Department of Surgery, Indiana University School of Medicine, 535 Barnhill Dr. RT 130, Indianapolis, IN 46202, USA.
J Gastrointest Surg. 2012 Sep;16(9):1680-5. doi: 10.1007/s11605-012-1931-5. Epub 2012 Jun 12.
Obesity accelerates pancreatic cancer growth; the mechanisms underlying this association are poorly understood. This study evaluated the hypothesis that obesity, rather than high-fat diet, is responsible for accelerated pancreatic cancer growth.
Male C57BL/6J mice were studied after 19 weeks of high-fat (60 % fat; n = 20) or low-fat (10 % fat; n = 10) diet and 5 weeks of Pan02 murine pancreatic cancer growth (flank).
By two-way ANOVA, diet did not (p = 0.58), but body weight, significantly influenced tumor weight (p = 0.01). Tumor weight correlated positively with body weight (R (2) = 0.562; p < 0.001). Tumors in overweight mice were twice as large as those growing in lean mice (1.2 ± 0.2 g vs. 0.6 ± .01 g, p < 0.01), had significantly fewer apoptotic cells than those in lean mice (0.8 ± 0.4 vs 2.4 ± 0.5; p < 0.05), and greater adipocyte volume (3.7 vs. 2.2 %, p < 0.05). Apoptosis (R (2) = 0.472; p = 0.008) and serum adiponectin correlated negatively with tumor weight (R = 0.45; p < 0.05).
These data suggest that body weight, and not high-fat diet, is responsible for accelerated murine pancreatic cancer growth observed in this model of diet-induced obesity. Decreased tumor apoptosis appears to play an important mechanistic role in this process. The concept that decreased apoptosis is potentiated by hypoadiponectinemia (seen in obesity) deserves further investigation.
肥胖会加速胰腺癌的生长；但人们对这种关联的潜在机制仍知之甚少。本研究评估了以下假说，即肥胖而非高脂肪饮食是导致胰腺癌生长加速的原因。
研究人员对接受了 19 周高脂肪（60%脂肪；n=20）或低脂肪（10%脂肪；n=10）饮食以及 5 周 Pan02 小鼠胰腺癌生长（侧腹）的雄性 C57BL/6J 小鼠进行了研究。
通过双因素方差分析，饮食（p=0.58）而非体重显著影响肿瘤重量。肿瘤重量与体重呈正相关（R 2=0.562；p<0.001）。超重小鼠的肿瘤是瘦小鼠的两倍大（1.2±0.2 g 比 0.6±0.01 g，p<0.01），比瘦小鼠的肿瘤具有显著更少的凋亡细胞（0.8±0.4 比 2.4±0.5；p<0.05），并且具有更大的脂肪细胞体积（3.7 比 2.2%，p<0.05）。凋亡（R 2=0.472；p=0.008）和血清脂联素与肿瘤重量呈负相关（R=0.45；p<0.05）。
这些数据表明，在该饮食诱导肥胖模型中，是体重而不是高脂肪饮食导致了观察到的小鼠胰腺癌生长加速。肿瘤凋亡减少似乎在这一过程中发挥了重要的机制作用。脂联素水平降低（肥胖时出现）增强凋亡减少的这一概念值得进一步研究。
