L-Arabinose Feeding Prevents Increases Due to Dietary Sucrose in Lipogenic Enzymes and Triacylglycer

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L-Arabinose Feeding Prevents Increases Due to Dietary Sucrose in Lipogenic Enzymes and Triacylglycerol Levels in Rats1

(Manuscript received 5 July 2000. Initial review completed 28 July 2000. Revision accepted 18 December 2000.)
Shigemitsu Osaki,Tomoe Kimura,* Tomomi Sugimoto,*Susumu Hizukuri** and Nobuko Iritani*2
*Faculty of Human and Cultural Studies, Tezukayama Gakuin University Sakai, Osaka 590-0113, Japan; Sanwa Cornstarch Co. Ltd., Kashiwara, Nara 634-0834, Japan and ** Faculty of Home Economics, Kobe Women’s University, Higashisuma, Kobe 654- 8585, Japan
ABSTRACT L-Arabinose is a natural, poorly absorbed pentose that selectively inhibits intestinal sucrase activity. To investigate the effects of L-arabinose feeding on lipogenesis due to its inhibition of sucrase, rats were fed 0–30 g sucrose/100 g diets containing 0–1 g L-arabinose/100 g for 10 d. Lipogenic enzyme activities and triacylglycerol concentrations in the liver were significantly increased by dietary sucrose, and arabinose significantly prevented these increases. Arabinose feeding reduced the weights of epididymal adipose tissue. Moreover, plasma insulin and triacylglycerol concentrations were significantly reduced by dietary L-arabinose. These findings suggest that L-arabinose inhibits intestinal sucrase activity, thereby reducing sucrose utilization, and consequently decreasing lipogenesis. J. Nutr. 131: 796–799, 2001.
 
KEY WORDS: c L-arabinose c sucrose c lipogenic enzymes c triacylglycerol levels c rats
 
L-Arabinose is a pentose with a sweet taste. It is absorbed from the intestinal tract in rats (1,2) and chicks (3,4) but at a lower rate than glucose. A portion of the ingested L-arabinose is excreted in the urine (1). Although widely present in nature, L-arabinose is rarely used, and its physiological effects in vivo have received little attention. Seri et al. (5) demonstrated that L-arabinose selectively inhibits intestinal sucrase activity in a noncompetitive manner and suppresses the plasma glucose increase due to sucrose ingestion. Neither D-arabinose nor the disaccharide L-arabinobiose inhibits sucrase activity. Sanai et al. (6) also examined the effects of L-arabinose on gastrointestinal digestion and absorption of14C-labeled sucrose in rats. After the oral administration of 14C-labeled sucrose, cumulative expiratory 14CO2 was significantly and dose-dependently reduced by L-arabinose, and a large quantity of undigested 14C-labeled sucrose and its metabolites was observed in the cecum of the arabinose-treated rats. The authors also observed suppressive effects of L-arabinose on the increase in blood glucose after sucrose loading in rats. Because the intestinal absorption of sucrose is inhibited in the presence of L-arabinose, the absorption of sucrose should be reduced by arabinose ingestion. Therefore, L-arabinose may also be useful in preventing excess sucrose utilization. In the present experiment, we investigated the effects of arabinose ingestion on the activities of lipogenic enzymes, which are involved in long-chain fatty acid synthesis, and on the plasma and liver triacylglycerol levels in rats.
 
MATERIALS AND METHODS
Materials. [1-14C]Acetyl coenzyme A (CoA)3 (1.85–2.22 MBq/ mmol) was purchased from Morevek Biochemicals (Brea, CA). [14C]Sodium bicarbonate (0.21 GBq/mmol) was obtained from New England Nuclear (Boston, MA). An insulin radioimmunoassay kit was obtained from Eiken Chemical Company (Tokyo, Japan). A glucose assay kit (Glucose CII test) was from Wako (Osaka, Japan). Most other reagents were obtained from Wako or Sigma Chemical Co. (St. Louis, MO). L-Arabinose and pregelatinized cornstarch were from Sanwa Starch (Nara, Japan).
Animals. Male 5-wk-old Wistar rats (Japan SLC, Hamamatsu, Japan) were deprived of food for 1 d and then fed synthetic diets for 10 d. Four basal synthetic diets with different sucrose concentrations were used: C (no sucrose), CS10 (containing 10 g sucrose/100 g by weight), CS20 (containing 20 g sucrose/100 g by weight) and CS30 (containing 30 g sucrose/100 g by weight). For a comparison, another dietary group was added: the sucrose in the CS20 diet was replaced with 10 g glucose and 10 g fructose (CGF20 diet). The composition of the C diet was 713.5 g pregelatinized cornstarch, 180 g casein, 50 g cellulose, 24.5 g salt mixture (7), 1 g choline chloride and 1 g vitamin mixture (7) per 100 g. When sucrose was added to the diet, pregelatinized cornstarch was replaced with sucrose by weight. In the 0.5 or 1 g L-arabinose/100 g diets, cellulose was replaced with 0.5 or 1 g L-arabinose/100 g. All of the experiments for these dietary groups (except the CGF20 diet) were repeated at least three times, andtypical results are shown in Table 1 and Figs. 1 and 2. The CGF20 diet containing 0–1 g L-arabinose/100 g was studied once in comparison with the CS20 diet.
 
