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© 2004 The American Society for Nutritional Sciences J. Nutr. 134:1942-1947, August 2004

Nutrient Interactions and Toxicity

Ingestion of Guar Gum Hydrolysate, a Soluble and Fermentable Nondigestible Saccharide, Improves Glucose Intolerance and Prevents Hypertriglyceridemia in Rats Fed Fructose

Takuya Suzuki and Hiroshi Hara1

Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo, Japan

1To whom correspondence should be addressed. E-mail: hara{at}chem.agr.hokudai.ac.jp.


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 
Fructose feeding provides a dietary model of insulin resistance accompanied by hypertriglyceridemia. We examined the effects of guar gum hydrolysate (GGH), a soluble and fermentable nondigestible saccharide with low viscosity, on glucose intolerance and hypertriglyceridemia in rats fed high-fructose diets. Rats were fed either a dextrin-based or a fructose-based diet with or without GGH (75 g/kg) for 30 d. Oral glucose tolerance tests (OGTTs) were performed 0, 14, and 28 d after feeding. High-fructose feeding negatively affected glucose tolerance on d 14 and 28. The addition of GGH to the diets improved glucose intolerance on d 28. Fructose feeding induced hyperinsulinemia after an oral glucose load; this was also improved by GGH on d 28. The glycogen concentration in the gastrocnemius muscles of rats was lowered by dietary fructose, and GGH supplementation abolished this decrease. Triglycerides in the plasma and livers of rats fed fructose diets were elevated, and the increases were ameliorated by supplemental GGH. Regardless of the type of carbohydrate, GGH enlarged the cecum and increased the cecal SCFA pools. In conclusion, supplemental feeding of GGH to rats improved the glucose intolerance and hypertriglyceridemia induced by a high-fructose diet. Possible mediators of these beneficial effects of GGH are the SCFAs produced by microbial fermentation of GGH in the large intestine.

KEY WORDS: • guar gum hydrolysate • fructose • glucose tolerance • hypertriglyceridemia • insulin resistance

Insulin resistance is a characteristic feature of type-2 diabetes mellitus, but other manifestations include hypertension, obesity, a hypercoagulable state, and dyslipidemia. The dyslipidemia associated with insulin-resistant states is characterized by hypertriglyceridemia, an increase in hepatic VLDL secretion, and a decrease in peripheral triglyceride clearance (1). The development of insulin resistance can be linked to both genetic and environmental factors (2). One of the most likely environmental factors is the habitual diet. Feeding a high-fructose diet provides a dietary model of insulin resistance associated with hyperinsulinemia (3,4), hypertriglyceridemia (3,5), and hypertension (6). Fructose stimulates de novo lipogenesis (3,5,6), although the mechanisms underlying this alteration are unclear. It was proposed that diet-induced hypertriglyceridemia is involved in impaired insulin sensitivity (1).

Feeding soluble nondigestible saccharides with a high viscosity, such as guar gum and pectin, modifies glucose tolerance because it delays gastric emptying and flattens increases in blood glucose (7,8). However, low-viscosity fibers, such as polydextrose and guar gum hydrolysates (GGH),2 are not expected to delay gastric emptying even though they are favored in food manufacturing due to their easy handling. Many soluble nondigestible saccharides are readily fermented by large intestinal microorganisms and produce organic acids, mainly SCFAs (acetic, propionic, and butyric acids). SCFAs are absorbed from the large intestine, and metabolized in the liver and the peripheral tissues in the body. These fermentation products may affect the metabolism of other nutrients. However, the effects of SCFAs on glucose metabolism are controversial. Propionic acid was shown to lower fasting plasma glucose concentration, but it has no effect on hepatic gluconeogenesis and whole-body glucose utilization in obese rats (9).

It was also reported that the feeding of some fermentable nondigestible saccharides lowers plasma triglyceride in rats (10–12). Previously, we demonstrated that an SCFA mixture lowered hepatic triglyceride accumulation in rats fed a high-sucrose diet (13). Further, it was observed that propionic acid inhibits incorporation of 1-[14C]acetate into fatty acids in isolated rat hepatocytes (14,15). However, the effects of SCFAs on diet-induced insulin resistance, which is associated with dyslipidemia, have not been investigated.

