Dataset Information

Overweight and obesity during adolescence increases the risk of renal cell carcinoma.

ABSTRACT: While overweight among adults has been linked with renal cell carcinoma (RCC) risk, little is known about the potential influence of overweight and obesity during adolescence. To ascertain if adolescent body mass index is associated with subsequent risk of RCC, we identified a cohort of 238,788 Swedish men who underwent mandatory military conscription assessment between 1969 and 1976 at a mean age of 18.5 years. At the time of conscription assessment, physical and psychological tests were performed including measurements of height and weight. Participants were followed through linkage to the Swedish Cancer Registry to identify incident diagnoses of RCC. The association between body mass index (BMI, kg/m² ) at conscription assessment and subsequent RCC was evaluated using multivariable Cox regression. During a follow-up of up to 37?years, 266 men were diagnosed with RCC. We observed a trend for higher RCC risk with increasing BMI during adolescence, where one-unit increase in BMI conferred a 6% increased risk of RCC (95% CI 1.01-1.10). compared to normal weight men (BMI 18.5-?

SUBMITTER: Landberg A

PROVIDER: S-EPMC6899622 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Overweight and obesity during adolescence increases the risk of renal cell carcinoma.

Landberg Anna A Fält Anna A Montgomery Scott S Sundqvist Pernilla P Fall Katja K

International journal of cancer 20190220 5

While overweight among adults has been linked with renal cell carcinoma (RCC) risk, little is known about the potential influence of overweight and obesity during adolescence. To ascertain if adolescent body mass index is associated with subsequent risk of RCC, we identified a cohort of 238,788 Swedish men who underwent mandatory military conscription assessment between 1969 and 1976 at a mean age of 18.5 years. At the time of conscription assessment, physical and psychological tests were perfor ...[more]

PMID: 30790271

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Project description:BACKGROUND:Rates of adolescent obesity and overweight are high. The offspring of overweight parents are at increased risk of becoming obese later in life. Investigating neural correlates of familial obesity risk and current overweight status in adolescence could help identify biomarkers that predict future obesity and that may serve as novel targets for obesity interventions. OBJECTIVE:Our primary aim was to use functional MRI to compare neural responses to words denoting high or low energy density (ED) foods and non-foods, in currently lean adolescents at higher compared with lower familial risk for obesity, and in overweight compared with lean adolescents. Secondary aims were to assess group differences in subjective appetite when viewing food and non-food words, and in objective ad libitum intake of high-ED foods in a laboratory setting. DESIGN:We recruited 36 adolescents (14-19y), of whom 10 were (obese/overweight "overweight"), 16 lean with obese/overweight mothers (lean high-risk, "lean-HR"), and 10 lean with lean mothers (lean low-risk, "lean-LR"). All underwent fMRI scanning while they viewed words representing high-ED foods, low-ED foods, or non-foods, and provided appetitive ratings in response to each word stimulus. They then consumed a multi-item ad libitum buffet meal. RESULTS:Food compared with non-food words activated a distributed emotion/reward system including insula and pregenual anterior cingulate cortex (ACC). Participants who were at increasing risk for obesity exhibited progressively weaker activation of an attentional/regulatory system including dorsolateral prefrontal cortex (PFC), dorsal ACC, and basal ganglia nuclei (activation was greatest in lean-LR, intermediate in lean-HR, and weakest in the overweight group). These group differences were most apparent for neural responses to high-compared with low-ED foods. Lean-HR (compared with lean-LR and overweight) adolescents reported greater desire for high-ED foods. Meal intake was greatest for the overweight, then lean-HR, then lean-LR groups. CONCLUSIONS:Adolescents at higher obesity risk exhibited reduced neural responses to high-ED food cues in a neural system that subserves attention and self-regulation. They also reported heightened appetitive responses to high-ED cues. Interventions that promote the capacity for self-regulation could prevent youth who have a familial predisposition for obesity from translating risk into reality.

Project description:BackgroundXp11.2 translocation renal cell carcinoma (tRCC) is defined by translocation of the transcription factor E3 (TFE3) gene located on chromosome Xp11.2. Due to the high incidence in women, 17β-estradiol (E2) may be a factor influencing TFE3 breaks, and the topoisomerase II (TOP2) poison is considered one of the important risk factors in mediating DNA breaks. In this study, we investigated the potential pathogenesis of Xp11.2 tRCC using the renal epithelial cell line HK-2.MethodsImmunofluorescence assay was performed to analyze DNA breaks by quantifying phosphorylation of H2AX (γH2AX), and the micronuclei (MN) assay was designed for monitoring chromosome breaks. The chromatin immunoprecipitation (CHIP) was used to detect whether proteins bound to specific DNA site, and the co-immunoprecipitation (Co-IP) was used to confirm whether proteins bound to other proteins. In some experiments, siRNA and shRNA were transfected to knockdown target genes.ResultsOur results demonstrated that DNA double-strand breaks were mediated by TOP2β in HK-2 cells, and this process could be amplified through estrogen receptor α (ERα)-dependent pathway induced by E2. After performing translocation site analysis using target region sequencing data in two Xp11.2 tRCC cell lines and ten Xp11.2 tRCC patients, we confirmed that TOP2β and ERα could both bind to TFE3 translocation sites directly to mediate DNA breaks in a E2-dependent manner. However, TOP2β and ERα were not observed to have direct interaction, indicating that their collaborative may be implemented in other ways. Besides, TFE3 was found to be upregulated through NRF1 with increasing E2 concentration, which could increase the risk of TFE3 breaks.ConclusionOur results indicate that E2 amplifies TOP2β-mediated TFE3 breaks by ERα-dependent pathway, and E2 upregulates TFE3 by NRF1 to increase the risk of TFE3 breaks. This suggests that E2 is an important pathogenic factor for Xp11.2 tRCC pathogenesis. Video Abstract.

Dataset Information

Overweight and obesity during adolescence increases the risk of renal cell carcinoma.

Publications

Overweight and obesity during adolescence increases the risk of renal cell carcinoma.

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