The rats were individually housed in wire-bottomed cages in a temperature-controlled room (24°C) with an automatic lighting schedule (0800–2000 h). They had free access to water and were fed equal energy-containing diets relative to body mass in all groups. The amount of diet consumed by the rats was measured at 1700 h everyday. Based on the measurement, the expected average amount of food consumed by rats fed the C, CS10, CS20 and CS30 diets containing 0–1 g L-arabinose/100 g was fed the next day. Only the rats consuming similar energy levels during the experimental period were used for the study.
 
Rats were killed by decapitation while under anesthesia with diethyl ether. An aliquot of liver was quickly removed and homogenized with three volumes of 0.25 mol sucrose/L. The liver homog-enate was centrifuged at 10,000 * g for 10 min, and then the supernatant was centrifuged at 105,000 * g for 45 min (model L5, type 40 rotor; Beckman Instruments, Palo Alto, CA). The 105,000 * g supernatant was used for measurement of lipogenic enzyme activities. Another aliquot of liver was immediately frozen in liquid nitrogen and stored at 280°C for subsequent extraction of total lipids and measurement of triacylglycerols. The care and treatment of experimental animals were in accordance with the National Institutes of Health “Guide for the Care and Use of Laboratory Animals”(8).
 
Lipogenic enzyme activities. Acetyl-CoA carboxylase (EC 6.4.1.2) activity was assayed according to the H14CO3 fixation method (9). To attain full activity, the enzyme was first preincubated with 10 mmol citrate/L. Fatty acid synthase (EC 2.3.1.85) activity was assayed according to Hsu et al. (10). Adenosine triphosphate (ATP) citrate-lyase (EC 4.1.3.8) activity was assayed as described by Takeda et al. (11). The enzyme activities in the supernatant of the liver homogenates are shown as mU/mg protein, where 1 mU is the amount that catalyzes the formation of 1 nmol product/min at 37°C. Protein was determined according to the method of Lowry et al. (12).
 
Plasma glucose and insulin analyses. Plasma glucose concentrations were determined according to the glucose-oxidase method (13). Plasma insulin concentrations were measured with a two-antibody system radioimmunoassay according to the method of Morgan and Lazarow (14).
 
Statistical analysis. For CS30, CS20, CS10 and C diets containing 0–1 g L-arabinose/100 g, two-way ANOVA was followed by an inspection of all differences between pairs of means using the least significant difference test (15). For the C diets containing 0–5 g L-arabinose/100 g, comparisons were made with the diet without arabinose by t test. The CGF20 diets containing 0–1 g L-arabinose/ 100 g were compared by t test with the no-arabinose diet and the CS20 diet containing the same amount of L-arabinose. Differences were considered significant at P 0.05.
 
RESULTS
Food intake, weights of body, adipose tissue and cecum with wet contents and cecum content pH. Changes in relative body weight [g/(100 g body ·d21)] did not differ among the groups (data not shown). Careful attention to the food consumption of rats ensured it was similar in the dietary groups. The standard deviations of relative food consumption [g/(100 g body z d)] were 3.3% of the mean values during the experimental period, except in rats fed the CS30 plus 1 g L-arabinose/100 g diet, in which food consumption was reduced to 85±1.3% of the CS30 group. However, food consumption in the CS30 plus 1 g L-arabinose/100 g group was reduced most for 3 d at the beginning of the feeding but was .90% of the CS30 group for the latter 5 d. No rats had diarrhea during the experiment.
 
The weights of epididymal adipose tissue were significantly (P0.001) reduced by L-arabinose in rats fed the diets containing sucrose (Table 1). The cecum weights including wet contents decreased (P 0.001) with increasing dietary sucrose and increased with increasing dietary L-arabinose. The pH of the cecum contents was markedly (P 0.001) lowered by L-arabinose.
 