The aims of the present study were to investigate the effects of the supplemental feeding of GGH, a low-viscosity and highly fermentable nondigestible saccharide (16,17), on glucose intolerance and hypertriglyceridemia in rats fed fructose-based diets.


   MATERIALS AND METHODS
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 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 LITERATURE CITED
 
    Animals and experimental protocols. Male Sprague-Dawley rats (n = 31; 5 wk old; Clea Japan) were housed in individual cages in a room with controlled temperature (22 ± 2°C), relative humidity (40 to 60%), and lighting (lights on from 2300 to 1100 h) throughout the study. Guar gum hydrolysate is a digestive product with ß-1,4-mannanase, having an average molecular weight of 15,000 (GGH, Guar Fiber, Meiji Seika Kaisha). Body weight and food intake were measured daily. The rats had free access to tap water and a high-dextrin diet (Table 1) for an acclimation period of 5–6 d. Then, they were divided into 4 groups on the basis of body weight, and glucose tolerance was assessed by oral glucose tolerance tests (OGTTs). Four experimental diets consisting of 2 types of dietary carbohydrate [dextrin (D) or fructose (F)] with or without GGH (–GGH or +GGH); D/–GGH, D/+GGH, F/–GGH, and F/+GGH were used. Rats had free access to each experimental diet for 30 d except for the days before OGTTs and dissection.


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  		TABLE 1 Composition of stock and experimental diets1

 
OGTTs were performed at 0900 h on d 0, 14, and 28 of the experimental period. The rats were food deprived for 10 h before the administration of an oral glucose load (2 g/kg body weight; 200 g/L solution). Blood samples (150 µL) were collected from the tail vein at 0 (before administration), 15, 30, 60, and 120 min after glucose administration. Blood samples were immediately centrifuged (1300 x g for 15 min at 4°C), and plasma was separated. The glucose concentration in plasma was measured on the day of study, and concentrations of triglycerides, nonesterified fatty acids (NEFAs), and insulin were analyzed after storage at –40°C.

At 1600 h on d 30, anesthetized rats were killed (Nembutal: sodium pentobarbital, 40 mg/kg body weight; Abbott Laboratories) 5 h after the start of feeding. The feeding period (1100–1600 h) took place after 12 h of food deprivation. The liver, gastrocnemius muscle, epididymal adipose tissue, and cecum were removed and immediately frozen in liquid nitrogen. Tissues, except the cecum (–40°C), were stored at –80°C until subsequent analyses.

This study was approved by the Hokkaido University Animal Committee, and the rats were maintained in accordance with the Hokkaido University guidelines for the care and use of laboratory animals.

    Analytical methods. Plasma glucose, NEFA, and triglyceride were assayed by enzymatic methods using commercially available kits (glucose CII Test Wako and NEFA C Test Wako, Wako Pure Chemical Industries; TG-EN Kainos, Kainos Laboratories). Plasma insulin was quantified by RIA using a commercially available kit (Rat Insulin [125I] Biotrak Assay System, Amersham Biosciences). Triglyceride concentrations in the liver and gastrocnemius muscle were estimated by an enzymatic method after Folch’s extraction (18). Glycogen concentrations in the liver and gastrocnemius muscle were estimated by the method of Anthrone after alkaline digestion of these tissues (19).

The activity of lipoprotein lipase (LPL) extracted from epididymal adipose tissues was measured by previously described methods without using radioactive substrates (20). The liberated NEFA were measured in an aliquot of the incubation solution using a commercially available kit (NEFA Test Wako, Wako Pure Chemical Industries).

The cecal contents were diluted with 4 volumes of deionized water and homogenized with a Teflon homogenizer. The pH of these homogenates was measured with a semiconducting electrode (ISFET pH sensor 0010–15C, HORIBA) as the pH of cecal contents. Organic acids (acetic, propionic, n-butyric, succinic, and lactic acids) in the homogenates of cecal contents were measured by the previously described method using HPLC (LC-10ADpv, Shimadzu) equipped with 2 Shim-pack SCR-102H columns (8-mm i.d., 30 cm long; Shimadzu) and an electroconductibility detector (CDD-6A, Shimadzu) (21,22).

