scholarly journals Melanocortin-4 Receptor and Lipocalin 2 Gene Variants in Spanish Children with Abdominal Obesity: Effects on BMI-SDS After a Lifestyle Intervention

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 960 ◽  
Author(s):  
Morell-Azanza ◽  
Ojeda-Rodríguez ◽  
Giuranna ◽  
Azcona-SanJulián ◽  
Hebebrand ◽  
...  

Mutations leading to a reduced function of the melanocortin-4 receptor (MC4R) exert a major gene effect on extreme obesity. Recently it was shown that the bone derived hormone lipocalin 2 (LCN2) binds to the MC4R and activates a MC4R dependent anorexigenic pathway. We identified mutations in both genes and screened the effects of MC4R and LCN2 mutations on eating behavior and weight change after a lifestyle intervention. One hundred and twelve children (11.24 ± 2.6 years, BMI-SDS 2.91 ± 1.07) with abdominal obesity participated in a lifestyle intervention. MC4R and LCN2 coding regions were screened by Sanger sequencing. Eating behavior was assessed at baseline with the Children Eating Behavior Questionnaire (CEBQ). We detected three previously described non-synonymous MC4R variants (Glu42Lys, Thr150Ile, and Arg305Gln) and one non-synonymous polymorphism (Ile251Leu). Regarding LCN2, one known non-synonymous variant (Thr124Met) was detected. Eating behavior was described in carriers of the MC4R and LCN2 mutation and in non-carriers. MC4R and LCN2 mutations were detected in 2.42% and 0.84%, respectively, of Spanish children with abdominal obesity. A number of subjects with functional mutation variants in MC4R and LCN2 were able to achieve a reduction in BMI-SDS after a lifestyle intervention.

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 289
Author(s):  
Amelia Marti ◽  
Isabel Martínez ◽  
Ana Ojeda-Rodríguez ◽  
María Cristina Azcona-Sanjulian

Background: Elevated circulating plasma levels of both lipopolysaccharide-binding protein (LBP) and chemerin are reported in patients with obesity, but few studies are available on lifestyle intervention programs. We investigated the association of both LBP and chemerin plasma levels with metabolic syndrome (MetS) outcomes in a lifestyle intervention in children and adolescents with abdominal obesity Methods: Twenty-nine patients enrolled in a randomized controlled trial were selected. The lifestyle intervention with a 2-month intensive phase and a subsequent 10-month follow-up consisted of a moderate calorie-restricted diet, recommendations to increase physical activity levels, and nutritional education. Results: Weight loss was accompanied by a significant reduction in MetS prevalence (−43%; p = 0.009). Chemerin (p = 0.029) and LBP (p = 0.033) plasma levels were significantly reduced at 2 months and 12 months, respectively. At the end of intervention, MetS components were associated with both LBP (p = 0.017) and chemerin (p < 0.001) plasma levels. Conclusions: We describe for the first time a reduction in both LBP and chemerin plasma levels and its association with MetS risk factors after a lifestyle intervention program in children and adolescents with abdominal obesity. Therefore, LBP and chemerin plasma levels could be used as biomarkers for the progression of cardiovascular risk in pediatric populations.


Medicine ◽  
2020 ◽  
Vol 99 (43) ◽  
pp. e22855
Author(s):  
Li-Hua Wang ◽  
Wei Huang ◽  
Wei Zhou ◽  
Li Zhou ◽  
Xiao-Li Zhou ◽  
...  

2015 ◽  
Vol 68 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Javier A. Vega ◽  
Gloria Salazar ◽  
María Isabel Hodgson ◽  
Luis Rodrigo Cataldo ◽  
Macarena Valladares ◽  
...  

Background/Aims: To evaluate the association between allelic variants of melanocortin receptors -3 and -4 (MC3R and MC4R, respectively) and leptin receptor (LEPR) genes with body mass index (BMI) and eating behavior. Methods: We selected 344 Chilean adults (57.8% women; age 39.1 ± 6.6 years) with a wide variation in BMI (30.3 ± 6.3 kg/m2). The Three-Factor Eating Questionnaire-R18 that measures uncontrolled eating (UE), emotional eating (EE) and cognitive restraint scores was adapted, validated and assessed for association with BMI. Genotypes were determined by polymerase chain reaction followed by restriction fragment length polymorphism techniques and Taqman assays. Results: Higher EE scores were found in obese vs. non-obese in both men (p = 0.01) and women (p < 0.001). UE scores were significantly associated with BMI only in women (p = 0.002). No significant differences in eating behavior scores or BMI were found by LEPR (rs1137101, rs8179183 and rs1137100 polymorphisms) or MC3R (rs3746619 and rs3827103). Carriers of the C allele for MC4R rs17782313 showed significantly higher scores of UE compared to non-carriers (2.3 ± 0.8 vs. 2.0 ± 0.7; p = 0.02). Additionally, we also report a monogenic case of obesity carrying the pathogenic mutation 449C>T (Thr150Ile) in MC4R gene with no apparent alterations in eating behavior scores. Conclusions: UE scores were higher in C-allele carriers of MC4R-rs17782313 compared to non-carriers.


2011 ◽  
Vol 90 (6) ◽  
pp. 735-739 ◽  
Author(s):  
R.I. Werneck ◽  
F.P. Lázaro ◽  
A. Cobat ◽  
A.V. Grant ◽  
M.B. Xavier ◽  
...  

2015 ◽  
Vol 15 (4) ◽  
pp. 203-209 ◽  
Author(s):  
Cícero B Menezes ◽  
Wilson R Maluf ◽  
Marcos V Faria ◽  
Sebastião M Azevedo ◽  
Juliano T V Resende ◽  
...  

Abstract The objective of this work was to study the genetic control of the PRSV-W (Papaya Ringspot Virus - Watermelon Strain) resistance in Cucurbita pepo 'Whitaker' line. Plants of parental lines Whitaker (resistant) and Caserta (susceptible), and of the generations F1, F2, BC11 and BC12 were evaluated for their reactions to PRSV-W. Caserta plants showed severe mosaic symptoms, while Whitaker grew vigorously and remained almost totally symptom-free. Most of the F1, F2 and backcross plants also presented severe mosaic symptoms. Data were used to test a hypothesis of monogenic inheritance under different presumed degrees of dominance, and genetic models were tested using maximum likelihood tests of genetic control. Broad-sense heritability was of 0.57 for the first evaluation. Resistance to PRSV-W in C. pepo 'Whitaker' is due to a major gene effect summed to polygenic effects.


Author(s):  
T.I. Axenovich ◽  
A.M. Zaidman ◽  
I.V. Zorkoltseva ◽  
I.L. Tregubova ◽  
P.M. Borodin

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