Department of Endocrinology & Metabolism, Academic Medical Centre Amsterdam, Netherlands.
Hepatology. 2014 Aug;60(2):545-53. doi: 10.1002/hep.27149. Epub 2014 May 13.
American children consume up to 27% of calories from high-fat and high-sugar snacks. Both sugar and fat consumption have been implicated as a cause of hepatic steatosis and obesity but the effect of meal pattern is largely understudied. We hypothesized that a high meal frequency, compared to consuming large meals, is detrimental in the accumulation of intrahepatic and abdominal fat. To test this hypothesis, we randomized 36 lean, healthy men to a 40% hypercaloric diet for 6 weeks or a eucaloric control diet and measured intrahepatic triglyceride content (IHTG) using proton magnetic resonance spectroscopy ((1) H-MRS), abdominal fat using magnetic resonance imaging (MRI), and insulin sensitivity using a hyperinsulinemic euglycemic clamp with a glucose isotope tracer before and after the diet intervention. The caloric surplus consisted of fat and sugar (high-fat-high-sugar; HFHS) or sugar only (high-sugar; HS) and was consumed together with, or between, the three main meals, thereby increasing meal size or meal frequency. All hypercaloric diets similarly increased body mass index (BMI). Increasing meal frequency significantly increased IHTG (HFHS mean relative increase of 45%; P = 0.016 and HS mean relative increase of 110%; P = 0.047), whereas increasing meal size did not (2-way analysis of variance [ANOVA] size versus frequency P = 0.03). Abdominal fat increased in the HFHS-frequency group (+63.3 ± 42.8 mL; P = 0.004) and tended to increase in the HS-frequency group (+46.5 ± 50.7 mL; P = 0.08). Hepatic insulin sensitivity tended to decrease in the HFHS-frequency group while peripheral insulin sensitivity was not affected.
A hypercaloric diet with high meal frequency increased IHTG and abdominal fat independent of caloric content and body weight gain, whereas increasing meal size did not. This study suggests that snacking, a common feature in the Western diet, independently contributes to hepatic steatosis and obesity. (
www.clinicaltrials.gov; nr.NCT01297738.)
美国儿童从高脂肪和高糖零食中摄入高达 27%的卡路里。糖和脂肪的摄入都被认为是肝脂肪变性和肥胖的原因，但用餐模式的影响在很大程度上仍未得到充分研究。我们假设，与摄入大餐相比，高进餐频率不利于肝内和腹部脂肪的积累。为了验证这一假设，我们将 36 名瘦且健康的男性随机分为高卡路里饮食组（40%热量过剩）或等热量对照组，进行 6 周的饮食干预，并在干预前后使用质子磁共振波谱（1 H-MRS）测量肝内甘油三酯含量（IHTG），使用磁共振成像（MRI）测量腹部脂肪，使用葡萄糖同位素示踪剂的高胰岛素正葡萄糖钳夹测量胰岛素敏感性。多余的热量来自脂肪和糖（高脂肪高糖；HFHS）或仅糖（高糖；HS），并与三餐一起或在三餐之间摄入，从而增加餐量或餐频。所有高热量饮食都使体重指数（BMI）增加。增加进餐频率显著增加 IHTG（HFHS 相对增加 45%；P=0.016，HS 相对增加 110%；P=0.047），而增加餐量则没有（2 因素方差分析[ANOVA]大小与频率 P=0.03）。HFHS 频率组腹部脂肪增加（+63.3±42.8 mL；P=0.004），HS 频率组腹部脂肪增加趋势（+46.5±50.7 mL；P=0.08）。HFHS 频率组肝胰岛素敏感性有下降趋势，而外周胰岛素敏感性不受影响。
高卡路里、高进餐频率的饮食会增加 IHTG 和腹部脂肪，这与热量含量和体重增加无关，而增加餐量则没有。本研究表明，零食是西方饮食的一个常见特征，它会独立导致肝脂肪变性和肥胖。（
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