    Statistical analyses. All values are expressed as means ± SEM. The effects of carbohydrates and fibers were analyzed by two-way ANOVA. Duncan’s multiple range test was used for comparisons among groups (23). A difference with P < 0.05 was considered significant. These statistical analyses were done by the general linear models procedure of the Statistical Analysis Systems program (version 6.07; SAS Institute).


   RESULTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 LITERATURE CITED
 
Initial body weights were similar in all groups (data not shown), whereas body weight gains and food intake for the 30-d experimental period were lower in the F/+GGH group than in the other groups (Table 2).


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  		TABLE 2 Body weight gains, food intake, and relative liver, epididymal adipose tissue, and gastrocnemius muscle weights of rats fed fructose or dextrin diets with or without GGH for 30 d1

 
Changes in plasma glucose and insulin (only on d 28) concentrations after an oral glucose load (OGTTs) 0, 14, and 28 d after the start of feeding the experimental diets are shown in Figure 1. On d 0, the plasma glucose concentrations of all groups reached maximum levels at 15 min after administration and returned to the baseline levels at 60 min. There were no differences among the groups. The area under the glucose curves from 0 to 60 min (glucose AUC 0–60) was also similar in all groups on d 0 [D/–GGH, 9.27 ± 0.32; D/+GGH, 9.32 ± 0.32; F/–GGH, 9.13 ± 0.16; F/+GGH, 9.20 ± 0.28 mmol/(h · L)]. On d 14, the plasma glucose concentrations of the fructose-fed groups increased more rapidly in response to the oral glucose load than did those of the groups fed dextrin. The plasma glucose concentrations of the fructose-fed groups were higher than those of the dextrin-fed groups at 15 and 30 min. The glucose AUC 0–60 was similarly higher in the F/–GGH (10.9 ± 0.26) and F/+GGH (10.5 ± 0.22) groups than in the D/–GGH (9.70 ± 0.14) and D/+GGH (9.82 ± 0.14) groups on d 14. For the OGTTs on d 28, the glucose tolerance curve of the F/+GGH group was similar to those of rats fed dextrin-based diets; however, the F/–GGH group was glucose intolerant as well as on d 14. The plasma glucose concentration of the F/–GGH group was higher than that of the F/+GGH group at 30 min and those of the dextrin-fed groups at 15 and 30 min. The glucose AUC 0–60 of the F/–GGH group (10.6 ± 0.18) was higher than those of the other groups, and the value in the F/+GGH group (9.88 ± 0.19) did not differ from those in the 2 dextrin groups (D/–GGH, 9.46 ± 0.17; D/+GGH, 9.79 ± 0.12). The plasma insulin concentrations on d 28 reached maximum levels at 15 min after administration in all groups, and returned to the baseline levels at 60 min. The concentration of the F/–GGH group was higher than those of the other 3 groups at 15 and 30 min, and the values at all time points in the F/+GGH group did not differ from those in the 2 dextrin-fed groups. There were no differences in the plasma insulin concentrations at 0, 60, and 120 min among the groups. The insulin AUC 0–60 of the F/–GGH group [0.54 ± 0.04 nmol/(h · L)] was higher than those of the other groups, and the value in the F/+GGH group (0.37 ± 0.03) did not differ from those of the 2 dextrin-fed groups (D/–GGH, 0.34 ± 0.02; D/+GGH, 0.29 ± 0.02).



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  		FIGURE 1 Plasma glucose (A, B, and C) and insulin concentrations (D) in rats fed fructose or dextrin diets with or without GGH in response to an oral glucose load (2 g/kg body weight). Oral glucose tolerance tests were performed on d 0 (A), 14 (B), and 28 (C, D) after the start of feeding the experimental diets. Each value represents mean ± SEM, n = 7–8. Means without a common letter differ, P < 0.05.

 
There were no significant differences in plasma triglyceride and NEFA concentrations on d 0 and 14 among the groups (Fig. 2). The plasma triglyceride concentration of the F/–GGH group was higher than those of the other 3 groups on d 21 and 28. Plasma NEFA concentration of the F/–GGH group was higher than those of the D/–GGH or F/+GGH groups on d 21, and was higher than those of the all other groups on d 28.



