DenBesten L, Reyna R H, Connor W E, Stegink L D
J Clin Invest. 1973 Jun;52(6):1384-93. doi: 10.1172/JCI107311.
The hypothesis that diets high in carbohydrate produce hyperlipidemia in man was tested in new experiments which provided all calories either by the intravenous route or orally. After a base-line general diet, eight healthy men were fed fat-free diets consisting of 80% of the calories from glucose and 20% from an amino acid hydrolysate. The calories were adequate to maintain body weight. The solutions (1 cal/ml) were infused by constant drip over a 24 h period through either a superior vena cava catheter or a nasogastric tube. Each feeding was for 12 days in sequence but assigned in random order. The high CHO diet given orally, as expected, increased the mean base-line serum triglyceride level from 176+/-29 (SE) to 274+/-47. The identical diet given intravenously (i.v.) failed to produce hypertriglyceridemia; triglyceride levels were not significantly changed, 154+/-37, nor were blood glucose levels. Serum insulin levels were higher during the intravenous feeding. In contrast, both i.v. and oral feedings greatly lowered mean serum cholesterol concentration from the base-line value of 220+/-13 mg/100 ml to 135+/-11 and 151+/-13, respectively. However, the serum cholesterol level was significantly lower (P < 0.01) with the intravenous feeding than with the oral feeding. In addition, the fecal excretion of both neutral sterols and bile acids diminished greatly during the period of intravenous feeding. The fecal mass was likewise decreased. The bacterial conversion of cholesterol to conprostanol did not occur with either intravenous or oral feeding, but with both regimens secondary bile acids predominated, as usual, in the bile acid fraction of the stool. These results emphasize the key role of the intestinal mucosa in the etiology of carbohydrate-induced hypertriglyceridemia and as a direct or indirect contributor to plasma triglyceride and cholesterol levels in the absence of dietary lipids. When the gut mucosa was bypassed, carbohydrate-induced hypertriglyceridemia did not occur and both serum triglyceride and serum cholesterol levels decreased greatly at a time when the excretion of steroids in the stool was also reduced.
高碳水化合物饮食会导致人体出现高脂血症这一假说，在新的实验中得到了验证。这些实验通过静脉途径或口服途径提供所有热量。在基线普通饮食之后，八名健康男性被给予无脂肪饮食，其中80%的热量来自葡萄糖，20%来自氨基酸水解物。热量足以维持体重。溶液（1千卡/毫升）通过上腔静脉导管或鼻胃管在24小时内持续滴注。每次喂食持续12天，按顺序进行，但随机分配。正如预期的那样，口服高碳水化合物饮食使平均基线血清甘油三酯水平从176±29（标准误）升高到274±47。静脉注射相同的饮食未能产生高甘油三酯血症；甘油三酯水平没有显著变化，为154±37，血糖水平也没有变化。静脉喂食期间血清胰岛素水平较高。相比之下，静脉注射和口服喂食都使平均血清胆固醇浓度从基线值220±13毫克/100毫升大幅降低至135±11和151±13。然而，静脉注射喂食时的血清胆固醇水平显著低于（P<0.01）口服喂食时的水平。此外，在静脉喂食期间，中性固醇和胆汁酸的粪便排泄量大幅减少。粪便量同样减少。无论是静脉注射还是口服喂食，胆固醇都不会转化为粪甾烷醇，但在两种方案中，粪便胆汁酸部分中次级胆汁酸照例占主导地位。这些结果强调了肠黏膜在碳水化合物诱导的高甘油三酯血症病因中的关键作用，以及在无膳食脂质情况下作为血浆甘油三酯和胆固醇水平的直接或间接影响因素的作用。当绕过肠黏膜时，不会发生碳水化合物诱导的高甘油三酯血症，并且在粪便中类固醇排泄减少的同时，血清甘油三酯和血清胆固醇水平都大幅下降。
