Effects of Inulin on the Plasma Lipid Profile of Normolipidemic and Hyperlipidemic Subjects

A Meta-analysis of Randomized Controlled Trials

Zhuang Guo; Xiao-Ming Liu; Qiu-Xiang Zhang; Feng-Wei Tian; Hao Zhang; He-Ping Zhang; Wei Chen

Disclosures

Clin Lipidology. 2012;7(2):215-222. 

In This Article

Discussion

The meta-analysis showed that the intake of inulin resulted in a significant decrease in total cholesterol (-11.97 mg/dl), LDL-C (-12.13 mg/dl) and triglyceride (-17.76 mg/dl) concentrations in the serum of hyperlipidemic patients treated with inulin compared with controls. The use of inulin did not appear to alter cholesterol and triglycerides in serum of normolipidemic subjects (p > 0.05), which can partly be accounted for by the fact that the initial serum cholesterol concentrations in normolipidemic subjects were already low. Oral inulin failed to provide a significant modification of HDL-C in normolipidemic and hyperlipidemic subjects (p > 0.05) and the mechanism is still unclear.

Previous studies have evaluated a number of mechanisms proposed for the cholesterol- and triglyceride-lowering effects of inulin. The proposed hypocholesterolemic mediation effect by inulin is via two mechanisms: decreasing the cholesterol level absorbed by intestinal epithelial cells and improving the production of short-chain fatty acids fermented by intestinal bacterial microflora.[20] Inulin is a soluble and viscous compound that can increase the thickness of the unstirred layer of the small intestine and thus inhibit the absorption of cholesterol.[21] Although inulin itself does not bind to bile acids in the upper digestive tract, it can help the soluble bile acids bind to bacteria or insoluble compounds such as calcium phosphate through decreasing the pH of the cecum.[22] As a result, higher fecal bile acid excretion increases the utilization of cholesterol to reconstruct bile acids in the liver and decrease the liver cholesterol concentrations. In the colon, inulin is degraded by bacteria into short-chain fatty acids such as acetate, butyrate and propionate. Butyrate, the major fermentation product of inulin, can inhibit the synthesis of cholesterol in the liver and provides a source of energy for human colon epithelial cells.[23,24] By reducing the rate of hepatic cholesterol synthesis, propionate can also lower the plasma cholesterol levels and inhibit fatty acid synthesis.[23]

Many human and animal experiments have demonstrated that inulin appears to be more effective in decreasing the level of triglyceridemia than cholesterolemia in hypertriglyceridemic conditions. With regard to the mechanism of action, it is suggested that oral inulin can modify the insulin levels and the absorption of macronutrients, as well as increase the production of fermentation end products and change the gut's peptide production.[25] Jackson et al. observed that oral administration of 10 g inulin per day could decrease fasting plasma insulin concentration in middle-aged men and women with a mean age of 52.2 years (SD 9.5 years; p < 0.05).[12] The decreasing levels of insulin can alleviate the biochemical process by which glucose increases gene transcription of lipogenic enzymes in the liver.[26] Although inulin is not digested in the upper part of the GI tract, it can influence the absorption of macronutrients, especially carbohydrates, delay gastric emptying and shorten small intestinal transit time. It is known that the body's cholesterol pool homeostasis is maintained via the intestinal absorption of cholesterol, the regulated pathways of de novo synthesis or enhanced endogenous cholesterol degradation and excretion. Although cholesterol absorption efficiency varies among different subjects, dietary cholesterol contributes 50% of the circulating cholesterol in humans.[27] Kirby et al. reported that stomach-emptying rate contributes directly to the rate of dietary cholesterol absorption, which is inversely correlated with the total amount of cholesterol absorbed from a single meal.[28] A number of gut peptides play significant roles in gastric motor processes. Gut peptides such as neurotensin (NT) and somatostatin (SST) are attributed to these processes. NT is a tridecapeptide localized mainly in the CNS hypothalamus and in endocrine cells of the jejunum and ileum.[29] SST is a peptide that is produced in the CNS and in most major peripheral organs, including the salivary glands, stomach, pancreas and intestine.[30] Both peptides have been demonstrated to strongly affect gastroduodenal motility by lowering gastric emptying rates. Russo et al. found that the release of gut peptides such as NT and SST in healthy young subjects increased with the administration of inulin-enriched pasta for 5 weeks.[31] Accordingly, by inhibiting the release of NT and SST, oral inulin can delay gastric emptying and induce slower absorption of nutrients. Although there are a number of gut peptides besides NT and SST that can affect gastric emptying, the evidence that oral inulin can cause changes in these requires further investigation.

It is known that the more weight gained the larger the risk of dyslipidemia, and controlling weight is of benefit for alleviating this disease. Obesity stems from the interaction between genetic and environmental factors and the main cause is excessive caloric intake. Backhed et al. detected that the conventionalization of adult germ-free mice with a normal microbiota harvested from the gut microbial community of conventionally raised animals produces a 60% increase in body fat content within 10–14 days, despite an associated decrease in food consumption.[32] Studies of healthy adults have revealed that the higher the BMI, the less diversity of microflora in the gut.[33] In addition, obesity is mainly associated with changes in the relative abundance of the Bacteroidetes and the Firmicutes, which are the two dominant bacteria groups in the host's GI tract.[34]Bifidobacterium and Lactobacillus, which constitute a significant proportion of probiotic cultures in nutritional supplements, pharmaceuticals and functional foods,[35] both belong to the Firmicutes genus. Inulin can be completely fermented by intestinal bacteria and thus is considered a prebiotic. In a human model, the growth of Bifidobacteria in the intestinal microflora was selectively stimulated by oral inulin, whereas a decrease in Enterococci numbers occurred.[36,37] The intake of inulin also affected the members of Lactobacilli, the Clostridium coccoidesEubacterium rectale cluster and even species that are not yet fully characterized.[38] The authors of the present review speculate that by changing the composition of Firmicutes in the host's GI tract, oral inulin may affect energy extraction from a given diet.

As with any meta-analysis, the potential for publication bias is a concern. Although visual inspection of this meta-analysis' funnel plot could not rule out the presence of publication bias, there are two limitations in the present meta-analysis that should be noted owing to their potential to add bias. Primarily, crossover studies are often subjected to additional biases, particularly when studies have insufficient washout periods.[39] In order to provide additional power to this meta-analysis, four crossover trials were included. In addition, the greater the amount of research and number of subjects, the less publication bias would appear. However, the largest number of participants in these trials was only 64. Different results might be obtained with larger numbers of subjects in the future.

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