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  		FIGURE 2 Plasma triglyceride (A) and NEFA (B) concentrations in rats fed fructose or dextrin diets with or without GGH at 14, 21, and 28 d after feeding. Each value represents mean ± SEM, n = 7–8. Means at a time without a common letter differ, P < 0.05.

 
The relative liver weights of the fructose-fed groups were higher than those of the dextrin-fed groups (Table 2); however, the weight in the F/+GGH group was lower than that of the F/–GGH group. The relative weight of the gastrocnemius muscle in the D/+GGH group was slightly but significantly lower than those of the D/–GGH and F/–GGH groups. There were no differences in the relative weights of epididymal adipose tissue among the 4 groups.

The triglyceride concentration in the livers of the F/–GGH group, but not the F/+GGH group, was much higher than those in the dextrin-fed groups (Table 3). However, there were no differences in triglyceride concentrations in the muscles among the groups. The glycogen concentration of the muscle in the F/+GGH group was higher than that in the F/–GGH group, but did not differ from those of the dextrin-fed groups. There were interactions between carbohydrate source and GGH supplementation on tissue glycogen concentrations.


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  		TABLE 3 Glycogen and triglyceride in the liver and gastrocnemius muscle of rats fed fructose or dextrin diets with or without GGH for 30 d1

 
Carbohydrate source affected LPL activity (P = 0.02). LPL activities in epididymal adipose tissue of the F/–GGH (2.85 ± 0.22 µmol NEFA release/g wet tissue) and F/+GGH (3.11 ± 0.30) groups were lower than those of the D/–GGH (3.66 ± 0.29) and D/+GGH (3.75 ± 0.34) groups.

Cecal and cecal content weights were higher, and the pH of the cecal contents was lower in rats fed diets with GGH than in those fed diets without GGH, regardless of the type of carbohydrate (Table 4).


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  		TABLE 4 Cecal weight, cecal content weight and pH of the cecal content of rats fed fructose or dextrin diets with or without GGH for 30 d1

 
Pools of acetic, propionic, and n-butyric acids and total SCFAs (the sum of acetic, propionic, and n-butyric acids) were higher and the pool of succinic acid was lower in rats fed diets with GGH than those in rats fed either fructose or dextrin without GGH (Table 5).


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  		TABLE 5 Pools of organic acids in the cecal content of rats fed fructose or dextrin diets with or without GGH for 30 d1

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
LITERATURE CITED
 
In this study, fructose feeding induced glucose intolerance and hypertriglyceridemia, which was consistent with previous reports (24,25). Supplemental GGH, a low-viscosity nondigestible saccharide, ameliorated these effects. GGH resists hydrolysis by digestive enzymes, but is highly fermentable by large intestinal microorganisms, producing organic acids, mainly SCFAs. Pools of SCFAs, but not lactic and succinic acids, were higher in the cecal contents of rats fed GGH, regardless of the type of carbohydrate in diets. Acetic, propionic, and butyric acids, the predominant SCFAs, are readily absorbed by colonocytes. SCFAs, especially acetic and/or propionic acids, may be possible mediators of the effects of GGH on glucose and lipid metabolism because the major part of butyric acid is utilized as an energy source by the colonocytes (26).

We demonstrated that GGH feeding ameliorated the glucose intolerance and hyperinsulinemia after an oral glucose load induced by feeding a fructose diet. Glucose tolerance depends on glucose uptake and oxidation in tissues as well as hepatic glucose production (27,28). Insulin is the most important factor for regulating these processes (29,30). Feeding fructose was shown to induce insulin resistance with accompanying decreases in glucose uptake in skeletal muscle and adipose tissue in rats using the euglycemic hyperinsulinemic clamp technique (31). High-fructose loading impairs phosphorylation of insulin receptor substrate-1 (IRS-1) and phosphatidylinositol 3-kinase after stimulation of insulin in muscles (32). In this study, supplemental feeding of GGH reversed the decrease in glycogen concentration of the gastrocnemius muscle induced by feeding the fructose diets. Our findings suggest that GGH feeding improves insulin resistance in the skeletal muscles of rats fed fructose diets. We also showed that plasma NEFA concentration in rats fed fructose diets was higher, and the increase was abolished with GGH feeding. NEFA accumulation in the tissues elevates fat oxidation and reduces glucose oxidation (33); it also causes insulin resistance through inhibition of IRS-1 signaling (34). SCFAs produced by GGH fermentation may be associated with the reduction of plasma NEFA, and be involved in the improvement of insulin resistance in skeletal muscle. It was reported that rectal infusion of a mixture of acetate and propionate in humans decreases plasma NEFA concentration (35). The effect of the experimental diets on hepatic glycogen concentration was complex. The interaction between the carbohydrate source and GGH supplementation was significant. Some previous reports showed that sucrose or fructooligosaccharide feeding affects hepatic glucose metabolism (36–38). Further investigations are required to clarify the effect of GGH feeding on carbohydrate metabolism in the liver.

Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are released from the intestine, are both incretin hormones that regulate postprandial insulin secretion (39). The effects of incretin are considered essential for the maintenance of glucose tolerance (40,41). Feeding oligofructose to rats enhances serum GIP concentration and GLP-1 in the cecum (11). However, we showed that plasma insulin levels after an oral glucose load were lower in the F/+GGH group than in the F/–GGH group. GIP or GLP-1 is not likely to be involved in the improvement of glucose intolerance under the current conditions.

Fructose induces glucose intolerance via the elevation of plasma triglyceride levels (5). The improvement in glucose intolerance with the amelioration of muscle insulin resistance by GGH may be secondary to the improvement of hepatic lipid metabolism impaired by feeding fructose diets. In agreement with previous reports (24,25), the triglyceride levels in the plasma and livers were increased in rats fed the fructose diets. Hypertriglyceridemia after fructose feeding results from the enhanced rate of hepatic VLDL-triglyceride synthesis (3,5,6) and a decrease in peripheral triglyceride clearance (25,42). The increased gene expression of several enzymes, including fatty acid synthase, is responsible for the enhanced synthesis of triglyceride in the liver of rats fed fructose (43,44). The addition of GGH to the fructose diets lowered triglyceride levels in liver, as well as in plasma. We reported previously that the ingestion of an SCFA mixture (acetic, propionic, and n-butyric acids) lowered triglycerides in the liver of rats fed high-sucrose diets (13). Propionate was reported to inhibit fatty acid synthesis in isolated rat hepatocytes (14,15). In the present study, fructose feeding also decreased LPL activity in epididymal adipose tissues, but GGH feeding did not reverse the reduction in LPL activity. These results suggest that the lowered hepatic triglyceride synthesis, not the increased peripheral triglyceride clearance, contributes to the hypolipidemic effect of GGH feeding, and SCFAs derived from GGH are likely responsible for the effects of GGH.

As described above, we speculate that the possible mediators of the effects of GGH are SCFAs. However, other possible mechanisms exist. The food intake of the F/+GGH group in the experimental period was lower than that of the other groups. Energy restriction is one of the most effective therapies for diet-induced obesity or diabetes (45). However, on d 14, both of the fructose-fed groups showed glucose intolerance and hypertriglyceridemia, and these metabolic impairments were no longer present on d 28 in the F/+GGH group. It is unlikely that the reduction in food intake in the F/+GGH group ameliorated the glucose intolerance and hyperlipidemia, but further studies under conditions of equalized food intakes among groups are warranted to eliminate the possibility. As another possible mechanism, nondigestible saccharides with high viscosity affect the intestinal absorption of carbohydrates and lipids (46,47). However, GGH is a nondigestible saccharide with very low viscosity (17) and the +GGH diets were prepared by substituting GGH for cellulose in the –GGH diet. The addition of GGH cannot be expected to alter intestinal absorption. It is clear that the effects of GGH are not caused merely by changes in intestinal fructose absorption.

In conclusion, supplemental feeding of GGH, a highly fermentable nondigestible saccharide, improves the glucose intolerance and hypertriglyceridemia induced by fructose feeding. The improvement in glucose intolerance after GGH feeding appears to be associated with the improvement in hepatic lipid metabolism impaired by feeding fructose diets. The possible mediators of the effects of GGH are the SCFAs produced by microbial fermentation of GGH in the large intestinal lumen.


