Magkos Faidon, Sullivan Shelby, Fitch Mark, Smith Gordon, Fabbrini Elisa, Mittendorfer Bettina, Hellerstein Marc, Klein Samuel
Center for Human Nutrition and Atkins Center of Excellence in Obesity Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore & Clinical Nutrition Research Centre, A*STAR, Singapore.
Obesity (Silver Spring). 2017 Nov;25 Suppl 2(Suppl 2):S81-S86. doi: 10.1002/oby.21983.
To evaluate the effects of diet-induced changes in energy balance and body weight on in vivo colonocyte fractional proliferation rates (FPR) in people with obesity.
In vivo colonocyte FPR was assessed in 31 men and women with obesity (BMI: 35.4 ± 4.0 kg/m , age: 52.6 ± 8.9 years) before and after diet-induced weight loss, weight gain, or weight maintenance. Subjects ingested aliquots of H O (heavy water) daily for 4 to 7 days, followed by flexible sigmoidoscopy with colon biopsies to assess the incorporation of H into the DNA of dividing colonocytes.
Colonocyte FPR averaged 12.7% ± 3.8% per day and correlated directly with intra-abdominal adipose tissue (IAAT) volume (r = 0.364, P = 0.044). Colonocyte FPR decreased in the weight loss group, did not change in the weight maintenance group, and increased in the weight gain group. The change in colonocyte FPR correlated directly with the percent change in body weight (r = 0.409, P = 0.028) and IAAT volume (r = 0.598, P = 0.001).
A high-calorie diet and weight gain increase, whereas a low-calorie diet and weight loss decrease, in vivo colonocyte proliferation rate in people with obesity. These results suggest that changes in energy balance influence the risk of developing colon cancer in people with obesity by regulating colonic mucosal growth rates.
评估饮食引起的能量平衡和体重变化对肥胖人群体内结肠细胞分数增殖率（FPR）的影响。
对31名肥胖男性和女性（BMI：35.4±4.0kg/m²，年龄：52.6±8.9岁）在饮食诱导的体重减轻、体重增加或体重维持前后，评估其体内结肠细胞FPR。受试者每天摄入等分的重水（H₂O），持续4至7天，随后进行乙状结肠镜检查并取结肠活检组织，以评估重氢掺入正在分裂的结肠细胞DNA中的情况。
结肠细胞FPR平均每天为12.7%±3.8%，且与腹内脂肪组织（IAAT）体积直接相关（r = 0.364，P = 0.044）。结肠细胞FPR在体重减轻组中降低，在体重维持组中未变化，在体重增加组中升高。结肠细胞FPR的变化与体重百分比变化（r = 0.409，P = 0.028）和IAAT体积（r = 0.598，P = 0.001）直接相关。
高热量饮食和体重增加会提高肥胖人群体内结肠细胞增殖率，而低热量饮食和体重减轻则会降低该增殖率。这些结果表明，能量平衡的变化通过调节结肠黏膜生长速率来影响肥胖人群患结肠癌的风险。
