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Procolipase gene: no association with early-onset obesity or fat intake.

ABSTRACT: BACKGROUND:Several lines of evidence in volvement of procolipase (CLPS) or its derivative enterostatin in dietary fat absorption, regulation of fat intake, and body weight in rodents. We explored the relationship between genetic variation in CLPS, early-onset obesity and fat intake in humans. METHODS:We screened the CLPS in 93 extremely obese children and adolescents and 96 underweight young adults for sequence variations and genotyped single nucleotide polymorphisms (SNPs) in extremely obese children and adolescents, healthy normal-and underweight young adults and obesity trios. Case-control and family-based association analyses were performed. RESULTS:Five sequence variations were identified: two non-synonymous SNPs: rs2766597 (Leu8Pro), rs41270082 (Arg109Cys); one SNP in the 5'UTR: rs3748050; one intronic SNP: rs3748051; and one infrequent novel non-synonymous variant: Arg55His. For rs2766597, rs3748050, and rs3748051 we obtained no evidence for an association with obesity in the case-control comparison. For rs41270082 there was a trend for association which could not be substantiated in the family-based association analysis. Additionally, we found no association in subgroup analyses pertaining to the extremely obese children and adolescents in the lowest and highest quartile of the percentage of energy consumed as fat. CONCLUSIONS:We found no evidence for an association of CLPS SNPs rs2766597, rs41270082, rs3748050, and rs3748051 with obesity or percentage of dietary fat intake.

SUBMITTER: Wermter AK

PROVIDER: S-EPMC6444705 | biostudies-literature | 2009

REPOSITORIES: biostudies-literature

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Procolipase gene: no association with early-onset obesity or fat intake.

Wermter Anne-Kathrin AK Scherag André A Holter Katja K Reichwald Kathrin K Lichtner Peter P Siegfried Wolfgang W Blundell John J Lawton Clare C Whybrow Stephen S Stubbs James J Arch Jonathan R JR Meitinger Thomas T Platzer Matthias M Hinney Anke A Hebebrand Johannes J

Obesity facts 20090209 1

<h4>Background</h4>Several lines of evidence in volvement of procolipase (CLPS) or its derivative enterostatin in dietary fat absorption, regulation of fat intake, and body weight in rodents. We explored the relationship between genetic variation in CLPS, early-onset obesity and fat intake in humans.<h4>Methods</h4>We screened the CLPS in 93 extremely obese children and adolescents and 96 underweight young adults for sequence variations and genotyped single nucleotide polymorphisms (SNPs) in ext ...[more]

PMID: 20054203

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Project description:ImportanceColorectal cancer (CRC) incidence and mortality among individuals younger than 50 years (early-onset CRC) are increasing. The reasons for such increases are largely unknown, although the increasing prevalence of obesity may be partially responsible.ObjectiveTo investigate prospectively the association between obesity and weight gain since early adulthood with the risk of early-onset CRC.Design, setting, and participantsThe Nurses' Health Study II is a prospective, ongoing cohort study of US female nurses aged 25 to 42 years at study enrollment (1989). A total of 85 256 women free of cancer and inflammatory bowel disease at enrollment were included in this analysis, with follow-up through December 31, 2011. Validated anthropomorphic measures and lifestyle information were self-reported biennially. Statistical analysis was performed from June 12, 2017, to June 28, 2018.ExposuresCurrent body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared), BMI at 18 years of age, and weight gain since 18 years of age.Main outcomes and measuresRelative risk (RR) for incident early-onset CRC.ResultsAmong the 85 256 women studied, 114 cases of early-onset CRC were documented (median age at diagnosis, 45 years; interquartile range, 41-47 years) during 1 196 452 person-years of follow-up. Compared with women with a BMI of 18.5 to 22.9, the multivariable RR was 1.37 (95% CI, 0.81-2.30) for overweight women (BMI, 25.0-29.9) and 1.93 (95% CI, 1.15-3.25) for obese women (BMI, ≥30.0). The RR for each 5-unit increment in BMI was 1.20 (95% CI, 1.05-1.38; P = .01 for trend). Similar associations were observed among women without a family history of CRC and without lower endoscopy within the past 10 years. Both BMI at 18 years of age and weight gain since 18 years of age contributed to this observation. Compared with women with a BMI of 18.5 to 20.9 at 18 years of age, the RR of early-onset CRC was 1.32 (95% CI, 0.80-2.16) for women with a BMI of 21.0 to 22.9 and 1.63 (95% CI, 1.01-2.61) for women with a BMI of 23.0 or greater at 18 years of age (P = .66 for trend). Compared with women who had gained less than 5.0 kg or had lost weight, the RR of early-onset CRC was 1.65 (95% CI, 0.96-2.81) for women gaining 20.0 to 39.9 kg and 2.15 (95% CI, 1.01-4.55) for women gaining 40.0 kg or more (P = .007 for trend).Conclusions and relevanceObesity was associated with an increased risk of early-onset CRC among women. Further investigations among men and to elucidate the underlying biological mechanisms are warranted.

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Dataset Information

Procolipase gene: no association with early-onset obesity or fat intake.

Publications

Procolipase gene: no association with early-onset obesity or fat intake.

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