   FOOTNOTES
 
2 Abbreviations used: AUC 0–60, the area under the curve from 0 to 60 min; D/–GGH diet, dextrin-based diet without guar gum hydrolysate; D/+GGH diet, dextrin-based diet with guar gum hydrolysate; F/–GGH diet, fructose-based diet without guar gum hydrolysate; F/+GGH diet, fructose-based diet with guar gum hydrolysate; GGH, guar gum hydrolysate; GIP, glucose-dependent insulinotropic polypeptide; GLP-1, glucagon-like peptide-1; IRS-1, insulin receptor substrate-1; LPL, lipoprotein lipase; NEFA, nonesterified fatty acid; OGTT, oral glucose tolerance test. Back

Manuscript received 10 December 2003. Initial review completed 1 March 2004. Revision accepted 4 May 2004.


   LITERATURE CITED
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 LITERATURE CITED
 

1. Watson, K. E., Horowitz, B. N. & Matson, G. (2003) Lipid abnormalities in insulin resistant states. Rev. Cardiovasc. Med 4:228-236.[Medline]

2. Hamman, R. F. (1992) Genetic and environmental determinants of non-insulin-dependent diabetes mellitus (NIDDM). Diabetes Metab. Rev. 8:287-338.[Medline]

3. Thorburn, A. W., Storlien, L. H., Jenkins, A. B., Khouri, S. & Kraegen, E. W. (1989) Fructose-induced in vivo insulin resistance and elevated plasma triglyceride levels in rats. Am. J. Clin. Nutr. 49:1155-1163.[Abstract/Free Full Text]

4. Tobey, T. A., Mondon, C. E., Zavaroni, I. & Reaven, G. M. (1982) Mechanism of insulin resistance in fructose-fed rats. Metabolism 31:608-612.[Medline]

5. Zavaroni, I., Chen, Y. D. & Reaven, G. M. (1982) Studies of the mechanism of fructose-induced hypertriglyceridemia in the rat. Metabolism 31:1077-1083.[Medline]

6. Hwang, I. S., Ho, H., Hoffman, B. B. & Reaven, G. M. (1987) Fructose-induced insulin resistance and hypertension in rats. Hypertension 10:512-516.[Abstract/Free Full Text]

7. Ou, S., Kwok, K., Li, Y. & Fu, L. (2001) In vitro study of possible role of dietary fiber in lowering postprandial serum glucose. J. Agric. Food Chem. 49:1026-1029.[Medline]

8. Tabatabai, A. & Li, S. (2000) Dietary fiber and type 2 diabetes. Clin. Excell. Nurse Pract. 4:272-276.[Medline]

9. Berggren, A. M., Nyman, E. M., Lundquist, I. & Bjorck, I. M. (1996) Influence of orally and rectally administered propionate on cholesterol and glucose metabolism in obese rats. Br. J. Nutr. 76:287-294.[Medline]

10. de Deckere, E. A., Kloots, W. J. & van Amelsvoort, J. M. (1995) Both raw and retrograded starch decrease serum triacylglycerol concentration and fat accretion in the rat. Br. J. Nutr. 73:287-298.[Medline]

11. Delzenne, N. M. & Kok, N. N. (1999) Biochemical basis of oligofructose-induced hypolipidemia in animal models. J. Nutr. 129:1467S-1470S.

12. Overton, P. D., Furlonger, N., Beety, J. M., Chakraborty, J., Tredger, J. A. & Morgan, L. M. (1994) The effects of dietary sugar-beet fibre and guar gum on lipid metabolism in Wistar rats. Br. J. Nutr. 72:385-395.[Medline]

13. Hara, H., Haga, S., Aoyama, Y. & Kiriyama, S. (1999) Short-chain fatty acids suppress cholesterol synthesis in rat liver and intestine. J. Nutr. 129:942-948.[Abstract/Free Full Text]

14. Demigné, C., Morand, C., Levrat, M. A., Besson, C., Moundras, C. & Rémésy, C. (1995) Effect of propionate on fatty acid and cholesterol synthesis and on acetate metabolism in isolated rat hepatocytes. Br. J. Nutr. 74:209-219.[Medline]

15. Nishina, P. M. & Freedland, R. A. (1990) Effects of propionate on lipid biosynthesis in isolated rat hepatocytes. J. Nutr. 120:668-673.

