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Colonic short-chain fatty acids (SCFA) may affect hepatic lipid metabolism. Lactulose increases colonic acetate production, whereas L-rhamnose increases propionate. To test the effects of oral L-rhamnose and lactulose for 28 d on fasting concentrations and hepatic synthesis of lipids in humans, 18 men were administered 25 g/d of L-rhamnose, lactulose, or D-glucose for 4 wk in a partially randomized crossover design, with blood collected from fasting subjects on the first and last day of each period. Cholesterol and triacylglycerol (TG) synthesis rates were determined using deuterated water uptake rate over the last 24 h of each period. Postprandial blood lipids, and glucose and insulin were assessed in 11 subjects on d 28. Fasting serum cholesterol was unchanged; however, when expressed as a percentage change, TG were decreased, relative to baseline (P < 0.04), by L-rhamnose (-10%) and lactulose (-10%), compared with D-glucose, which increased serum TG (+11%). Net TG-fatty acid (TGFA) synthesis on d 28 was lower with L-rhamnose (2.42 [+ or -] 0.38 g/d) and lactulose (2.62 [+ or -] 0.35 g/d) than with D-glucose (2.96 [+ or -] 0.31 g/d, P< 0.01). We conclude that these results do not support a primary role for propionate in the cholesterol-lowering effect of soluble fiber. However, both lactulose and L-rhamnose lowered serum TG (expressed as a percentage change) and TGFA synthesis, compared with D-glucose, which increased them. Although these data are consistent with inhibition of TGFA synthesis by SCFA, other aspects of the metabolism of these sugars cannot be ruled out as putative agents of their TG-lowering effects.

Butyrate inhibits colonic cell proliferation in vitro but reportedly has an opposite effect in vivo. Because lactulose feeding decreases cecal cell proliferation, an effect attenuated by prefeeding inulin, we hypothesized that lactulose feeding would decrease colonic luminal synthesis of butyrate, and that prefeeding and cofeeding inulin would prevent this effect. Piglets (n = 31) were catheterized and randomly assigned to 1 of 4 groups: Control formula (C); control formula + lactulose (L); control formula + lactulose + inulin (L + I); and control formula + inulin (I). At 6 and 7 d postsurgery, the rate of cecal synthesis of butyrate, cecal cell proliferation and apoptosis, and cecal and distal colon butyrate concentration were measured. In groups C, L, L + I, and I, the rates of synthesis of butyrate (mean [+ or -] SEM) were 10.6 [+ or ] 3.2, 23.3 [+ or -] 4.5, 12.4 [+ or] 3.6, and 14.6 [+ or -] 4.0 [micro]mol/min, respectively (Group Effect, P= 0.1; C vs. L, P = 0.03; L vs. L + I, P = 0.06). The cecal butyrate concentrations did not differ among the 4 groups and were 8.7 [+ or -] 3.2, 2.4 [+ or -] 0.8, 3.4 [+ or -] 1.9, and 2.0 [+ or -] 0.7 [micro]mol/g dry wt, respectively. The total cecal cell proliferation index was higher in C than in L (P = 0.008) or I (P = 0.026) and was higher in L + I than in L (P = 0.013) or I (P = 0.046). The increased supply of butyrate to the cecum was associated with decreased cell proliferation, but cecal butyrate concentration did not reflect synthesis. J. Nutr. 136: 64-69, 2006. KEY WORDS: * butyrate * lactulose * inulin * swine * colon