; Scores in Arab Children and Adolescents Treated with Risperidone

Almandil, Noor B.; Lodhi, Rohit J.; Ren, Hongyan; Besag, Frank; Rossolatos, David; Ohlsen, Ruth; Slomp, Caitlin; Lapetina, Diego L.; Plazzotta, Giona; Murray, Macey L; Al-Sulaiman, Abdulsalam A.; Gringras, Paul; Wong, Ian C. K.; Aitchison, Katherine J.

doi:10.1159/000490463

Cited by 5 publications

(3 citation statements)

References 36 publications

(42 reference statements)

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“…The associations seen with the G allele of the LEPR SNP rs1137101 were observed with both weight gain and weight relatively stable for T1D and T2D groups versus controls. This is in keeping with previous reports about this allele and its relation to BMI in people prescribed sodium valproate [ 32 ] although the GG genotype was associated with less BMI increase over time in that study [ 33 ]…”

Section: Discussionsupporting

confidence: 92%

A study to investigate genetic factors associated with weight gain in people with diabetes: analysis of polymorphisms in four relevant genes

Heald,

Qin,

Loureiro

et al. 2023

Adipocyte

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Background Weight change is often seen in people with diabetes. We investigated the effects of genes associated with weight change/glucose handling/insulin-signalling. Materials/methods DNA from diabetes individuals and non-diabetes individuals, plus clinical data, were available from the DARE study ( n = 379 individuals: T1D n = 111; T2D n = 222; controls n = 46). Weight gain was assessed by temporal change of Body Mass Index (BMI). Genotyping was performed for CAV1 rs926198, LEPR rs1137101, BDNF rs6265 and FTO rs9939609. Results No differences in genotype distributions were observed for the four SNPs in all groups un-stratified by weight gain. Following stratification differences in genotype distribution were observed. For those BMI relatively stable; controls showed a difference in genotype distributions versus T1D ( CAV1 rs926198, LEPR rs1137101). In T2D vs controls, significant differences were observed in genotype distribution for all four genes. For BMI increase, the only difference by category was LEPR rs1137101 (bothT1D/T2D vs controls). In BMI-stable groups, CAV1 rs926198, T1D individuals showed lower T allele frequency ( p =0.004) vs non-diabetes and for LEPR rs1137101 a higher G allele frequency versus controls ( p =0.002). For T2D, CAV1 rs926198, T allele frequency was lower in T2D than controls ( p =0.005). For LEPR rs1137101, the G allele frequency was higher than in controls ( p =0.004). In those with BMI increase, LEPR rs1137101 T1D individuals had higher G allele frequency versus controls ( p =0.002) as did T2D vs controls ( p =0.03). Conclusion Differences in allele frequency were seen between diabetes individuals and non-diabetes diagnosed at baseline in relation to the likelihood of BMI increase of >10%. It is established that the G allele of LEPR rs1137101 is associated with weight gain/obesity. However, this is the first report of CAV1 rs926198 polymorphism being associated with weight stability/gain in diabetes.

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Section: Discussionsupporting

confidence: 92%

A study to investigate genetic factors associated with weight gain in people with diabetes: analysis of polymorphisms in four relevant genes

Heald,

Qin,

Loureiro

et al. 2023

Adipocyte

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“…Se ha revisado otro estudio en el que ciertas variantes genéticas se asocian con diferencias en el incremento de índice de masa corporal en niños y adolescentes que comienzan tratamiento con risperidona (32). La variante genética rs1137101 del receptor de leptina (LEPR) está directamente relacionada con el incremento de peso durante el tratamiento con dicho fármaco.…”

Section: Otrosunclassified

Farmacogenómica en psiquiatría de niños y adolescentes: Una revisión del estado actual de la cuestión

Alario¹,

Cuesta²

2021

Rev Psiquiatr Infanto-Juv

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La farmacogenómica estudia el rol de los diferentes componentes del genoma humano en la respuesta a fármacos. Conocer la información sobre estos factores podría ser de utilidad en el ámbito de la psicofarmacología de niños y adolescentes para individualizar la selección de tratamientos y minimizar reacciones adversas. Material y métodos: Se ha realizado una búsqueda bibliográfica de publicaciones en los últimos diez años en la base de datos PubMed, utilizando las siguientes palabras clave: Psychiatry AND child and adolescent AND pharmacogenomic/pharmacogenetic. Se seleccionaron 35 artículos siguiendo criterios de in-clusión previamente establecidos. Resultados: Los resultados más consistentes son los relativos a los polimorfismos en los genes de la familia CYP450, sobre todo los diferentes fenotipos metabolizadores (lento, intermedio, rápido) que influyen en la respuesta farmacológica de Inhibidores Selectivos de la Recaptación de Serotonina (ISRS), Risperidona y Atomoxetina. Además, los polimorfismos funcionales del gen HTR2A están relacionados con la respuesta clínica de los ISRS y varios polimorfismos de COMT se relacionan con una menor respuesta al Metilfenidato y a otros estimulantes. Variantes de los receptores serotoninérgicos como 5HT2A, 5HT1B, influyen en la respuesta y en la probabilidad de efectos secundarios de los ISRS. Conclusiones: El uso de test farmacogenéticos puede llegar a ser una herramienta complementaria de ayuda en la toma de decisiones terapéuticas en la psiquiatría de niños y adolescentes. No obstante, según los resultados revisados, no está justificado su uso generalizado, aunque podría considerarse en algunos pacientes con enfermedades graves y con respuesta insuficiente a los fármacos ensayados.