16. Hara, H., Suzuki, T., Kasai, T., Aoyama, Y. & Ohta, A. (1999) Ingestion of guar gum hydrolysate, a soluble fiber, increases calcium absorption in totally gastrectomized rats. J. Nutr. 129:39-45.[Abstract/Free Full Text]

17. Takahashi, H., Yang, S. I., Ueda, Y., Kim, M. & Yamamoto, T. (1994) Influence of intact and partially hydrolysed guar gum on iron utilization in rats fed on iron-deficient diets. Comp. Biochem. Physiol. Physiol. 109:75-82.[Medline]

18. Folch, J., Lees, M. & Sloane-Stanley, G. (1957) A simple method for the isolation and purification of total lipids from animal tissues. J. Biol. Chem. 226:497-509.[Free Full Text]

19. Passonneau, J. V. & Lauderdale, V. R. (1974) A comparison of three methods of glycogen measurement in tissues. Anal. Biochem. 60:405-412.[Medline]

20. Nilsson-Ehle, P. & Schotz, M. C. (1976) A stable, radioactive substrate emulsion for assay of lipoprotein lipase. J. Lipid Res. 17:536-541.[Abstract]

21. Hoshi, S., Sakata, T., Mikuni, K., Hashimoto, H. & Kimura, S. (1994) Galactosylsucrose and xylosylfructoside alter digestive tract size and concentrations of cecal organic acids in rats fed diets containing cholesterol and cholic acid. J. Nutr. 124:52-60.

22. Shiga, K., Hara, H., Takahashi, T., Aoyama, Y., Furuta, H. & Maeda, H. (2002) Ingestion of water-soluble soybean fiber improves gastrectomy-induced calcium malabsorption and osteopenia in rats. Nutrition 18:636-642.[Medline]

23. Duncan, D. B. (1955) Multiple range and multiple F test. Biometrics 1:1-42.

24. Anurag, P. & Anuradha, C. V. (2002) Metformin improves lipid metabolism and attenuates lipid peroxidation in high fructose-fed rats. Diabetes Obes. Metab. 4:36-42.[Medline]

25. Tsutsumi, K., Inoue, Y., Shima, A., Iwasaki, K., Kawamura, M. & Murase, T. (1993) The novel compound NO-1886 increases lipoprotein lipase activity with resulting elevation of high density lipoprotein cholesterol, and long- term administration inhibits atherogenesis in the coronary arteries of rats with experimental atherosclerosis. J. Clin. Investig. 92:411-417.

26. Cummings, J. H. & Macfarlane, G. T. (1991) The control and consequences of bacterial fermentation in the human colon. J. Appl. Bacteriol. 70:443-459.[Medline]

27. Bergman, R. N., Finegood, D. T. & Ader, M. (1985) Assessment of insulin sensitivity in vivo. Endocr. Rev. 6:45-86.[Abstract/Free Full Text]

28. Bergman, R. N., Hope, I. D., Yang, Y. J., Watanabe, R. M., Meador, M. A., Youn, J. H. & Ader, M. (1989) Assessment of insulin sensitivity in vivo: a critical review. Diabetes Metab. Rev. 5:411-429.[Medline]

29. Kahn, C. R. & Goldfine, A. B. (1993) Molecular determinants of insulin action. J. Diabet. Complicat. 7:92-105.

30. Rosen, O. M. (1987) After insulin binds. Science (Washington, DC) 237:1452-1458.[Abstract/Free Full Text]

31. Thresher, J. S., Podolin, D. A., Wei, Y., Mazzeo, R. S. & Pagliassotti, M. J. (2000) Comparison of the effects of sucrose and fructose on insulin action and glucose tolerance. Am. J. Physiol. 279:R1334-R1340.

32. Pagliassotti, M. J., Kang, J., Thresher, J. S., Sung, C. K. & Bizeau, M. E. (2002) Elevated basal PI 3-kinase activity and reduced insulin signaling in sucrose-induced hepatic insulin resistance. Am. J. Physiol. 282:E170-E176.