Plasma glucose and insulin concentrations. The plasma glucose concentrations were slightly (P0.05) elevated by sucrose (Table 1) but were not affected by dietary L-arabinose. Plasma insulin concentrations were significantly lowered by L-arabinose feeding (Fig. 1).
Plasma and liver triacylglycerol concentrations. Liver
triacylglycerol concentrations were increased (P 0.001) by
dietary sucrose, and L-arabinose feeding prevented the increases
(P 0.001) (Fig. 1). Plasma triacylglycerol concentrations
were not significantly affected by dietary sucrose.
L-Arabinose feeding (P 0.01) reduced plasma triacylglycerol
concentrations.
Liver lipogenic enzyme activities. The activities of acetyl-
CoA carboxylase, fatty acid synthase and ATP citrate-lyase
were significantly (P 0.01) increased by dietary sucrose, and
these increases were prevented by dietary L-arabinose (Fig. 2,
P 0.001).
Effects of extra L-arabinose feeding in rats fed the C diet.
The lipogenic enzyme activities and the plasma and liver
triacylglycerol concentrations of rats fed the C diet were not
affected by the addition of 0.5 or 1 g L-arabinose/100 g to the
diet compared with no addition of arabinose. Therefore, the
results for rats fed the C diet containing a large amount (2 or
5 g/100 g) of L-arabinose are also shown in Table 1 and Figs.
1 and 2. The lipogenic enzyme activities and plasma and liver
triacylglycerol levels were not reduced even by the addition of
2 or 5 g arabinose/100 g to the C diet compared with no
addition of arabinose. Compared with no arabinose, however,
the epididymal adipose tissue weights were reduced by feeding
5 gL-arabinose/100 g. Moreover, the cecum weights with
contents were significantly increased, and the pH of the cecum
content was markedly lowered by feeding 2 or 5 g L-arabinose/
100 g.
Effects of L-arabinose feeding in rats fed a fructose-plusglucose
diet. Compared with not being fed arabinose, Larabinose
feeding did not affect the weights of the cecum with
wet contents in the CGF20 groups but lowered the pH of the
cecum contents. No effects of L-arabinose on plasma and liver
triacylglycerol concentrations or on liver lipogenic enzyme
activities were observed in the CGF20 groups. The weights of
epididymal adipose tissue were also not affected by L-arabinose
feeding. Plasma glucose and insulin concentrations were not
affected by L-arabinose in the CGF20 groups.
 
 
 
 
 
DISCUSSION
The concentrations of liver triacylglycerols were significantly increased with dietary sucrose. The lipogenic enzyme activities in the liver were also significantly increased with dietary sucrose. Fukuda et al. (16) previously reported that the lipogenic enzyme activities were higher of rats fed diets of (in
order) fructose sucrose a-cornstarch in both normal and diabetic states. The concentrations of the substrate (acetyl- CoA) and the activator (citrate) of acetyl-CoA carboxylase, a key enzyme of fatty acid synthesis in the livers, were significantly higher in that order. This may be one of the reasons that fructose stimulates lipogenic enzyme activities and lipogenesis. Thus, dietary sucrose is considered to be more lipogenic than starch.
In rats fed the C (no sucrose) diets containing the higher concentrations (2 or 5 g/100 g) of arabinose, the cecum with content weights were increased and the pH was acidified compared with no arabinose. Bacteria in the small intestine may ferment L-arabinose. Schutte et al. (17) found in a study with pigs that the presence of L-arabinose in the diet increased ileal flow of volatile fatty acids and lactic acid, suggesting the occurrence of microbial degradation of L-arabinose in the small
intestine.
In rats fed sucrose, the cecum with content weights were dose-dependently increased by arabinose feeding, and the pH of the cecum contents was markedly lowered. We suggest that L-arabinose inhibited the sucrase activity of intestinal mucosa and that dietary sucrose was fermented by intestinal bacteria to generate the acidic products, in addition to arabinose degradation.
Sanai et al. (6) observed the suppressive effects of L-arabinose on the increase in blood glucose after sucrose loading in rats. In the present experiment, plasma glucose concentrations were significantly increased with dietary sucrose, but the increase was not significantly suppressed by arabinose. In rats fed the CS30 diet, however, plasma glucose levels were significantly lowered by the arabinose, and plasma insulin concentrations were also lowered. The lowered insulin concentrations were possibly due to the suppression of hyperglycemia.
L-Arabinose feeding prevented the increases due to sucrose feeding in activities of lipogenic enzymes and the increases in triacylglycerol concentrations of livers. Moreover, arabinose feeding reduced the weights of adipose tissue. However, no effects of L-arabinose feeding on the increases due to fructose
plus glucose were found in rats fed the CFG20 diet. Therefore, the suppression of lipogenesis could be ascribed to the reduction in sucrose utilization due to inhibition of intestinal sucrase by L-arabinose. We previously reported that the lipogenic enzyme activities were sigmoidly increased relative to the quantity of a high sucrose diet and were greatly increased by feeding 75% of ad libitum intake (18). L-Arabinose may be useful for preventing obesity due to extreme sucrose ingestion.
 

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