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“…Analysis of the scientometric PubMed database showed that the most studied association between obesity and type 2 diabetes are the following SNPs of the LEPR gene: rs3790435 [11] and missense mutations rs1137100 [12,13], rs1137101 [14,15], rs1805094 [16], rs8179183 [17], which are located in gene regions encoding functionally significant domains of the LEPR protein.…”

mentioning

confidence: 99%

Association of leptin receptor gene polymorphisms and meta-inflammation markers with metabolically unhealthy obesity in children

Абатуров¹,

Никулина

2021

ZMJ

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The aim: to study the contribution of single-nucleotide polymorphisms (SNP) of the leptin receptor (LEPR) gene and meta-inflammation markers to the formation of metabolically unhealthy obesity (MUO) in children. Materials and methods. A total of 109 obese children aged 6–18 years were examined. Based on the recommendations of the National Heart, Lung, and Blood Institute (NHLBI), 2 observation groups were formed. The main group (n = 56) was represented by patients with MUO. The control group (n = 53) comprised children with metabolically healthy obesity (MHO). Serum levels of interleukin-1β (IL-1β) were measured using a chemiluminescent immunoassay (CLIA) method, interleukin-6, leptin, adiponectin – by enzyme-linked immunosorbent assay (ELISA) and the serum level of C-reactive protein were quantified by latex turbidimetric method (Synevo, Ukraine). The method of next-generation sequencing (NGS) (CeXGat, Germany) was used to identify LEPR SNP. Statistical methods were used: analysis of variance, Spearman’s correlation analysis and multiple discriminant analysis. Results. In obese children aged 6 to 18 years, there was an increase in pro-inflammatory adipokines IL-6 and leptin and a decrease in anti-inflammatory adiponectin. Statistically significant changes in these indicators were more expressed in the main group: IL-6 – 7.4 ± 0.5 pg/ml (ρ = 0.65; P ≤ 0.001); adiponectin – 3.9 ± 0.8 μg/ml (ρ = -0.27; P = 0.007) among all the children examined, leptin in girls – 47.8 ± 4.4 ng/ml (ρ = -0.28; P = 0.003) compared with the results of patients in the control group: IL-6 – 4.3 ± 0.3 pg/ml, adiponectin – 7.7 ± 2.4 μg/ml, leptin in girls – 32.5 ± 4.3 ng/ml, P ≤ 0.05. The most important in the development of MUO were the following SNP of the LEPR gene: rs3790435 (CiMUO = 0.939), rs2186248 (CiMUO = 0.862), P < 0.05. A strong correlation was found between MUO and serum IL-6 level (ρ = 0.7), LEPR SNP rs3790435 (ρ = 0.7), basal hyperinsulinemia (ρ = 0.72); Р ≤ 0.001. The risk of IL-6-dependent meta-inflammation in the presence of SNP rs3790435 of the LEPR gene: OR = 17.11; 95 % CI 2.8–20.4. Conclusions. Meta-inflammation in MUO is IL-6-dependent. Among the 10 SNPs of the LEPR gene that we identified, SNP rs3790435 of the LEPR gene has a strong association with the formation of MUO. SNP rs2186248 LEPR was described by us for the first time when it was found in 94.1 % of obese children, but it was characterized by the presence of a weak association with MUO.

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Associations between the <b><i>LEP</i></b> -2548G/A Promoter and Baseline Weight and between <b><i>LEPR</i></b> Gln223Arg and Lys656Asn Variants and Change in BMI <b><i>z</i></b> Scores in Arab Children and Adolescents Treated with Risperidone

Cited by 5 publications

References 36 publications

A study to investigate genetic factors associated with weight gain in people with diabetes: analysis of polymorphisms in four relevant genes

A study to investigate genetic factors associated with weight gain in people with diabetes: analysis of polymorphisms in four relevant genes

Farmacogenómica en psiquiatría de niños y adolescentes: Una revisión del estado actual de la cuestión

Association of leptin receptor gene polymorphisms and meta-inflammation markers with metabolically unhealthy obesity in children

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