33. Randle, P. J. (1998) Regulatory interactions between lipids and carbohydrates: the glucose fatty acid cycle after 35 years. Diabetes Metab. Rev. 14:263-283.[Medline]

34. Shulman, G. I. (2000) Cellular mechanisms of insulin resistance. J. Clin. Investig. 106:171-176.[Medline]

35. Wolever, T. M., Brighenti, F., Royall, D., Jenkins, A. L. & Jenkins, D. J. (1989) Effect of rectal infusion of short chain fatty acids in human subjects. Am. J. Gastroenterol. 84:1027-1033.[Medline]

36. Luo, J., Rizkalla, S. W., Alamowitch, C., Boussairi, A., Blayo, A., Barry, J. L., Laffitte, A., Guyon, F., Bornet, F. R. & Slama, G. (1996) Chronic consumption of short-chain fructooligosaccharides by healthy subjects decreased basal hepatic glucose production but had no effect on insulin-stimulated glucose metabolism. Am. J. Clin. Nutr. 63:939-945.[Abstract/Free Full Text]

37. Luo, J., Van Yperselle, M., Rizkalla, S. W., Rossi, F., Bornet, F. R. & Slama, G. (2000) Chronic consumption of short-chain fructooligosaccharides does not affect basal hepatic glucose production or insulin resistance in type 2 diabetics. J. Nutr. 130:1572-1577.[Abstract/Free Full Text]

38. Pagliassotti, M. J., Prach, P. A., Koppenhafer, T. A. & Pan, D. A. (1996) Changes in insulin action, triglycerides, and lipid composition during sucrose feeding in rats. Am. J. Physiol. 271:R1319-R1326.

39. Holst, J. J. & Orskov, C. (2001) Incretin hormones—an update. Scand. J. Clin. Lab. Investig. Suppl. 234:75-85.[Medline]

40. Tseng, C. C., Kieffer, T. J., Jarboe, L. A., Usdin, T. B. & Wolfe, M. M. (1996) Postprandial stimulation of insulin release by glucose-dependent insulinotropic polypeptide (GIP). Effect of a specific glucose-dependent insulinotropic polypeptide receptor antagonist in the rat. J. Clin. Investig. 98:2440-2445.[Medline]

41. Wang, Z., Wang, R. M., Owji, A. A., Smith, D. M., Ghatei, M. A. & Bloom, S. R. (1995) Glucagon-like peptide-1 is a physiological incretin in rat. J. Clin. Investig. 95:417-421.

42. Mayes, P. A. (1993) Intermediary metabolism of fructose. Am. J. Clin. Nutr. 58:754S-765S.[Abstract/Free Full Text]

43. Katsurada, A., Iritani, N., Fukuda, H., Matsumura, Y., Nishimoto, N., Noguchi, T. & Tanaka, T. (1990) Effects of nutrients and hormones on transcriptional and post-transcriptional regulation of fatty acid synthase in rat liver. Eur. J. Biochem. 190:427-433.[Medline]

44. Katsurada, A., Iritani, N., Fukuda, H., Matsumura, Y., Nishimoto, N., Noguchi, T. & Tanaka, T. (1990) Effects of nutrients and hormones on transcriptional and post-transcriptional regulation of acetyl-CoA carboxylase in rat liver. Eur. J. Biochem. 190:435-441.[Medline]

45. Scheen, A. J. (1998) Aggressive weight reduction treatment in the management of type 2 diabetes. Diabetes Metab. 24:116-123.[Medline]

46. Wolever, T. M., Jenkins, D. J., Leeds, A. R., Gassull, M. A., Dilawari, J. B., Goff, D. V., Metz, G. L. & Alberti, G. M. (1978) Dietary fibre and glucose tolerance importance of viscosity. Proc. Nutr. Soc. 37:47A (abs.).[Medline]

47. Jenkins, D. J., Wolever, T. M., Leeds, A. R., Gassull, M. A., Haisman, P., Dilawari, J., Goff, D. V., Metz, G. L. & Alberti, K. G. (1978) Dietary fibres, fibre analogues, and glucose tolerance: importance of viscosity. Br. Med. J. 1:1392-1394.

48. Reeves, P. G., Nielsen, F. H. & Fahey, G. C., Jr (1993) AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet. J. Nutr. 123:1939-1951.




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