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1.
BMC Pediatr ; 23(1): 87, 2023 02 21.
Artigo em Inglês | MEDLINE | ID: mdl-36810017

RESUMO

BACKGROUND: Obesity is defined as a multifactorial disease, marked by excessive accumulation of body fat, responsible for compromising the individual's health over the years. The energy balance is essential for the proper functioning of the body, as the individual needs to earn and spend energy in a compensatory way. Mitochondrial Uncoupling Proteins (UCP) help in energy expenditure through heat release and genetic polymorphisms could be responsible for reducing energy consumption to release heat and consequently generate an excessive accumulation of fat in the body. Thus, this study aimed to investigate the potential association between six UCP3 polymorphisms, that have not yet been represented in ClinVar®, and pediatric obesity susceptibility. METHODS: A case-control study was conducted with 225 children from Central Brazil. The groups were subdivided into obese (123) and eutrophic (102) individuals. The polymorphisms rs15763, rs1685354, rs1800849, rs11235972, rs647126, and rs3781907 were determined by real-time Polymerase Chain Reaction (qPCR). RESULTS: Biochemical and anthropometric evaluation of obese group showed higher levels of triglycerides, insulin resistance, and LDL-C and low level of HDL-C. Insulin resistance, age, sex, HDL-C, fasting glucose, triglyceride levels, and parents' BMI explained up to 50% of body mass deposition in the studied population. Additionally, obese mothers contribute 2 × more to the Z-BMI of their children than the fathers. The SNP rs647126 contributed to 20% to the risk of obesity in children and the SNP rs3781907 contribute to 10%. Mutant alleles of UCP3 increase the risk for triglycerides, total cholesterol, and HDL-C levels. The polymorphism rs3781907 is the only one that could not be a biomarker for obesity as the risk allele seem to be protective gains the increase in Z-BMI in our pediatric population. Haplotype analysis demonstrated two SNP blocks (rs15763, rs647126, and rs1685534) and (rs11235972 and rs1800849) that showed linkage disequilibrium, with LOD 76.3% and D' = 0.96 and LOD 57.4% and D' = 0.97, respectively. CONCLUSIONS: The causality between UCP3 polymorphism and obesity were not detected. On the other hand, the studied polymorphism contributes to Z-BMI, HOMA-IR, triglycerides, total cholesterol, and HDL-C levels. Haplotypes are concordant with the obese phenotype and contribute minimally to the risk of obesity.


Assuntos
Resistência à Insulina , Obesidade Infantil , Proteína Desacopladora 3 , Criança , Humanos , Índice de Massa Corporal , Estudos de Casos e Controles , Colesterol , Frequência do Gene , Genótipo , Obesidade Infantil/genética , Polimorfismo de Nucleotídeo Único , Triglicerídeos , Proteína Desacopladora 3/genética
2.
Orthop J Sports Med ; 5(5): 2325967117708190, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-28607939

RESUMO

BACKGROUND: A subset of patients have clinical internal and/or external knee rotational instability despite no apparent injury to the cruciate or collateral ligaments. PURPOSE/HYPOTHESIS: The purpose of this study was to assess the effect of sequentially cutting the posterolateral, anterolateral, posteromedial, and anteromedial structures of the knee on rotational stability in the setting of intact cruciate and collateral ligaments. It was hypothesized that cutting of the iliotibial band (ITB), anterolateral ligament and lateral capsule (ALL/LC), posterior oblique ligament (POL), and posteromedial capsule (PMC) would significantly increase internal rotation, while sectioning of the anteromedial capsule (AMC) and the popliteus tendon and popliteofibular ligament (PLT/PFL) would lead to a significant increase in external knee rotation. STUDY DESIGN: Controlled laboratory study. METHODS: Ten pairs (N = 20) of cadaveric knees were assigned to 2 sequential cutting groups (group 1: posterolateral-to-posteromedial [PL → PM] and group 2: posteromedial-to-posterolateral [PM → PL]). Specimens were subjected to applied 5-N·m internal and external rotation torques at knee flexion angles of 0°, 30°, 60°, and 90° while intact and after each cut state. Rotational changes were measured and compared with the intact and previous cut states. RESULTS: Sectioning of the ITB significantly increased internal rotation at 60° and 90° by 5.4° and 6.2° in group 1 (PL → PM) and 3.5° and 3.8° in group 2 (PM → PL). PLT/PFL complex sectioning significantly increased external rotation at 60° and 90° by 2.7° and 2.9° in group 1 (PL → PM). At 60° and 90° in group 2 (PM → PL), ALL/LC sectioning produced significant increases in internal rotation of 3.1° and 3.5°, respectively. In group 2 (PM → PL), POL sectioning produced a significant increase in internal rotation of 2.0° at 0°. AMC sectioning significantly increased external rotation at 30° to 90° of flexion with a magnitude of change of <1° in both groups 1 (PL → PM) and 2 (PM → PL). CONCLUSION: Collectively, the anterolateral corner structures provided primary internal rotation control of the knee from 60° to 90° of knee flexion in knees with intact cruciate and collateral ligaments. The ITB was the most significant primary stabilizer of internal rotation. The POL had a primary role for internal rotational stability at full extension. The PLT/PFL complex was a primary stabilizer for external rotation of the knee at 60° and 90°. CLINICAL RELEVANCE: This study delineates the primary and secondary roles of the ITB, ALL/LC, POL, and PLT/PFL to rotatory stability of the knee and provides new information to understand knee rotational instabilities.

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